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Related Concept Videos

Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

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PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
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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.
Insulin and C-peptide are...
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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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Type II Diabetes I: Introduction01:26

Type II Diabetes I: Introduction

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Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
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Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

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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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Type I Diabetes II: Pathophysiology01:26

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Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular...
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Related Experiment Video

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Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance
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[Insulin secretion and insulin resistance].

Yasuharu Ohta1, Yukio Tanizawa1

  • 1Division of Endocrinology, Metabolism, Hematological Sciences and Therapeutics, Department of Bio-Signal Analysis, Yamaguchi University, Graduate School of Medicine.

Nihon Rinsho. Japanese Journal of Clinical Medicine
|January 9, 2014
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Summary

Aging significantly impacts glucose tolerance and diabetes risk. This review explores how aging affects pancreatic beta cells, insulin secretion, and sensitivity, crucial for understanding and treating type 2 diabetes in older adults.

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Area of Science:

  • Gerontology
  • Endocrinology
  • Metabolic Diseases

Background:

  • Aging is a primary risk factor for impaired glucose tolerance and type 2 diabetes (T2DM).
  • In Japan, a significant portion of the 8.9 million diabetes cases (37%) involve individuals over 70.
  • Understanding age-related changes in glucose metabolism is critical for public health.

Purpose of the Study:

  • To review current evidence on how aging impacts pancreatic beta cell function and mass.
  • To examine the effects of aging on insulin secretion and peripheral insulin sensitivity.
  • To elucidate mechanisms underlying impaired glucose homeostasis and T2DM in the elderly.

Main Methods:

  • Literature review of existing research on aging and diabetes.
  • Analysis of studies focusing on pancreatic beta cell physiology in aging.
  • Examination of data on insulin resistance and secretion changes with age.

Main Results:

  • Aging is associated with reduced pancreatic beta cell function and mass.
  • Insulin secretion capacity declines with age.
  • Peripheral insulin resistance increases in older individuals, contributing to T2DM pathogenesis.

Conclusions:

  • Impaired insulin secretion and peripheral insulin resistance are key features of T2DM in aging.
  • Understanding these age-related mechanisms is vital for developing targeted interventions.
  • Novel treatments could prevent or delay diabetes, improving longevity and quality of life in the elderly.