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Related Concept Videos

Hormones Regulating Blood Glucose01:16

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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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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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Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

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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: The Receptor and Signaling Pathways01:28

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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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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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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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Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes
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Glucose, exercise and insulin: emerging concepts.

E A Richter1, W Derave, J F Wojtaszewski

  • 1Copenhagen Muscle Research Centre, Department of Human Physiology, Institute of Exercise and Sports Sciences, University of Copenhagen, DK-2100 Copenhagen, Denmark. erichter@aki.ku.dk

The Journal of Physiology
|September 5, 2001
PubMed
Summary
This summary is machine-generated.

Physical exercise boosts glucose uptake in muscles by moving glucose transporters (GLUT4) to the cell membrane. Glycogen plays a key role in signaling for glucose metabolism during and after exercise.

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Area of Science:

  • Exercise physiology
  • Skeletal muscle metabolism
  • Cellular signaling

Background:

  • Physical activity rapidly increases glucose uptake in contracting skeletal muscles.
  • This enhancement is mediated by the translocation of glucose transporters (GLUT4) to the muscle cell membrane (sarcolemma and t-tubules).

Purpose of the Study:

  • To review recent advancements in understanding the signals that initiate GLUT4 translocation in exercising muscle.
  • To discuss the mechanisms underlying improved insulin action on glucose uptake and glycogen synthase activity post-exercise.

Main Methods:

  • Literature review of signaling pathways involved in exercise-induced glucose uptake.
  • Discussion of the roles of calcium, protein kinase C (PKC), nitric oxide (NO), glycogen, and AMP-activated protein kinase (AMPK).

Main Results:

  • Exercise triggers GLUT4 translocation to the sarcolemma and t-tubules, increasing glucose uptake.
  • Glycogen appears to be a significant modulator of signaling events in glucose metabolism.
  • Post-exercise, insulin sensitivity for glucose uptake and glycogen synthesis is enhanced.

Conclusions:

  • Glycogen is a crucial modulator of signaling pathways governing glucose metabolism during and after muscle contractions.
  • Understanding these signaling mechanisms is key to optimizing metabolic health through exercise.