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Related Concept Videos

Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

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.
Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

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 this inhibition is released...
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

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 uptake of...
Insulin: Dosing Regimen and Adverse Effects01:16

Insulin: Dosing Regimen and Adverse Effects

Insulin-replacement therapy usually includes both long-acting insulin (basal) and short-acting insulin (to cater to postprandial needs). In a diverse group of type 1 diabetes patients, the average daily insulin dose is typically 0.5-0.7 units/kg body weight. However, obese patients and pubertal adolescents may need more due to insulin resistance.
The basal dose constitutes about 40%-50% of the total daily dose, with the rest as premeal insulin. The mealtime insulin dose should mirror...
Type II Diabetes I: Introduction01:26

Type II Diabetes I: Introduction

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...
Oral Hypoglycemic Agents: Biguanides and Glitazones01:26

Oral Hypoglycemic Agents: Biguanides and Glitazones

Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood glucose levels...

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Related Experiment Video

Updated: May 18, 2026

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance
09:48

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance

Published on: February 17, 2023

[RAAS and insulin resistance].

Hiroyuki Motoshima1, Eiichi Araki

  • 1Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University.

Nihon Rinsho. Japanese Journal of Clinical Medicine
|September 28, 2012
PubMed
Summary

The renin-angiotensin-aldosterone system (RAAS) contributes to insulin resistance and type 2 diabetes. Blocking the RAAS reduces type 2 diabetes incidence, highlighting its therapeutic potential.

Area of Science:

  • Endocrinology and Metabolism
  • Cardiovascular Disease Pathophysiology

Context:

  • The renin-angiotensin-aldosterone system (RAAS) is increasingly implicated in metabolic disorders.
  • Insulin resistance and type 2 diabetes (T2DM) are significant global health challenges.

Purpose:

  • To review the role of the RAAS in the development of insulin resistance and T2DM.
  • To discuss the clinical relevance of RAAS blockade in metabolic syndrome and pre-diabetes.

Summary:

  • RAAS activation, particularly via angiotensin II (Ang II) and aldosterone, promotes insulin resistance through oxidative stress and inflammation in insulin-sensitive organs.
  • Experimental and clinical studies link RAAS activity to insulin resistance, diabetes, and cardiovascular diseases.
  • RAAS blockade with ACE inhibitors or ARBs has been shown to decrease T2DM incidence.

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Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
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Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice

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Hyperinsulinemic-Euglycemic Clamp in the Conscious Rat
11:12

Hyperinsulinemic-Euglycemic Clamp in the Conscious Rat

Published on: February 7, 2011

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Last Updated: May 18, 2026

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance
09:48

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance

Published on: February 17, 2023

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
11:10

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice

Published on: November 16, 2011

Hyperinsulinemic-Euglycemic Clamp in the Conscious Rat
11:12

Hyperinsulinemic-Euglycemic Clamp in the Conscious Rat

Published on: February 7, 2011

Impact:

  • Understanding RAAS involvement offers insights into preventing and treating metabolic syndrome and pre-diabetes.
  • RAAS blockade presents a viable strategy for managing T2DM risk and potentially improving insulin sensitivity.
  • This review consolidates current knowledge on RAAS and metabolic health, guiding future research and clinical practice.