http://sedici.unlp.edu.ar:80/handle/10915/73646 Sun, 08 Nov 2026 04:43:16 GMT 2026-11-08T04:43:16Z http://sedici.unlp.edu.ar:80/handle/10915/200373 Objeto de conferencia I Jornada de Divulgación en Biotecnología (La Plata, 20 y 21 de octubre de 2022); Revista digital de la 1ra Jornada de Divulgación en Biotecnología; 2022; https://sedici.unlp.edu.ar/handle/10915/155920; Libro de resúmenes del Congreso de Investigaciones Formativas IFLP – 2026 La administración de una dieta rica en fructosa (DRF) a ratas normales induce cambios endocrinometabólicos similares a los de la prediabetes (PD) humana, donde el estrés del retículo endoplasmático (RE) tendría un rol crucial. Nuestro objetivo fue estudiar el rol del estrés del RE y de la respuesta inflamatoria en la disfunción de las células β pancreáticas inducida por DRF. Para ello, ratas macho normales se alimentaron 21 días con una dieta comercial estándar y agua corriente (C), o con el mismo alimento y una solución acuosa de fructosa al 10% p/v (DRF). Al sacrificio se midieron los niveles séricos de glucosa, triglicéridos (TG), col-total, col-HDL y se calculó el índice de insulinorresistencia (IR) dado por la relación TG/col-HDL. Se extrajo el páncreas y se aislaron los islotes para medir secreción de insulina estimulada por glucosa (SIEG) y los niveles de expresión génica (qPCR) de marcadores de estrés del RE, autofagia, inflamación y apoptosis. Las ratas DRF aumentaron significativamente los niveles de TG, colnoHDL y el índice IR, y no tuvieron cambios en col-total y col-HDL. En ellas también aumentó la SIEG (con glucosa 16,7 mM) y los niveles de ARNm de los marcadores de estrés del RE (CHOP, ATF4 y XBP1s), autofagia (HSc70), apoptosis (Casp-3, Casp-12, Bcl-2 y Bad) e inflamación (TNF-α, IL-1β y PAI-1); p&lt;0,05. En conclusión, la DRF induce dislipemia, IR, sobrecarga funcional de las células β, estrés del RE, apoptosis y la respuesta inflamatoria, contribuyendo a promover la disfunción y disminución de la masa de células β. Una alternativa prometedora para desarrollar nuevas herramientas terapéuticas de prevención y tratamiento de la DT2 podría ser la atenuación del estrés del RE a través de chaperonas químicas. Sat, 01 Jan 2022 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/200373 2022-01-01T00:00:00Z La administración de una dieta rica en fructosa (DRF) a ratas normales induce cambios endocrinometabólicos similares a los de la prediabetes (PD) humana, donde el estrés del retículo endoplasmático (RE) tendría un rol crucial. Nuestro objetivo fue estudiar el rol del estrés del RE y de la respuesta inflamatoria en la disfunción de las células β pancreáticas inducida por DRF. Para ello, ratas macho normales se alimentaron 21 días con una dieta comercial estándar y agua corriente (C), o con el mismo alimento y una solución acuosa de fructosa al 10% p/v (DRF). Al sacrificio se midieron los niveles séricos de glucosa, triglicéridos (TG), col-total, col-HDL y se calculó el índice de insulinorresistencia (IR) dado por la relación TG/col-HDL. Se extrajo el páncreas y se aislaron los islotes para medir secreción de insulina estimulada por glucosa (SIEG) y los niveles de expresión génica (qPCR) de marcadores de estrés del RE, autofagia, inflamación y apoptosis. Las ratas DRF aumentaron significativamente los niveles de TG, colnoHDL y el índice IR, y no tuvieron cambios en col-total y col-HDL. En ellas también aumentó la SIEG (con glucosa 16,7 mM) y los niveles de ARNm de los marcadores de estrés del RE (CHOP, ATF4 y XBP1s), autofagia (HSc70), apoptosis (Casp-3, Casp-12, Bcl-2 y Bad) e inflamación (TNF-α, IL-1β y PAI-1); p&lt;0,05. En conclusión, la DRF induce dislipemia, IR, sobrecarga funcional de las células β, estrés del RE, apoptosis y la respuesta inflamatoria, contribuyendo a promover la disfunción y disminución de la masa de células β. Una alternativa prometedora para desarrollar nuevas herramientas terapéuticas de prevención y tratamiento de la DT2 podría ser la atenuación del estrés del RE a través de chaperonas químicas. http://sedici.unlp.edu.ar:80/handle/10915/195369 Articulo Magnetochemistry; vol. 12, no. 2 In this work, we evaluate the efficiency of a DNA purification protocol from gynecological samples using locally synthesized Fe3 O4 @SiO2 magnetic microparticles and a low-cost, guanidinium thiocyanate (GITC)-free lysis buffer. The microparticles were characterized by SEM, EDS, FTIR, and magnetic measurements, confirming the formation of compact silica- coated aggregates with suitable magnetic responsiveness for rapid and complete capture. Using this material in combination with a simple, GITC-free lysis buffer, we achieved DNA extraction yields comparable to those obtained with standard methods based on chaotropic salts. The purified DNA showed high compatibility with molecular assays for the detection of Chlamydia trachomatis, Ureaplasma urealyticum, Mycoplasma hominis, and human papilloma virus. Clinical validation demonstrated excellent diagnostic performance, with only a few discrepancies observed in samples near the detection threshold of qPCR, a limitation shared with commercial kits. Overall, the method represents a low-cost, safe, and sustainable alternative for routine clinical and epidemiological applications, compared to methods based on chaotropic salt buffers. Furthermore, it reduces reliance on imported commercial consumables and minimizes the handling of hazardous reagents. Thu, 01 Jan 2026 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/195369 2026-01-01T00:00:00Z In this work, we evaluate the efficiency of a DNA purification protocol from gynecological samples using locally synthesized Fe3 O4 @SiO2 magnetic microparticles and a low-cost, guanidinium thiocyanate (GITC)-free lysis buffer. The microparticles were characterized by SEM, EDS, FTIR, and magnetic measurements, confirming the formation of compact silica- coated aggregates with suitable magnetic responsiveness for rapid and complete capture. Using this material in combination with a simple, GITC-free lysis buffer, we achieved DNA extraction yields comparable to those obtained with standard methods based on chaotropic salts. The purified DNA showed high compatibility with molecular assays for the detection of Chlamydia trachomatis, Ureaplasma urealyticum, Mycoplasma hominis, and human papilloma virus. Clinical validation demonstrated excellent diagnostic performance, with only a few discrepancies observed in samples near the detection threshold of qPCR, a limitation shared with commercial kits. Overall, the method represents a low-cost, safe, and sustainable alternative for routine clinical and epidemiological applications, compared to methods based on chaotropic salt buffers. Furthermore, it reduces reliance on imported commercial consumables and minimizes the handling of hazardous reagents. http://sedici.unlp.edu.ar:80/handle/10915/193797 Articulo Cell Death and Disease; vol. 16, art. 744 Pancreatic β-cells fine-tune glucose homeostasis through insulin secretion. The endoplasmic reticulum (ER) is critical for insulin production, relying on the unfolded protein response (UPR) to adapt to the body's fluctuating demands. Islets from both type 1 (T1D) and type 2 diabetes (T2D) exhibit inflammation, β-cell dysfunction, and loss. ER stress is present in the inflamed islets of autoimmune diabetes-prone mice and individuals with T1D and T2D. Inflammatory cytokines induce ER stress and disrupt UPR regulation, driving β-cell apoptosis and contributing to diabetes development. Inflammatory cytokines, e.g., IL-1β, impair β-cell function and survival, contributing to diabetes pathogenesis by inducing stress, altering gene expression, driving dedifferentiation, and reducing insulin production. Paradoxically, β-cells exhibit a high density of IL-1R1, and IL-1R1/KO mice display impaired glucose tolerance and reduced insulin secretion. Postprandial IL-1β secreted by macrophages helps maintain blood glucose homeostasis. These observations suggest that circulating low IL-1β concentrations may have physiologically relevant roles; however, their effects on β-cell function and survival remain unclear due to conflicting reports. Preconditioning β-cells with physiological circulating levels of IL-1β (IL-1β^low) induced a resilient state, protecting them from pro-inflammatory cytokine (CYT)-induced cell death while preserving glucose-stimulated insulin secretion through hormesis. IL-1β^low-treated INS-1E cells reduced CYT-induced NO secretion by suppressing NF-κB signaling and decreasing iNOS expression, correlating with reduced β-cell death. IL-1β^low conditioning reduced ER stress and upregulated p-eIF2α in response to CYT, thereby enhancing the expression of ER chaperones and biomarkers linked to improved β-cell identity/functionality. Transcriptomic analysis revealed that IL-1β^low preconditioning mitigated the CYT-induced loss of genes involved in β-cell function/identity, and suppressed the expression of genes linked to NF-κB signaling, cytokine-induced inflammation, and apoptosis. IL-1β^low treatment counteracted the upregulation of stress-related genes triggered by pro-inflammatory stimuli. Enhancing IL-1β^low-induced stress-response hormesis may provide a novel strategy to sustain β-cell function and survival during harmful diabetic inflammation. Tue, 21 Oct 2025 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/193797 2025-10-21T00:00:00Z Pancreatic β-cells fine-tune glucose homeostasis through insulin secretion. The endoplasmic reticulum (ER) is critical for insulin production, relying on the unfolded protein response (UPR) to adapt to the body's fluctuating demands. Islets from both type 1 (T1D) and type 2 diabetes (T2D) exhibit inflammation, β-cell dysfunction, and loss. ER stress is present in the inflamed islets of autoimmune diabetes-prone mice and individuals with T1D and T2D. Inflammatory cytokines induce ER stress and disrupt UPR regulation, driving β-cell apoptosis and contributing to diabetes development. Inflammatory cytokines, e.g., IL-1β, impair β-cell function and survival, contributing to diabetes pathogenesis by inducing stress, altering gene expression, driving dedifferentiation, and reducing insulin production. Paradoxically, β-cells exhibit a high density of IL-1R1, and IL-1R1/KO mice display impaired glucose tolerance and reduced insulin secretion. Postprandial IL-1β secreted by macrophages helps maintain blood glucose homeostasis. These observations suggest that circulating low IL-1β concentrations may have physiologically relevant roles; however, their effects on β-cell function and survival remain unclear due to conflicting reports. Preconditioning β-cells with physiological circulating levels of IL-1β (IL-1β^low) induced a resilient state, protecting them from pro-inflammatory cytokine (CYT)-induced cell death while preserving glucose-stimulated insulin secretion through hormesis. IL-1β^low-treated INS-1E cells reduced CYT-induced NO secretion by suppressing NF-κB signaling and decreasing iNOS expression, correlating with reduced β-cell death. IL-1β^low conditioning reduced ER stress and upregulated p-eIF2α in response to CYT, thereby enhancing the expression of ER chaperones and biomarkers linked to improved β-cell identity/functionality. Transcriptomic analysis revealed that IL-1β^low preconditioning mitigated the CYT-induced loss of genes involved in β-cell function/identity, and suppressed the expression of genes linked to NF-κB signaling, cytokine-induced inflammation, and apoptosis. IL-1β^low treatment counteracted the upregulation of stress-related genes triggered by pro-inflammatory stimuli. Enhancing IL-1β^low-induced stress-response hormesis may provide a novel strategy to sustain β-cell function and survival during harmful diabetic inflammation. http://sedici.unlp.edu.ar:80/handle/10915/167349 Articulo International Journal of Molecular Sciences; vol. 25, no. 2 The aim of this work was to evaluate possible mechanisms involved in the protective effect of N-acetyl-L-cysteine (NAC) on hepatic endocrine-metabolic, oxidative stress, and inflammatory changes in prediabetic rats. For that, normal male Wistar rats (60 days old) were fed for 21 days with 10% sucrose in their drinking water and 5 days of NAC administration (50 mg/kg, i.p.) and thereafter, we determined: serum glucose, insulin, transaminases, uric acid, and triglyceride levels; hepatic fructokinase and glucokinase activities, glycogen content, lipogenic gene expression; enzymatic and non-enzymatic oxidative stress, insulin signaling pathway, and inflammatory markers. Results showed that alterations evinced in sucrose-fed rats (hypertriglyceridemia, hyperinsulinemia, and high liver fructokinase activity together with increased liver lipogenic gene expression and oxidative stress and inflammatory markers) were prevented by NAC administration. P-endothelial nitric oxide synthase (P-eNOS)/eNOS and pAKT/AKT ratios, decreased by sucrose ingestion, were restored after NAC treatment. In conclusion, the results suggest that NAC administration improves glucose homeostasis, oxidative stress, and inflammation in prediabetic rats probably mediated by modulation of the AKT/NOS pathway. Administration of NAC may be an effective complementary strategy to alleviate or prevent oxidative stress and inflammatory responses observed in type 2 diabetes at early stages of its development (prediabetes). Mon, 01 Jan 2024 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/167349 2024-01-01T00:00:00Z The aim of this work was to evaluate possible mechanisms involved in the protective effect of N-acetyl-L-cysteine (NAC) on hepatic endocrine-metabolic, oxidative stress, and inflammatory changes in prediabetic rats. For that, normal male Wistar rats (60 days old) were fed for 21 days with 10% sucrose in their drinking water and 5 days of NAC administration (50 mg/kg, i.p.) and thereafter, we determined: serum glucose, insulin, transaminases, uric acid, and triglyceride levels; hepatic fructokinase and glucokinase activities, glycogen content, lipogenic gene expression; enzymatic and non-enzymatic oxidative stress, insulin signaling pathway, and inflammatory markers. Results showed that alterations evinced in sucrose-fed rats (hypertriglyceridemia, hyperinsulinemia, and high liver fructokinase activity together with increased liver lipogenic gene expression and oxidative stress and inflammatory markers) were prevented by NAC administration. P-endothelial nitric oxide synthase (P-eNOS)/eNOS and pAKT/AKT ratios, decreased by sucrose ingestion, were restored after NAC treatment. In conclusion, the results suggest that NAC administration improves glucose homeostasis, oxidative stress, and inflammation in prediabetic rats probably mediated by modulation of the AKT/NOS pathway. Administration of NAC may be an effective complementary strategy to alleviate or prevent oxidative stress and inflammatory responses observed in type 2 diabetes at early stages of its development (prediabetes). http://sedici.unlp.edu.ar:80/handle/10915/164889 Objeto de conferencia XXIX Congreso Argentino de Ciencias de la Computación (CACIC) (Luján, 9 al 12 de octubre de 2023); https://sedici.unlp.edu.ar/handle/10915/163107; Libro de actas - XXIX Congreso Argentino de Ciencias de la Computación - CACIC 2023 La detección de Diabetes Tipo 2 (DT2) y prediabetes (PDM) representa un verdadero desafío para la medicina debido a la ausencia de síntomas patogenómicos y a la falta de conocimiento de los factores de riesgo asociados. Si bien existen algunas propuestas de modelos de aprendizaje automático que permiten identificar a personas en riesgo, las características de esta enfermedad hacen que uno que resulte adecuado para una población, no necesariamente lo sea para otra. Este artículo propone desarrollar y evaluar modelos predictivos que permitan identificar personas con riesgo de DT2 y PDM específicos para la población argentina. Partiendo de un cuidadoso preprocesamiento de la base de datos, se generaron dos datasets particulares considerando el compromiso entre cantidad de registros y de variables disponibles. Luego de aplicar 5 diferentes modelos de clasificación, los resultados obtenidos muestran que algunos de ellos obtuvieron muy buenos rendimientos para ambos datasets. En particular, RF, DT y ANN demostraron gran poder de clasificación, con altos valores en las métricas consideradas. Considerando la vacancia de herramientas de este tipo para la población argentina, este trabajo representa el primer paso hacia modelos más sofisticados. Mon, 01 Jan 2024 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/164889 2024-01-01T00:00:00Z La detección de Diabetes Tipo 2 (DT2) y prediabetes (PDM) representa un verdadero desafío para la medicina debido a la ausencia de síntomas patogenómicos y a la falta de conocimiento de los factores de riesgo asociados. Si bien existen algunas propuestas de modelos de aprendizaje automático que permiten identificar a personas en riesgo, las características de esta enfermedad hacen que uno que resulte adecuado para una población, no necesariamente lo sea para otra. Este artículo propone desarrollar y evaluar modelos predictivos que permitan identificar personas con riesgo de DT2 y PDM específicos para la población argentina. Partiendo de un cuidadoso preprocesamiento de la base de datos, se generaron dos datasets particulares considerando el compromiso entre cantidad de registros y de variables disponibles. Luego de aplicar 5 diferentes modelos de clasificación, los resultados obtenidos muestran que algunos de ellos obtuvieron muy buenos rendimientos para ambos datasets. En particular, RF, DT y ANN demostraron gran poder de clasificación, con altos valores en las métricas consideradas. Considerando la vacancia de herramientas de este tipo para la población argentina, este trabajo representa el primer paso hacia modelos más sofisticados. http://sedici.unlp.edu.ar:80/handle/10915/162061 Articulo Pharmaceuticals; vol. 17, no. 1 A high-fructose diet (HFD) induces murine alterations like those recorded in human prediabetes. Protective effects of isoespintanol (monoterpene isolated from Oxandra cf. xylopioides) on changes induced by HFD were evaluated. Animals were maintained for 21 days with a standard diet (C), 10% fructose (F), and F plus isoespintanol (FI, 10 mg/kg, i.p.). Glycemia, triglyceridemia, total and HDL-cholesterol, and insulin resistance index (IRX) were determined. Intraperitoneal glucose tolerance test (IGTT) was performed. In the liver, we measured glycogen, lipogenic gene expression (SREBP-1c, GPAT, FAS, and CPT1), oxidative stress (GSH and 3′-nitrotyrosine content), inflammation markers (iNOS, TNF-α, and PAI-1 gene expression; iNOS and COX-2 protein levels), p-eNOS, p-Akt, and p-GSK3β protein levels. Isoespintanol corrected enhanced triglycerides, lipogenic genes, and IRX, and reduced HDL-cholesterol induced by HFD. Increased liver glycogen and inflammatory markers and decreased GSH, p-Akt, and p-GSK3β measured in F rats were reversed by isoespintanol, and p-eNOS/e-NOS and iNOS/GADPH ratios were normalized. Isoespintanol restored glucose tolerance (IGTT) compared to F rats. These results demonstrate for the first time that isoespintanol prevents endocrine–metabolic alterations induced by HFD in prediabetic rats. These effects could be mediated by Akt/eNOS and Akt/GSK3β pathways, suggesting its possible use as a therapeutic tool for the prevention of diabetes at early stages of its development (prediabetes). Thu, 28 Dec 2023 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/162061 2023-12-28T00:00:00Z A high-fructose diet (HFD) induces murine alterations like those recorded in human prediabetes. Protective effects of isoespintanol (monoterpene isolated from Oxandra cf. xylopioides) on changes induced by HFD were evaluated. Animals were maintained for 21 days with a standard diet (C), 10% fructose (F), and F plus isoespintanol (FI, 10 mg/kg, i.p.). Glycemia, triglyceridemia, total and HDL-cholesterol, and insulin resistance index (IRX) were determined. Intraperitoneal glucose tolerance test (IGTT) was performed. In the liver, we measured glycogen, lipogenic gene expression (SREBP-1c, GPAT, FAS, and CPT1), oxidative stress (GSH and 3′-nitrotyrosine content), inflammation markers (iNOS, TNF-α, and PAI-1 gene expression; iNOS and COX-2 protein levels), p-eNOS, p-Akt, and p-GSK3β protein levels. Isoespintanol corrected enhanced triglycerides, lipogenic genes, and IRX, and reduced HDL-cholesterol induced by HFD. Increased liver glycogen and inflammatory markers and decreased GSH, p-Akt, and p-GSK3β measured in F rats were reversed by isoespintanol, and p-eNOS/e-NOS and iNOS/GADPH ratios were normalized. Isoespintanol restored glucose tolerance (IGTT) compared to F rats. These results demonstrate for the first time that isoespintanol prevents endocrine–metabolic alterations induced by HFD in prediabetic rats. These effects could be mediated by Akt/eNOS and Akt/GSK3β pathways, suggesting its possible use as a therapeutic tool for the prevention of diabetes at early stages of its development (prediabetes). http://sedici.unlp.edu.ar:80/handle/10915/160006 Articulo Plants; vol. 12, no. 14 “Yerba mate” (YM), an aqueous extract of Ilex paraguariensis, has antioxidant, diuretic, cardio-protective and hypoglycaemic properties. Since its effect on the pancreatic islets remains unclear, we evaluated insulin sensitivity and glucose-stimulated insulin secretion (GSIS) in rats consuming YM or tap water (C) for 21 days. Glucose tolerance, glycemia, triglyceridemia, insulinemia, TBARS and FRAP serum levels were evaluated. GSIS and mRNA levels of insulin signaling pathway and inflammatory markers were measured in isolated pancreatic islets from both groups. In C rats, islets were incubated with YM extract or its phenolic components to measure GSIS. YM improved glucose tolerance, enhanced GSIS, increased FRAP plasma levels and islet mRNA levels of IRS-1 and PI3K (p110), and decreased TBARS plasma levels and islet gene expression of TNF-α and PAI-1. Islets from C rats incubated with 100 µg/mL dry YM extract, 1 µM chlorogenic acid, 0.1 and 1 µM rutin, 1 µM caffeic acid or 1 µM quercetin showed an increase in GSIS. Our results suggest that YM enhances glucose tolerance because of its positive effects on GSIS, oxidative stress rate and insulin sensitivity in rat islets, suggesting that long-term dietary supplementation with YM may improve glucose homeostasis in pre-diabetes or type 2 diabetes. Sun, 01 Jan 2023 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/160006 2023-01-01T00:00:00Z “Yerba mate” (YM), an aqueous extract of Ilex paraguariensis, has antioxidant, diuretic, cardio-protective and hypoglycaemic properties. Since its effect on the pancreatic islets remains unclear, we evaluated insulin sensitivity and glucose-stimulated insulin secretion (GSIS) in rats consuming YM or tap water (C) for 21 days. Glucose tolerance, glycemia, triglyceridemia, insulinemia, TBARS and FRAP serum levels were evaluated. GSIS and mRNA levels of insulin signaling pathway and inflammatory markers were measured in isolated pancreatic islets from both groups. In C rats, islets were incubated with YM extract or its phenolic components to measure GSIS. YM improved glucose tolerance, enhanced GSIS, increased FRAP plasma levels and islet mRNA levels of IRS-1 and PI3K (p110), and decreased TBARS plasma levels and islet gene expression of TNF-α and PAI-1. Islets from C rats incubated with 100 µg/mL dry YM extract, 1 µM chlorogenic acid, 0.1 and 1 µM rutin, 1 µM caffeic acid or 1 µM quercetin showed an increase in GSIS. Our results suggest that YM enhances glucose tolerance because of its positive effects on GSIS, oxidative stress rate and insulin sensitivity in rat islets, suggesting that long-term dietary supplementation with YM may improve glucose homeostasis in pre-diabetes or type 2 diabetes. http://sedici.unlp.edu.ar:80/handle/10915/159808 Articulo Life Sciences; vol. 322 Aim: Glucocorticoids (GCs) play a crucial role in energy homeostasis including white adipose tissue function; however, chronic GC excess is detrimental to mammals' health. White hypertrophic adiposity is a main factor for neuroendocrine-metabolic dysfunctions in monosodium L-glutamate (MSG)-damaged hypercorticosteronemic rat. Nevertheless, little is known about the receptor path in endogenous GC impact on white adipose tissueresident precursor cells to bring them into beige lineage. Thus, our aim was to explore whether transient/ chronic endogenous hypercorticosteronemia affects browning capacity in white adipose tissue pads from MSG rats during development. Main methods: Control and MSG male rats aged 30 and 90 days were 7-day exposed to cold conditions in order to stimulate wet white epidydimal adipose tissue (wEAT) beiging capacity. This procedure was also replicated in adrenalectomized rats. Key findings: Data indicated that whereas epidydimal white adipose tissue pads from prepubertal hypercorticosteronemic rats retained full expression of GR/MR genes resulting in a drastic reduction in wEAT beiging capacity, conversely, chronic hypercorticosteronemic adult MSG rats developed down-regulation of corticoid genes (and reduced GR cytosolic mediators) in wEAT pads and consequently partially restored local beiging capacity. Finally, wEAT pads from adrenalectomized rats revealed up-regulation of GR gene accompanied by full local beiging capacity. Significance: This study strongly supports a GR-dependent inhibitory effect of GC excess on white adipose tissue browning, an issue strongly supporting a key role of GR in the non-shivering thermogenic process. As a consequence, normalizing the GC milieu could be a relevant factor to handle dysmetabolism in white hyperadipose phenotypes. Sun, 01 Jan 2023 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/159808 2023-01-01T00:00:00Z Aim: Glucocorticoids (GCs) play a crucial role in energy homeostasis including white adipose tissue function; however, chronic GC excess is detrimental to mammals' health. White hypertrophic adiposity is a main factor for neuroendocrine-metabolic dysfunctions in monosodium L-glutamate (MSG)-damaged hypercorticosteronemic rat. Nevertheless, little is known about the receptor path in endogenous GC impact on white adipose tissueresident precursor cells to bring them into beige lineage. Thus, our aim was to explore whether transient/ chronic endogenous hypercorticosteronemia affects browning capacity in white adipose tissue pads from MSG rats during development. Main methods: Control and MSG male rats aged 30 and 90 days were 7-day exposed to cold conditions in order to stimulate wet white epidydimal adipose tissue (wEAT) beiging capacity. This procedure was also replicated in adrenalectomized rats. Key findings: Data indicated that whereas epidydimal white adipose tissue pads from prepubertal hypercorticosteronemic rats retained full expression of GR/MR genes resulting in a drastic reduction in wEAT beiging capacity, conversely, chronic hypercorticosteronemic adult MSG rats developed down-regulation of corticoid genes (and reduced GR cytosolic mediators) in wEAT pads and consequently partially restored local beiging capacity. Finally, wEAT pads from adrenalectomized rats revealed up-regulation of GR gene accompanied by full local beiging capacity. Significance: This study strongly supports a GR-dependent inhibitory effect of GC excess on white adipose tissue browning, an issue strongly supporting a key role of GR in the non-shivering thermogenic process. As a consequence, normalizing the GC milieu could be a relevant factor to handle dysmetabolism in white hyperadipose phenotypes. http://sedici.unlp.edu.ar:80/handle/10915/156981 Articulo HemaSphere; vol. 6, supl. 3 The aim of the study was to estimate the cost-effectiveness of VenG in the treatment of first-line unfit CLL patients in Argentina. XXVII Congress of the European Hematology Association (Viena, 9 al 17 de junio de 2022) Wed, 01 Jun 2022 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/156981 2022-06-01T00:00:00Z The aim of the study was to estimate the cost-effectiveness of VenG in the treatment of first-line unfit CLL patients in Argentina. http://sedici.unlp.edu.ar:80/handle/10915/145237 Articulo Cell and Tissue Research; vol. 201, no. 1 The ultrastructural changes in pancreatic β cells were studied following glucose-induced insulin secretion in vitro, at two different extracellular pH (7.4 and 7.8). The pancreata perfused at pH 7.4 exhibited a biphasic insulin response to glucose challenge together with signs of increased emiocytotic activity and numerous microtubules in the β cells. Conversely, the pancreata perfused at pH 7.8 showed a significant decrease in insulin secretion, and their β cells revealed scarce emiocytotic images and a marked increase of intracellular granulolysis. These results represent the ultrastructural correlate of the reduced insulin secretion produced by metabolic alkalosis in the perfused rat pancreas. Sun, 02 Sep 1979 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/145237 1979-09-02T00:00:00Z The ultrastructural changes in pancreatic β cells were studied following glucose-induced insulin secretion in vitro, at two different extracellular pH (7.4 and 7.8). The pancreata perfused at pH 7.4 exhibited a biphasic insulin response to glucose challenge together with signs of increased emiocytotic activity and numerous microtubules in the β cells. Conversely, the pancreata perfused at pH 7.8 showed a significant decrease in insulin secretion, and their β cells revealed scarce emiocytotic images and a marked increase of intracellular granulolysis. These results represent the ultrastructural correlate of the reduced insulin secretion produced by metabolic alkalosis in the perfused rat pancreas. http://sedici.unlp.edu.ar:80/handle/10915/144137 Articulo Diabetologia; vol. 26, no. 4 Localization and quantification of calcium pyroantimonate precipitates within the B cells, and determination of insulin secretion were performed in rat pancreas perfused with 3.3 and 16.6 mmol/l glucose. Observations were carried out during the peak, the refractory period, and at 10 and 20 min in the second phase of glucose secretion after the start of a glucose challenge. Specific calcium pyroantimonate precipitates, assessed by EGTA cross-incubation, appeared attached to plasma membrane, Golgi complex, mitochondria, cytoplasmic matrix and secretory granules. The total number of cellular calcium pyroantimonate precipitates increased with perfusion time, being significantly higher at every time-point with the higher concentration of glucose (16.6 mmol/l) than with the 3.3 mmol/l glucose concentration. Calcium pyroantimonate precipitates showed a progressive increment both in plasma membranes and mitochondria. In the cytoplasmic matrix, B granules and Golgi complex, a sharp increase in the number of precipitates was detected at the refractory period, followed by a continuous decrease until the end of the experiment. These results show that the number of calcium pyroantimonate precipitates, localized in different organelles, changes according to the functional state of B cells. They stress the importance of intracellular readily exchangeable pools as regulators of calcium availability for insulin stimulus-secretion coupling. Sun, 01 Jan 1984 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/144137 1984-01-01T00:00:00Z Localization and quantification of calcium pyroantimonate precipitates within the B cells, and determination of insulin secretion were performed in rat pancreas perfused with 3.3 and 16.6 mmol/l glucose. Observations were carried out during the peak, the refractory period, and at 10 and 20 min in the second phase of glucose secretion after the start of a glucose challenge. Specific calcium pyroantimonate precipitates, assessed by EGTA cross-incubation, appeared attached to plasma membrane, Golgi complex, mitochondria, cytoplasmic matrix and secretory granules. The total number of cellular calcium pyroantimonate precipitates increased with perfusion time, being significantly higher at every time-point with the higher concentration of glucose (16.6 mmol/l) than with the 3.3 mmol/l glucose concentration. Calcium pyroantimonate precipitates showed a progressive increment both in plasma membranes and mitochondria. In the cytoplasmic matrix, B granules and Golgi complex, a sharp increase in the number of precipitates was detected at the refractory period, followed by a continuous decrease until the end of the experiment. These results show that the number of calcium pyroantimonate precipitates, localized in different organelles, changes according to the functional state of B cells. They stress the importance of intracellular readily exchangeable pools as regulators of calcium availability for insulin stimulus-secretion coupling. http://sedici.unlp.edu.ar:80/handle/10915/143741 Articulo Molecular Diagnosis; vol. 8, no. 1 Background: The different clinical presentations of latent autoimmune diabetes in adults (LADA) and type 1 diabetes mellitus may be the result of susceptibility genes in determining the mode of onset. We analyzed the 5′ polymorphisms of the insulin mini-satellite region (INS), a variable number of tandem repeats (VNTR) [repeat units; RU]. We evaluated the association of the different INS-VNTR alleles in patient susceptibility to LADA autoimmune diabetes. To our knowledge, this constitutes the first study of this kind performed in a Caucasian population. Methods: From an group of 160 Argentinean patients previously characterized as having LADA, we selected 44 patients who presented with humoral autoimmunity for genotyping and compared them to 88 patients with type 1 diabetes and 138 healthy individuals. The INS-VNTR allele classes were determined by Southern blotting (class I: 21–44RU; class III: 138–159RU). Subjects with class I alleles were further studied using PCR amplification to determine the exact length of the alleles (short 1S: 22–37RU; medium 1M: 38–41RU; large 1L: 42–43RU). Allelic and genotype frequencies were estimated by χ2 tests for independence with 2 × 2 contingency tables and the relative risks (RR) were determined using GraphPad InStat software. Results: We observed differential associations among the class I alleles when comparing patients with LADA (80.6%) and type 1 diabetes (81.3%) with the controls (70%; p < 0.005). This increase was largely due to the high frequency of the 1S/S genotype (63.6% LADA vs 37% controls, with a p-value of 0.0019 [p1]; 53.4% type 1 diabetes vs 37% controls, with a p-value of 0.0149 [p2]). Remarkably, all LADA patients genotyped as class I homozygous had the shorter (S) class I allele (100%). Differences in the overall 1S distribution were observed: in LADA the 94.4% of the alleles were equal to or smaller than 35RU, while in patients with type 1 diabetes it was 78.3% and in controls 74.1%. Moreover, the relative risks associated with the 1S/S genotype for patients with LADA showed a substantial increase with respect to those with type 1 diabetes (52%) when we compare them to the controls (1S/S LADA/control, 2.282 [RR1] vs type 1 diabetes/control, 1.497 [RR2]). Conclusion: The presence of the 1S allele could be considered a risk factor in LADA patients, as previously reported for type 1 diabetes. The class I INS-VNTR allele in LADA increases genetic susceptibility to disease development. Thu, 01 Jan 2004 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/143741 2004-01-01T00:00:00Z Background: The different clinical presentations of latent autoimmune diabetes in adults (LADA) and type 1 diabetes mellitus may be the result of susceptibility genes in determining the mode of onset. We analyzed the 5′ polymorphisms of the insulin mini-satellite region (INS), a variable number of tandem repeats (VNTR) [repeat units; RU]. We evaluated the association of the different INS-VNTR alleles in patient susceptibility to LADA autoimmune diabetes. To our knowledge, this constitutes the first study of this kind performed in a Caucasian population. Methods: From an group of 160 Argentinean patients previously characterized as having LADA, we selected 44 patients who presented with humoral autoimmunity for genotyping and compared them to 88 patients with type 1 diabetes and 138 healthy individuals. The INS-VNTR allele classes were determined by Southern blotting (class I: 21–44RU; class III: 138–159RU). Subjects with class I alleles were further studied using PCR amplification to determine the exact length of the alleles (short 1S: 22–37RU; medium 1M: 38–41RU; large 1L: 42–43RU). Allelic and genotype frequencies were estimated by χ2 tests for independence with 2 × 2 contingency tables and the relative risks (RR) were determined using GraphPad InStat software. Results: We observed differential associations among the class I alleles when comparing patients with LADA (80.6%) and type 1 diabetes (81.3%) with the controls (70%; p < 0.005). This increase was largely due to the high frequency of the 1S/S genotype (63.6% LADA vs 37% controls, with a p-value of 0.0019 [p1]; 53.4% type 1 diabetes vs 37% controls, with a p-value of 0.0149 [p2]). Remarkably, all LADA patients genotyped as class I homozygous had the shorter (S) class I allele (100%). Differences in the overall 1S distribution were observed: in LADA the 94.4% of the alleles were equal to or smaller than 35RU, while in patients with type 1 diabetes it was 78.3% and in controls 74.1%. Moreover, the relative risks associated with the 1S/S genotype for patients with LADA showed a substantial increase with respect to those with type 1 diabetes (52%) when we compare them to the controls (1S/S LADA/control, 2.282 [RR1] vs type 1 diabetes/control, 1.497 [RR2]). Conclusion: The presence of the 1S allele could be considered a risk factor in LADA patients, as previously reported for type 1 diabetes. The class I INS-VNTR allele in LADA increases genetic susceptibility to disease development. http://sedici.unlp.edu.ar:80/handle/10915/143263 Articulo Cell and Tissue Research; vol. 206, no. 2 The ultrastructural changes induced by partial hepatectomy in the STH cells of mice were examined. These changes suggest an increased secretory activity of STH cells. Therefore, several experimental procedures elucidating the possible mechanism of this effect were undertaken. Normal mice were starved for 52 h or treated with insulin, glucagon, or cAMP. Serum glucose level measurements as well as electron microscopy of pituitary STH cells were carried out in each group of animals. It was found that STH cells of glucagon and cAMP-treated mice showed some of the ultrastructural features observed in partially hepatectomized animals. Tue, 01 Jan 1980 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/143263 1980-01-01T00:00:00Z The ultrastructural changes induced by partial hepatectomy in the STH cells of mice were examined. These changes suggest an increased secretory activity of STH cells. Therefore, several experimental procedures elucidating the possible mechanism of this effect were undertaken. Normal mice were starved for 52 h or treated with insulin, glucagon, or cAMP. Serum glucose level measurements as well as electron microscopy of pituitary STH cells were carried out in each group of animals. It was found that STH cells of glucagon and cAMP-treated mice showed some of the ultrastructural features observed in partially hepatectomized animals. http://sedici.unlp.edu.ar:80/handle/10915/142726 Articulo International Journal of Clinical Practice; vol. 73, no. 4, e13336 Aims: to examine the relationship between costs of hyperglycemia drug treatment and glycemic control among people with type 2 diabetes (T2D). Methods: This observational study utilized data from the QUALIDIAB database on 3,452 T2D patients seen in Diabetes Centers in Argentina. Patients were classified according to their HbA1c value into two groups: On Target (OT; HbA1c≤7%), and Not on Target (NOT; HbA1c>7%); within each category we considered clinical and metabolic indicators, as well as type of hyperglycemia treatment. Monthly expenditure on drugs was estimated by micro‐costing. Multivariable regression analysis was used to evaluate the association between cost of hyperglycemia treatment and HbA1c values. Results: 48.9% of the participants have HbA1c on target values. Overall monthly per capita costs of this treatment increased significantly (134%) in the NOT group. Multivariable regression analysis showed that expenditure for hyperglycemia drugs treatment was significant associated with glycemic control (OR:0.705), diabetes duration (OR:1.017), systolic blood pressure (OR:1.006), and treatment of T2D (OR:2.622). Conclusions: HbA1c not on target significantly increases drugs monthly cost of hyperglycemia treatment in people with T2D in a country with an emerging market economy. This article is protected by copyright. All rights reserved. Fri, 15 Feb 2019 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/142726 2019-02-15T00:00:00Z Aims: to examine the relationship between costs of hyperglycemia drug treatment and glycemic control among people with type 2 diabetes (T2D). Methods: This observational study utilized data from the QUALIDIAB database on 3,452 T2D patients seen in Diabetes Centers in Argentina. Patients were classified according to their HbA1c value into two groups: On Target (OT; HbA1c≤7%), and Not on Target (NOT; HbA1c>7%); within each category we considered clinical and metabolic indicators, as well as type of hyperglycemia treatment. Monthly expenditure on drugs was estimated by micro‐costing. Multivariable regression analysis was used to evaluate the association between cost of hyperglycemia treatment and HbA1c values. Results: 48.9% of the participants have HbA1c on target values. Overall monthly per capita costs of this treatment increased significantly (134%) in the NOT group. Multivariable regression analysis showed that expenditure for hyperglycemia drugs treatment was significant associated with glycemic control (OR:0.705), diabetes duration (OR:1.017), systolic blood pressure (OR:1.006), and treatment of T2D (OR:2.622). Conclusions: HbA1c not on target significantly increases drugs monthly cost of hyperglycemia treatment in people with T2D in a country with an emerging market economy. This article is protected by copyright. All rights reserved. http://sedici.unlp.edu.ar:80/handle/10915/139527 Articulo Diabetes Care; vol. 44, no. 5 Objetive: Depression is common in people with diabetes, but data from developing countries are scarce. We evaluated the prevalence and risk factors for depressive symptoms in patients with diabetes using data from the International Diabetes Management Practices Study (IDMPS). Research and methods: IDMPS is an ongoing multinational, cross-sectional study investigating quality of care in patients with diabetes in real-world settings. Data from wave 5 (2011), including 21 countries, were analyzed using the 9-item Patient Health Questionnaire (PHQ-9) to evaluate depressive symptoms. Logistic regression analyses were conducted to identify risk factors of depressive symptoms. Results: Of 9,865 patients eligible for analysis, 2,280 had type 1 and 7,585 had type 2 diabetes (treatment: oral glucose-lowering drugs [OGLD] only, n = 4,729; OGLDs plus insulin, n = 1,892; insulin only, n = 964). Depressive symptoms (PHQ-9 score ≥5) were reported in 30.7% of those with type 1 diabetes. In patients with type 2 diabetes, the respective figures were 29.0% for OGLDs-only, 36.6% for OGLDs-plus-insulin, and 46.7% for insulin-only subgroups. Moderate depressive symptoms (PHQ-9 score 10–19) were observed in 8–16% of patients with type 1 or type 2 diabetes. Female sex, complications, and low socioeconomic status were independently associated with depressive symptoms. In type 1 diabetes and in the type 2 diabetes OGLDs-only group, depression was associated with poor glycemic control. Conclusions: Depressive symptoms are common in patients with diabetes from developing countries, calling for routine screening, especially in high-risk groups, to reduce the double burden of diabetes and depression and their negative interaction. Fri, 07 May 2021 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/139527 2021-05-07T00:00:00Z Objetive: Depression is common in people with diabetes, but data from developing countries are scarce. We evaluated the prevalence and risk factors for depressive symptoms in patients with diabetes using data from the International Diabetes Management Practices Study (IDMPS). Research and methods: IDMPS is an ongoing multinational, cross-sectional study investigating quality of care in patients with diabetes in real-world settings. Data from wave 5 (2011), including 21 countries, were analyzed using the 9-item Patient Health Questionnaire (PHQ-9) to evaluate depressive symptoms. Logistic regression analyses were conducted to identify risk factors of depressive symptoms. Results: Of 9,865 patients eligible for analysis, 2,280 had type 1 and 7,585 had type 2 diabetes (treatment: oral glucose-lowering drugs [OGLD] only, n = 4,729; OGLDs plus insulin, n = 1,892; insulin only, n = 964). Depressive symptoms (PHQ-9 score ≥5) were reported in 30.7% of those with type 1 diabetes. In patients with type 2 diabetes, the respective figures were 29.0% for OGLDs-only, 36.6% for OGLDs-plus-insulin, and 46.7% for insulin-only subgroups. Moderate depressive symptoms (PHQ-9 score 10–19) were observed in 8–16% of patients with type 1 or type 2 diabetes. Female sex, complications, and low socioeconomic status were independently associated with depressive symptoms. In type 1 diabetes and in the type 2 diabetes OGLDs-only group, depression was associated with poor glycemic control. Conclusions: Depressive symptoms are common in patients with diabetes from developing countries, calling for routine screening, especially in high-risk groups, to reduce the double burden of diabetes and depression and their negative interaction. http://sedici.unlp.edu.ar:80/handle/10915/139180 Articulo Acta Diabetologica; vol. 53, no. 1 Aims. Test strips for self-monitoring of blood glucose (SMBG) represent in Argentina, around 50 % of diabetes treatment cost; the frequency of their use is closely associated with hyperglycemia treatment. However, the favorable impact of SMBG on attainment of HbA1c goal in different treatment conditions remains controversial. We therefore attempted to estimate the relationship between use of SMBG test strips and degree of attainment of metabolic control in an institution of our social security subsector (SSS) in which provision is fully covered and submitted to a regular audit system. Methods. Observational retrospective study using information of 657 patients with T2DM (period 2009–2010) from the database of the Diabetes and Other Cardiovascular Risk Factors Program (DICARO) of one institution of our SSS. DICARO provides—with an audit system—100 % coverage for all drugs and keeps records of clinical, metabolic and treatment data from every patient. Results. The average monthly test strips/patient used for SMBG increased as a function of treatment intensification: Monotherapy with oral antidiabetic drugs (OAD) < combined OAD therapy < insulin treatment. In every condition, the number was larger in people with target HbA1c levels. Test strips represented the larger percentage of total prescription cost. Conclusions. In our population, the type of hyperglycemia treatment was the main driver of test strip use for SMBG; in every condition tested, targeted HbA1c values were associated with greater strip use. Patient education and prescription audit may optimize its use and treatment outcomes. Mon, 01 Feb 2016 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/139180 2016-02-01T00:00:00Z Aims. Test strips for self-monitoring of blood glucose (SMBG) represent in Argentina, around 50 % of diabetes treatment cost; the frequency of their use is closely associated with hyperglycemia treatment. However, the favorable impact of SMBG on attainment of HbA1c goal in different treatment conditions remains controversial. We therefore attempted to estimate the relationship between use of SMBG test strips and degree of attainment of metabolic control in an institution of our social security subsector (SSS) in which provision is fully covered and submitted to a regular audit system. Methods. Observational retrospective study using information of 657 patients with T2DM (period 2009–2010) from the database of the Diabetes and Other Cardiovascular Risk Factors Program (DICARO) of one institution of our SSS. DICARO provides—with an audit system—100 % coverage for all drugs and keeps records of clinical, metabolic and treatment data from every patient. Results. The average monthly test strips/patient used for SMBG increased as a function of treatment intensification: Monotherapy with oral antidiabetic drugs (OAD) < combined OAD therapy < insulin treatment. In every condition, the number was larger in people with target HbA1c levels. Test strips represented the larger percentage of total prescription cost. Conclusions. In our population, the type of hyperglycemia treatment was the main driver of test strip use for SMBG; in every condition tested, targeted HbA1c values were associated with greater strip use. Patient education and prescription audit may optimize its use and treatment outcomes. http://sedici.unlp.edu.ar:80/handle/10915/139101 Articulo Acta diabetologica latina; vol. 20, no. 3 Previously, we reported that change from the normal pH of 7.4 surrounding the islet cells to 7.8 results in a decreased B-cell response to 16.6 mM glucose, 10 mM arginine or 400 µg/ml tolbutamide. In the present report we studied the effect of modifications in the extracellular pH on glucose- and arginine-induced glucagon and insulin secretion by the perfused rat pancreas. It was found that at pH 7.8, arginine-induced glucagon secretion was significantly greater than at pH 7.4. On the other hand, the switch from pH 7.4 to 7.8 in a pancreas already stimulated by either low glucose or arginine, produced fast and transient glucagon release. Sequential extracellular pH changes from 7.4 to 7.8 and back to 7.4 in the presence of 8.3 mM glucose and a 5 mM arginine stimulus demonstrated that A- and B-cells rapidly modify their secretion in response to extracellular alkalosis in opposite directions. While glucagon output was enhanced (mean secretory rates at pH 7.4, 0.692 ± 0.042 ng/min and 0.948 ± 0.57 at pH 7.8), insulin secretion was clearly reduced (72.6 ± 6.2 ng/min and 35.7 ± 2.8 ng/min at pH 7.4 and 7.8, respectively). The above observations, together with our previously reported data, indicate that extracellular pH plays an important role in the regulation of glucagon and insulin release. Particularly, extracellular alkalosis enhances A-cell response to 2.3 mM glucose and 5 mM arginine while partially inhibiting B-cell secretion in the perfused rat pancreas. Sat, 01 Jan 1983 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/139101 1983-01-01T00:00:00Z Previously, we reported that change from the normal pH of 7.4 surrounding the islet cells to 7.8 results in a decreased B-cell response to 16.6 mM glucose, 10 mM arginine or 400 µg/ml tolbutamide. In the present report we studied the effect of modifications in the extracellular pH on glucose- and arginine-induced glucagon and insulin secretion by the perfused rat pancreas. It was found that at pH 7.8, arginine-induced glucagon secretion was significantly greater than at pH 7.4. On the other hand, the switch from pH 7.4 to 7.8 in a pancreas already stimulated by either low glucose or arginine, produced fast and transient glucagon release. Sequential extracellular pH changes from 7.4 to 7.8 and back to 7.4 in the presence of 8.3 mM glucose and a 5 mM arginine stimulus demonstrated that A- and B-cells rapidly modify their secretion in response to extracellular alkalosis in opposite directions. While glucagon output was enhanced (mean secretory rates at pH 7.4, 0.692 ± 0.042 ng/min and 0.948 ± 0.57 at pH 7.8), insulin secretion was clearly reduced (72.6 ± 6.2 ng/min and 35.7 ± 2.8 ng/min at pH 7.4 and 7.8, respectively). The above observations, together with our previously reported data, indicate that extracellular pH plays an important role in the regulation of glucagon and insulin release. Particularly, extracellular alkalosis enhances A-cell response to 2.3 mM glucose and 5 mM arginine while partially inhibiting B-cell secretion in the perfused rat pancreas. http://sedici.unlp.edu.ar:80/handle/10915/139083 Articulo Acta diabetologica; vol. 32, no. 3 The aim of this study was to evaluate the effect of a structured teaching/treatment programme on the clinical and metabolic control of non-insulin-dependent (type 2) diabetic patients. The programme was aimed at improving the overall treatment quality in these patients through measures involving self-care, diet, exercise and weight reduction. Four theoretical-practical teaching units were given once a week to group of 5–8 ambulatory patients by previously trained general practitioners. Clinical and biochemical parameters were recorded at the beginning of the course and 1 year after its completion in 40 patients attending the programme and in 39 patients of similar clinical characteristics under conventional diabetes treatment, but receiving no structured teaching before or during the survey period (control group). The drop-out percentage in the intervention group (25%) was significantly lower than in the control group (45%),P<0.05, suggesting an incentive toward greater compliance in the former. At the end of the 1-year follow-up, the mean differences observed in the control and in the intervention groups were: body weight loss −2.4±0.5 kg vs −0.4±0.5 (P<0.001); haemoglobin HbA1 −0.2%±0.4% vs +0.8±0.4% (NS); number of daily oral hypoglycaemic agent intake −1.4±0.2 vs +0.9±0.2 tablets (P<0.001). Our results strongly suggest that this programme, applied through family doctors, may constitute an efficient tool to improve the compliance and clinico-metabolic control of type 2 patients at the primary health care level. Sun, 01 Jan 1995 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/139083 1995-01-01T00:00:00Z The aim of this study was to evaluate the effect of a structured teaching/treatment programme on the clinical and metabolic control of non-insulin-dependent (type 2) diabetic patients. The programme was aimed at improving the overall treatment quality in these patients through measures involving self-care, diet, exercise and weight reduction. Four theoretical-practical teaching units were given once a week to group of 5–8 ambulatory patients by previously trained general practitioners. Clinical and biochemical parameters were recorded at the beginning of the course and 1 year after its completion in 40 patients attending the programme and in 39 patients of similar clinical characteristics under conventional diabetes treatment, but receiving no structured teaching before or during the survey period (control group). The drop-out percentage in the intervention group (25%) was significantly lower than in the control group (45%),P<0.05, suggesting an incentive toward greater compliance in the former. At the end of the 1-year follow-up, the mean differences observed in the control and in the intervention groups were: body weight loss −2.4±0.5 kg vs −0.4±0.5 (P<0.001); haemoglobin HbA1 −0.2%±0.4% vs +0.8±0.4% (NS); number of daily oral hypoglycaemic agent intake −1.4±0.2 vs +0.9±0.2 tablets (P<0.001). Our results strongly suggest that this programme, applied through family doctors, may constitute an efficient tool to improve the compliance and clinico-metabolic control of type 2 patients at the primary health care level. http://sedici.unlp.edu.ar:80/handle/10915/138315 Comunicacion Value in Health; vol. 20, no. 9 Objectivos: Evaluar el impacto de un programa de capacitación de médicos y enfermeras, asociado a cambios en el sistema de gestión de pacientes y registro sistemático de variables clínico-metabólicas y terapéuticas, implementado en el nivel primario de atención, sobre la calidad de atención brindada a personas con diabetes tipo 2 (DT2). Sun, 01 Jan 2017 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/138315 2017-01-01T00:00:00Z Objectivos: Evaluar el impacto de un programa de capacitación de médicos y enfermeras, asociado a cambios en el sistema de gestión de pacientes y registro sistemático de variables clínico-metabólicas y terapéuticas, implementado en el nivel primario de atención, sobre la calidad de atención brindada a personas con diabetes tipo 2 (DT2). http://sedici.unlp.edu.ar:80/handle/10915/131051 Articulo The Journal of membrane biology; vol. 171, no. 1 We have previously demonstrated (Diabetes 39:707–711, 1990) that in vitro glycation of the red cell Ca2+ pump diminishes the Ca2+-ATPase activity of the enzyme up to 50%. Such effect is due to the reaction of glucose with lysine residues of the Ca2+ pump (Biochem. J. 293:369–375, 1993). The aim of this work was to determine whether the effect of glucose is due to a full inactivation of a fraction of the total population of Ca2+ pump, or to a partial inactivation of all the molecules. Glycation decreased the Vmax; for the ATPase activity leaving unaffected the apparent affinities for Ca2+, calmodulin or ATP. The apparent turnover was identical in both, the glycated and the native enzyme. Glycation decreased the Vmax; for the ATP-dependent but not for the calmodulin-activated phosphatase activities. Concomitantly with the inhibition, up to 6.5% of the lysine residues were randomly glycated. The probabilistic analysis of the relation between the enzyme activity and the fraction of nonmodified residues indicates that only one Lys residue is responsible for the inhibition. We suggest that glucose decreases the Ca2+-ATPase activity by reacting with one essential Lys residue probably located in the vicinity of the catalytic site, which results in the full inactivation of the enzyme. Thus, Ca2+-ATPase activity measured in erythrocyte membranes or purified enzyme preparations preincubated with glucose depends on the remaining enzyme molecules in which the essential Lys residue stays unglycated. Wed, 01 Sep 1999 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/131051 1999-09-01T00:00:00Z We have previously demonstrated (Diabetes 39:707–711, 1990) that in vitro glycation of the red cell Ca2+ pump diminishes the Ca2+-ATPase activity of the enzyme up to 50%. Such effect is due to the reaction of glucose with lysine residues of the Ca2+ pump (Biochem. J. 293:369–375, 1993). The aim of this work was to determine whether the effect of glucose is due to a full inactivation of a fraction of the total population of Ca2+ pump, or to a partial inactivation of all the molecules. Glycation decreased the Vmax; for the ATPase activity leaving unaffected the apparent affinities for Ca2+, calmodulin or ATP. The apparent turnover was identical in both, the glycated and the native enzyme. Glycation decreased the Vmax; for the ATP-dependent but not for the calmodulin-activated phosphatase activities. Concomitantly with the inhibition, up to 6.5% of the lysine residues were randomly glycated. The probabilistic analysis of the relation between the enzyme activity and the fraction of nonmodified residues indicates that only one Lys residue is responsible for the inhibition. We suggest that glucose decreases the Ca2+-ATPase activity by reacting with one essential Lys residue probably located in the vicinity of the catalytic site, which results in the full inactivation of the enzyme. Thus, Ca2+-ATPase activity measured in erythrocyte membranes or purified enzyme preparations preincubated with glucose depends on the remaining enzyme molecules in which the essential Lys residue stays unglycated.