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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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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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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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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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Complex carbohydrates consumed cannot be absorbed into the small intestine in their original form. First, they must be hydrolyzed to a monosaccharide form such as glucose or galactose. These monosaccharides are then transported across the intestinal membrane and into the blood via transcellular transport. The intestinal epithelial cells allow the movement of these monosaccharides with a defined 'entry' through membrane transporter proteins present on their apical membrane and...
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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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Related Experiment Video

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Membrane Potential Dye Imaging of Ventromedial Hypothalamus Neurons From Adult Mice to Study Glucose Sensing
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Hypothalamic glucose-sensing mechanisms.

Nal Ae Yoon1,2, Sabrina Diano3,4

  • 1Institute of Human Nutrition, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY, USA.

Diabetologia
|February 5, 2021
PubMed
Summary

Disruptions in the brain

Keywords:
AstrocytesBrainCounterregulatory responsesDiabetesGlucose-sensingHypothalamusNeuronsObesityReviewTanycytes

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Area of Science:

  • Neuroscience
  • Metabolic disease research

Background:

  • Chronic metabolic diseases like diabetes and obesity pose significant global health challenges.
  • Glucose homeostasis is vital for mammalian survival, involving complex regulation by the central nervous system (CNS).
  • The hypothalamus is a key CNS area for glucose regulation, and its dysfunction is linked to obesity and type 2 diabetes.

Purpose of the Study:

  • To review current literature on hypothalamic glucose-sensing mechanisms.
  • To discuss how alterations in these mechanisms contribute to diabetes pathogenesis.

Main Methods:

  • Literature review of studies on hypothalamic glucose sensing.
  • Analysis of intracellular mechanisms involved in glucose detection within the hypothalamus.

Main Results:

  • The hypothalamus plays a critical role in maintaining glucose homeostasis.
  • Dysfunctional glucose sensing in the hypothalamus is associated with obesity and type 2 diabetes.
  • Intracellular mechanisms of hypothalamic glucose sensing require further elucidation.

Conclusions:

  • Understanding hypothalamic glucose sensing is crucial for addressing metabolic diseases.
  • Further research into the specific intracellular pathways is needed to clarify the pathogenesis of diabetes.