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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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Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
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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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Glucagon-like Receptor Agonists01:24

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Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
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Glucose Homeostasis: Regulation of Blood Glucose01:02

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Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
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Metabolic States of the Body: The Postabsorptive State01:18

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The postabsorptive state usually starts about four hours after a meal and lasts until the next meal is eaten. During this time, the digestive system stops absorbing nutrients, and the body uses stored energy reserves to maintain stable blood glucose levels.
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Postprandial Glucagon Action in the Human Brain.

Robert Wagner1,2,3, Stephanie Kullmann2,4,5, Julia Hummel6

  • 1Institute for Clinical Diabetology, German Diabetes Center, Leibnitz Center for Diabetes Research at Heinrich Heine University Düsseldorf, Düsseldorf, Germany.

Diabetes, Obesity & Metabolism
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Summary

Postprandial glucagon influences brain regions regulating metabolism and food intake. This study shows glucagon

Keywords:
MRI neuroimagingOGTT (oral glucose tolerance test)brain metabolismcerebral blood flowglucagonhypothalamusinsulin sensitivitymetabolic regulation

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Area of Science:

  • Metabolic Research
  • Neuroendocrinology
  • Human Physiology

Background:

  • Elevated fasting glucagon is linked to hyperglycemia, but postprandial glucagon's role is less understood.
  • Emerging evidence suggests metabolic benefits from rising postprandial glucagon, potentially via brain pathways.
  • Understanding glucagon's effects on the human brain is crucial for its translational relevance.

Purpose of the Study:

  • To investigate the postprandial effects of glucagon on the human brain.
  • To determine if experimentally elevated glucagon influences brain activity related to metabolism and food intake.

Main Methods:

  • Oral glucose tolerance tests (OGTT) combined with functional magnetic resonance imaging (fMRI) in 30 volunteers.
  • Measurement of brain activity and connectivity at fasting, 30, and 120 minutes post-glucose.
  • Comparison between participants with suppressed glucagon (receiving low-dose glucagon infusion) and those with endogenous glucagon rise.

Main Results:

  • Experimentally increasing glucagon during OGTT significantly enhanced postprandial brain responsivity in the hippocampus, hypothalamus, and ventral striatum.
  • These brain regions are critical for regulating appetite, systemic metabolism, and food intake.
  • The observed brain responses correlated with the rise in glucagon, irrespective of its source (endogenous or exogenous).

Conclusions:

  • Postprandial glucagon exerts significant effects on key human brain areas involved in metabolic regulation.
  • These findings may explain the body weight management benefits observed with multi-agonists targeting the glucagon receptor.