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Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
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The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
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Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
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Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but...
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The endoplasmic reticulum (ER) of pancreatic β-cells synthesizes preproinsulin, which consists of a signal peptide, A and B chains, and a C-peptide. Preproinsulin is then cleaved and folded into proinsulin, which translocates to the Golgi apparatus for sorting and packaging into secretory granules. In these granules, enzymatic clipping generates insulin and C-peptide.
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Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
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Initial hyperinsulinemia and subsequent β-cell dysfunction is associated with elevated palmitate levels.

Johan Staaf1,2, Sarojini J K A Ubhayasekera3, Ernest Sargsyan1

  • 1Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.

Pediatric Research
|April 12, 2016
PubMed
Summary
This summary is machine-generated.

Elevated palmitate levels in obese children and adolescents are linked to altered insulin secretion. This suggests that fatty acid exposure impacts pancreatic islet function, potentially contributing to diabetes development.

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Area of Science:

  • Endocrinology
  • Metabolic disorders
  • Pediatric research

Background:

  • Childhood obesity and diabetes prevalence are rising.
  • Nonesterified fatty acids, like palmitate, may link obesity to diabetes.
  • Understanding palmitate's role in insulin secretion is crucial.

Purpose of the Study:

  • To investigate the association between palmitate and insulin secretion in children and adolescents.
  • To examine the in vivo and in vitro effects of palmitate on pancreatic islet function.

Main Methods:

  • Studied 80 obese and lean children/adolescents, measuring fasting palmitate and glucose-stimulated insulin secretion (OGTT).
  • Cultured human islets with palmitate, assessing glucose-stimulated insulin secretion (GSIS), insulin content, and apoptosis.
  • Analyzed palmitate levels, insulin response during OGTT, GSIS, insulin content, and apoptosis markers.

Main Results:

  • Obese subjects showed higher fasting palmitate levels.
  • Elevated palmitate correlated with accentuated insulin levels in younger obese children but delayed first-phase insulin response in obese adolescents.
  • In vitro, palmitate initially enhanced GSIS but attenuated it after 7 days, while decreasing insulin content and increasing apoptosis.

Conclusions:

  • High palmitate levels in obese youth are associated with altered insulin secretory patterns.
  • These changes in insulin secretion and islet integrity may be induced by prolonged palmitate exposure.
  • Palmitate's impact on pancreatic islets could be a key factor in obesity-related diabetes development.