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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.
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...
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...
Carbohydrate Metabolism01:36

Carbohydrate Metabolism

Carbohydrates are polymers composed of molecules containing atoms of carbon, hydrogen and oxygen. One gram of carbohydrate can provide four kilo-calories of energy, which makes it the most efficient instant energy source.
Starch accounts for approximately 60% of the carbohydrates consumed by humans. Since amylase enzymes cannot function in the stomach's acidic environment, starch can only be digested in the mouth and small intestine. Simple sugars are found naturally in milk and fruits in the...
Diabetes Mellitus: Type 2 and Gestational01:22

Diabetes Mellitus: Type 2 and Gestational

Type 2 diabetes, characterized by insulin resistance, arises when the insulin receptors on cells lose responsiveness to insulin, diminishing the cell's capacity to take up glucose, resulting in elevated blood glucose levels. To receive a diagnosis of Type 2 diabetes, a series of blood glucose tests are necessary to assess whether the blood glucose falls within normal parameters. If the result is out of the normal range, a patient may be diagnosed as prediabetic or diabetic, depending on the...
Pathophysiology of Diabetes01:20

Pathophysiology of Diabetes

Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility, suggesting a...

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Related Experiment Video

Updated: Jul 1, 2026

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
09:40

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

Published on: January 19, 2017

Mitochondrial dysfunction in type 2 diabetes and obesity.

Kurt Højlund1, Martin Mogensen, Kent Sahlin

  • 1Diabetes Research Center, Department of Endocrinology, Odense University Hospital, Kloevervaenget 6, 3 DK-5000 Odense C, Denmark. k.hojlund@dadlnet.dk

Endocrinology and Metabolism Clinics of North America
|September 9, 2008
PubMed
Summary
This summary is machine-generated.

Insulin resistance in skeletal muscle, a key feature of type 2 diabetes and obesity, is linked to mitochondrial dysfunction. This review explores molecular mechanisms connecting these conditions in human skeletal muscle.

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Measurement of Mitochondrial Respiration in Human and Mouse Skeletal Muscle Fibers by High-Resolution Respirometry
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Measurement of Mitochondrial Respiration in Human and Mouse Skeletal Muscle Fibers by High-Resolution Respirometry

Published on: October 4, 2024

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Last Updated: Jul 1, 2026

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
09:40

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

Published on: January 19, 2017

Measurement of Mitochondrial Respiration in Human and Mouse Skeletal Muscle Fibers by High-Resolution Respirometry
08:12

Measurement of Mitochondrial Respiration in Human and Mouse Skeletal Muscle Fibers by High-Resolution Respirometry

Published on: October 4, 2024

Area of Science:

  • Metabolic disorders
  • Mitochondrial biology
  • Skeletal muscle physiology

Background:

  • Insulin resistance in skeletal muscle is central to type 2 diabetes mellitus (T2D) and obesity.
  • It involves impaired glucose transport, reduced glycogen synthesis, and lipid accumulation.
  • Mitochondrial dysfunction is increasingly implicated in skeletal muscle insulin resistance.

Purpose of the Study:

  • To review recent advances in understanding molecular mechanisms of insulin resistance in human skeletal muscle.
  • To focus on the potential links between insulin resistance and mitochondrial dysfunction in T2D and obesity.

Main Methods:

  • Literature review of recent studies on skeletal muscle insulin resistance.
  • Analysis of molecular pathways connecting mitochondrial function and insulin signaling.
  • Focus on data from human subjects with T2D and obesity.

Main Results:

  • Skeletal muscle insulin resistance is associated with reduced mitochondrial content (biogenesis).
  • Potential decrease in the functional capacity of individual mitochondria.
  • Accumulation of intramyocellular lipid metabolites contributes to insulin resistance.

Conclusions:

  • Mitochondrial dysfunction is a significant factor in skeletal muscle insulin resistance in T2D and obesity.
  • Understanding these molecular links is crucial for developing targeted therapies.
  • Further research into mitochondrial mechanisms may reveal new treatment strategies.