We are analyzing https://link.springer.com/article/10.1007/s00125-009-1347-2.

Title:
Autophagy in human type 2 diabetes pancreatic beta cells | Diabetologia
Description:
Aims/hypothesis Beta cell loss contributes to type 2 diabetes, with increased apoptosis representing an underlying mechanism. Autophagy, i.e. the physiological degradation of damaged organelles and proteins, may, if altered, be associated with a distinct form of cell death. We studied several features of autophagy in beta cells from type 2 diabetic patients and assessed the role of metabolic perturbation and pharmacological intervention. Methods Pancreatic samples were obtained from organ donors and isolated islets prepared both by collagenase digestion and density gradient centrifugation. Beta cell morphology and morphometry were studied by electron microscopy. Gene expression studies were performed by quantitative RT-PCR. Results Using electron microscopy, we observed more dead beta cells in diabetic (2.24 ± 0.53%) than control (0.66 ± 0.52%) samples (p < 0.01). Massive vacuole overload (suggesting altered autophagy) was associated with 1.18 ± 0.54% dead beta cells in type 2 diabetic samples and with 0.36 ± 0.26% in control samples (p < 0.05). Density volume of autophagic vacuoles and autophagosomes was significantly higher in diabetic beta cells. Unchanged gene expression of beclin-1 and ATG1 (also known as ULK1), and reduced transcription of LAMP2 and cathepsin B and D was observed in type 2 diabetic islets. Exposure of non-diabetic islets to increased NEFA concentration led to a marked increase of vacuole accumulation, together with enhanced beta cell death, which was associated with decreased LAMP2 expression. Metformin ameliorated autophagy alterations in diabetic beta cells and beta cells exposed to NEFA, a process associated with normalisation of LAMP2 expression. Conclusions/interpretation Beta cells in human type 2 diabetes have signs of altered autophagy, which may contribute to loss of beta cell mass. To preserve beta cell mass in diabetic patients, it may be necessary to target multiple cell-death pathways.
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Keywords {🔍}

beta, cell, cells, autophagy, type, diabetic, diabetes, death, autophagic, article, islets, pancreatic, metformin, expression, vacuoles, lamp, cas, google, scholar, pubmed, altered, dead, vacuole, nefa, accumulation, control, fig, cathepsin, increased, samples, autophagosomes, atg, signs, human, apoptosis, organelles, gene, observed, exposure, mass, pisa, results, massive, beclin, nondiabetic, alterations, removal, membrane, privacy, cookies,

Topics {✒️}

diabetes-induced oxidative stress multiple cell-death pathways beta cell-specific deletion amp-activated protein kinase nefa-induced ceramide formation amp-regulated kinase family nefa-exposed beta cells ubiquinated-protein aggregates form pancreatic beta cells pancreatic beta-cells privacy choices/manage cookies beta cell mass human pancreatic islets messenger rna level gene expression studies beta cells exposed high-fat diet beta cell death beta-cell death autophagy-related gene dead beta cells beta cell morphology beta cell identity beta cell line beta cell dysfunction beta cell damage normal beta cell unchanged gene expression normal beta cells programmed cell death apoptotic cell death cell death modalities free fatty acids diabetic beta cells plasma membrane integrity autophagy-mediated death related subjects digesting mechanism responsible tumor suppressor mechanism major chromatin condensation reduced lamp2 expression quantitative rt-pcr defined cytoplasmic regions hydrolytic enzymes responsible local ethics committee close double membranes quantitative rt-pcr [2] realistic therapeutic target unique neuronal functions significantly lower expression

Questions {❓}

Meier JJ (2008) Beta cell mass in diabetes: a realistic therapeutic target?

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         headline:Autophagy in human type 2 diabetes pancreatic beta cells
         description:Beta cell loss contributes to type 2 diabetes, with increased apoptosis representing an underlying mechanism. Autophagy, i.e. the physiological degradation of damaged organelles and proteins, may, if altered, be associated with a distinct form of cell death. We studied several features of autophagy in beta cells from type 2 diabetic patients and assessed the role of metabolic perturbation and pharmacological intervention. Pancreatic samples were obtained from organ donors and isolated islets prepared both by collagenase digestion and density gradient centrifugation. Beta cell morphology and morphometry were studied by electron microscopy. Gene expression studies were performed by quantitative RT-PCR. Using electron microscopy, we observed more dead beta cells in diabetic (2.24 ± 0.53%) than control (0.66 ± 0.52%) samples (p < 0.01). Massive vacuole overload (suggesting altered autophagy) was associated with 1.18 ± 0.54% dead beta cells in type 2 diabetic samples and with 0.36 ± 0.26% in control samples (p < 0.05). Density volume of autophagic vacuoles and autophagosomes was significantly higher in diabetic beta cells. Unchanged gene expression of beclin-1 and ATG1 (also known as ULK1), and reduced transcription of LAMP2 and cathepsin B and D was observed in type 2 diabetic islets. Exposure of non-diabetic islets to increased NEFA concentration led to a marked increase of vacuole accumulation, together with enhanced beta cell death, which was associated with decreased LAMP2 expression. Metformin ameliorated autophagy alterations in diabetic beta cells and beta cells exposed to NEFA, a process associated with normalisation of LAMP2 expression. Beta cells in human type 2 diabetes have signs of altered autophagy, which may contribute to loss of beta cell mass. To preserve beta cell mass in diabetic patients, it may be necessary to target multiple cell-death pathways.
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      headline:Autophagy in human type 2 diabetes pancreatic beta cells
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