نتایج جستجو برای: insulin expression and secretion
تعداد نتایج: 16981496 فیلتر نتایج به سال:
Type 2 diabetes is characterized by hyperglycemia due to insulin resistance in the target tissue and insufficient insulin secretion from the beta cells. Finding new mechanisms and pathways involved in the regulation of insulin secretion from the pancreatic beta cells is of great importance. Our group has earlier found, miRNA-212 and miRNA-132 to be upregulated in the non-obese type 2 diabetic G...
Type 2 diabetes is caused by both insulin resistance and relative insulin deficiency. To investigate age-related changes in glucose metabolism and development of type 2 diabetes, we compared glucose homeostasis in different groups of C57BL/6J mice ranging in age from 4 months to 20 months (4, 8, 12, 16 and 20 months). Interestingly, we observed that non-fasting glucose levels were not significa...
Insulin is secreted as discrete insulin secretory bursts at ~5-min intervals into the hepatic portal vein, these pulses being attenuated early in the development of type 1 and type 2 diabetes mellitus (T2DM). Intraportal insulin infusions (pulsatile, constant, or reproducing that in T2DM) indicated that the pattern of pulsatile insulin secretion delivered via the portal vein is important for he...
background resistance exercise is recommended as a useful therapeutic tool for the treatment of type 2 diabetes (t2d); however, the frequency of studies is inadequate to establish the precise mechanisms of any association between them. objectives in this study, we aimed to assess the effect of three months of resistance training on tcf7l2 expression in pancreatic tissues, serum insulin and gluc...
Obesity is often associated with insulin resistance, low-grade systemic inflammation, and reduced plasma adiponectin. Inflammation is also increased in adipose tissue, but it is not clear whether the reductions of adiponectin levels are related to dysregulation of insulin activity and/or increased proinflammatory mediators. In this study, we investigated the interactions of insulin, tumor necro...
Glucagon secretion involves a combination of paracrine, autocrine, hormonal, and autonomic neural mechanisms. Type 2 diabetes often presents impaired glucagon suppression by insulin and glucose. Insulin-like growth factor-I (IGF-1) has elevated homology with insulin, and regulates pancreatic β-cells insulin secretion. Insulin and IGF-1 receptors share considerable structure homology and functio...
Cytokines, released in and around pancreatic islets during insulitis, have been proposed to participate in beta-cell destruction associated with autoimmune diabetes. In this study we have evaluated the hypothesis that local release of the cytokine interleukin 1 (IL-1) by nonendocrine cells of the islet induce the expression of inducible nitric oxide synthase (iNOS) by beta cells which results i...
Cytokines, released in and around pancreatic islets during insulitis, have been proposed to participate in B-cell destruction associated with autoimmune diabetes. In this study we have evaluated the hypothesis that local release of the cytokine interleukin 1 (IL-1) by nonendocrine cells of the islet induce the expression of inducible nitric oxide synthase (iNOS) by 3 cells which results in the ...
background: eukaryotic proteins generally have signal peptides, which are not only crucial for their secretion efficiencies but are important for their expression levels. the coagulation factor ix (fix) is a glycoprotein that plays a fundamental role in a blood coagulation pathway. reduced levels or dysfunctional fix are associated with hemophilia b. to improve the hfix secretion efficiency in ...
It is known that the LIM homeodomain transcription factor Isl1 is highly expressed in all pancreatic endocrine cells and functions in regulating pancreatic development and insulin secretion. The Isl1 mutation has been found to be associated with type 2 diabetes, but the mechanism responsible for Isl1 regulation of insulin synthesis and secretion still needs to be elucidated. In the present stud...
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