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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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The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
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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: 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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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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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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Adiponectin signaling and function in insulin target tissues.

Hong Ruan1, Lily Q Dong2

  • 1Department of Pharmacology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA dongq@uthscsa.edu ruanh@uthscsa.edu.

Journal of Molecular Cell Biology
|March 20, 2016
PubMed
Summary

Adiponectin improves insulin sensitivity and energy metabolism, offering a potential therapeutic target for obesity-linked type 2 diabetes. Further research into adiponectin signaling is crucial for developing effective treatments for insulin resistance.

Keywords:
APPL1APPL2adiponectinadiponectin receptorcell signalinginsulin resistance

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Area of Science:

  • Metabolic disease research
  • Endocrinology
  • Molecular biology

Background:

  • Obesity-linked type 2 diabetes is a major global health burden.
  • Current treatments for insulin resistance are inadequate.
  • Adiponectin, an adipocyte-secreted factor, enhances insulin sensitivity and regulates metabolism.

Purpose of the Study:

  • To explore adiponectin's therapeutic potential for type 2 diabetes.
  • To elucidate the mechanisms of adiponectin signaling and its regulation.
  • To identify novel therapeutic targets for insulin resistance.

Main Methods:

  • Review of tissue- and cell-specific functions of adiponectin.
  • Analysis of adiponectin signaling pathways.
  • Investigation of crosstalk with other metabolic signaling pathways.

Main Results:

  • Adiponectin demonstrates broad biological activities, including improving insulin sensitivity and modulating inflammation.
  • Understanding adiponectin's role in energy metabolism is key.
  • Potential for therapeutic intervention targeting adiponectin signaling.

Conclusions:

  • Adiponectin holds significant promise as a therapeutic agent for type 2 diabetes and insulin resistance.
  • Further research into adiponectin signaling mechanisms is essential.
  • Targeting adiponectin pathways could lead to novel treatments for metabolic disorders.