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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.
Overview of Lipid Metabolism01:24

Overview of Lipid Metabolism

Lipid metabolism is a crucial process in the human body that involves the synthesis and degradation of lipids. This process is essential for energy production, cell membrane formation, and hormone production, among other functions.
Lipolysis: The Breakdown of Lipids:
Lipolysis is the process of breaking down lipids, particularly triglycerides, into glycerol and fatty acids. This process typically occurs in the adipose tissue and is triggered by various hormones, including glucagon and...
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...
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...
Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
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...

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Related Experiment Video

Updated: Jun 19, 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

Insulin resistance, lipotoxicity and endothelial dysfunction.

Helen Imrie1, Afroze Abbas, Mark Kearney

  • 1Division of Cardiovascular and Diabetes Research, Leeds Multidisciplinary Cardiovascular Research Centre, The LIGHT Laboratories, Clarendon Way, Leeds, LS29JT, UK. h.imrie@leeds.ac.uk

Biochimica Et Biophysica Acta
|October 13, 2009
PubMed
Summary

Insulin resistance, common in type 2 diabetes and obesity, drives endothelial dysfunction and atherosclerosis. Free fatty acids may harm endothelial cells, contributing to cardiovascular disease risk.

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Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)
08:13

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)

Published on: January 7, 2018

Related Experiment Videos

Last Updated: Jun 19, 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

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)
08:13

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)

Published on: January 7, 2018

Area of Science:

  • Endocrinology
  • Cardiovascular Science
  • Metabolic Disorders

Background:

  • Type 2 diabetes mellitus (T2DM) and obesity are global epidemics.
  • Cardiovascular atherosclerosis complications cause 80% of T2DM deaths.
  • Insulin resistance leads to endothelial dysfunction, a key factor in atherosclerosis.

Purpose of the Study:

  • To review mechanisms linking insulin resistance to endothelial dysfunction.
  • To highlight the role of free fatty acids in endothelial cell homeostasis.

Main Methods:

  • Literature review of studies on insulin resistance, endothelial dysfunction, and atherosclerosis.
  • Focus on the impact of free fatty acids on endothelial cells.

Main Results:

  • Insulin resistance is characterized by endothelial dysfunction.
  • An imbalance between nitric oxide (NO) and reactive oxygen species (ROS) is a hallmark of endothelial dysfunction.
  • Free fatty acids may exert toxic effects on endothelial cell function.

Conclusions:

  • Insulin resistance contributes significantly to endothelial dysfunction and atherosclerosis.
  • Free fatty acids are implicated as a potential cause of endothelial cell damage.
  • Understanding these mechanisms is crucial for preventing cardiovascular complications in T2DM and obesity.