We are analyzing https://link.springer.com/article/10.1007/s00125-012-2801-0.

Title:
Modulation of hypovitaminosis D-induced islet dysfunction and insulin resistance through direct suppression of the pancreatic islet renin–angiotensin system in mice | Diabetologia
Description:
Aims/hypothesis Vitamin D is necessary for normal insulin action and suppresses renin production. Increased renin–angiotensin system (RAS) activity causes islet damage, including reduced insulin secretion. We therefore sought to determine whether hypovitaminosis D-induced upregulation of islet RAS in vivo impairs islet cell function and increases insulin resistance, and whether pharmacological suppression of the RAS during continuing vitamin D deficiency might correct this. Methods C57BL/6 mice were rendered vitamin D-deficient by diet, and glucose and insulin tolerance was assessed. The expression and translation of islet functional, and islet RAS, genes were measured and the effects of pharmacological renin suppression examined. Results Mice with diet-induced hypovitaminosis D developed impaired glucose tolerance, increased RAS component expression and impaired islet function gene transcription. Treatment with pharmacological renin inhibition (aliskiren), without vitamin D status correction, reduced islet RAS over-reactivity, islet dysfunction and insulin resistance, and improved glucose tolerance. Conclusions/interpretation Upregulation of islet RAS genes can contribute to hypovitaminosis D-induced impairment of islet function and increase insulin resistance independently of vitamin D status. Thus, our findings support the use of RAS inhibitors in impaired glucose homeostasis or early diabetes. They also suggest that combining RAS inhibition with correction of hypovitaminosis D might be useful in treating impaired glycaemic control and also in type 2 diabetes prevention. However, the use of aliskiren in established diabetes is contraindicated due to the increased risk of side effects such as hyperkalaemia, so other more suitable RAS blockers need to be identified.
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Keywords {🔍}

vitamin, insulin, islet, mice, ras, ddeficient, glucose, article, fig, google, scholar, diabetes, pubmed, cas, renin, expression, islets, function, resistance, aliskiren, diet, cell, pancreatic, increased, type, serum, receptor, system, effects, beta, blood, deficiency, mouse, mrna, concentrations, levels, normal, activity, treatment, gene, ohd, data, secretion, tolerance, homeostasis, fasting, esm, reduced, control, risk,

Topics {✒️}

full size image normal-diet-fed control mice oxidative stress-related genes local angiotensin-generating system islet insulin-signalling-related genes local renin-angiotensin system air-dried pancreatic sections mouse pancreatic beta-cells pancreatic islet beta-cells increased renin–angiotensin system hanks’-balanced-salt-solution air-dried cryo-sections o'keefe jh jr gov/drugs/drugsafety/ucm300889 normal-diet-fed mice fluorescent-conjugated secondary antibodies rendered vitamin d-deficient vitamin d-deficient diet vitamin d-deficient diets vitamin d-deficient states angiotensin-converting enzyme inhibitors 1alpha-hydroxylase knockout mice rate-limiting ras component cardoso-de-lemos fs perform real-time-pcr normal-diet-fed controls vitamin d-deficient mice randomized clinical trials double distilled h2o sybr-green-i-mix vitamin d-deficient animals vitamin d-deficient islets dahl salt-sensitive animals hypovitaminosis d-induced upregulation islet ras mediates glucose-stimulated insulin release hypovitaminosis d-induced impairment modulating oxidative stress glucagon-secreting alpha cells reduced oxidative stress islet cross-sectional areas deficiency-related tcf7l2 downregulation glucose-stimulated insulin secretion renin–angiotensin system renin-angiotensin system vdr-ko mice limit related gene activity increased islet size gene defects related catalase mrna expression

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         description:Vitamin D is necessary for normal insulin action and suppresses renin production. Increased renin–angiotensin system (RAS) activity causes islet damage, including reduced insulin secretion. We therefore sought to determine whether hypovitaminosis D-induced upregulation of islet RAS in vivo impairs islet cell function and increases insulin resistance, and whether pharmacological suppression of the RAS during continuing vitamin D deficiency might correct this. C57BL/6 mice were rendered vitamin D-deficient by diet, and glucose and insulin tolerance was assessed. The expression and translation of islet functional, and islet RAS, genes were measured and the effects of pharmacological renin suppression examined. Mice with diet-induced hypovitaminosis D developed impaired glucose tolerance, increased RAS component expression and impaired islet function gene transcription. Treatment with pharmacological renin inhibition (aliskiren), without vitamin D status correction, reduced islet RAS over-reactivity, islet dysfunction and insulin resistance, and improved glucose tolerance. Upregulation of islet RAS genes can contribute to hypovitaminosis D-induced impairment of islet function and increase insulin resistance independently of vitamin D status. Thus, our findings support the use of RAS inhibitors in impaired glucose homeostasis or early diabetes. They also suggest that combining RAS inhibition with correction of hypovitaminosis D might be useful in treating impaired glycaemic control and also in type 2 diabetes prevention. However, the use of aliskiren in established diabetes is contraindicated due to the increased risk of side effects such as hyperkalaemia, so other more suitable RAS blockers need to be identified.
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      headline:Modulation of hypovitaminosis D-induced islet dysfunction and insulin resistance through direct suppression of the pancreatic islet renin–angiotensin system in mice
      description:Vitamin D is necessary for normal insulin action and suppresses renin production. Increased renin–angiotensin system (RAS) activity causes islet damage, including reduced insulin secretion. We therefore sought to determine whether hypovitaminosis D-induced upregulation of islet RAS in vivo impairs islet cell function and increases insulin resistance, and whether pharmacological suppression of the RAS during continuing vitamin D deficiency might correct this. C57BL/6 mice were rendered vitamin D-deficient by diet, and glucose and insulin tolerance was assessed. The expression and translation of islet functional, and islet RAS, genes were measured and the effects of pharmacological renin suppression examined. Mice with diet-induced hypovitaminosis D developed impaired glucose tolerance, increased RAS component expression and impaired islet function gene transcription. Treatment with pharmacological renin inhibition (aliskiren), without vitamin D status correction, reduced islet RAS over-reactivity, islet dysfunction and insulin resistance, and improved glucose tolerance. Upregulation of islet RAS genes can contribute to hypovitaminosis D-induced impairment of islet function and increase insulin resistance independently of vitamin D status. Thus, our findings support the use of RAS inhibitors in impaired glucose homeostasis or early diabetes. They also suggest that combining RAS inhibition with correction of hypovitaminosis D might be useful in treating impaired glycaemic control and also in type 2 diabetes prevention. However, the use of aliskiren in established diabetes is contraindicated due to the increased risk of side effects such as hyperkalaemia, so other more suitable RAS blockers need to be identified.
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         Internal Medicine
         Metabolic Diseases
         Human Physiology
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