Related Experiment Video
Updated: May 24, 2026
12:32
High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds
Published on: January 23, 2018
Role of mitochondrial function in insulin resistance
Myrte Brands1, Arthur J Verhoeven, Mireille J Serlie
1Department of Endocrinology and Metabolism, Academic Medical Center, Amsterdam, The Netherlands. M.Brands@amc.uva.nl
Advances in Experimental Medicine and Biology
|March 9, 2012
Summary
Obesity and type 2 diabetes (DM2) are linked to insulin resistance. Skeletal muscle mitochondrial function
Area of Science:
- Metabolic disorders
- Exercise physiology
- Cellular metabolism
Background:
- The global obesity pandemic is a major driver for the increasing prevalence of type 2 diabetes (DM2).
- Insulin resistance, a key factor in DM2 pathogenesis, occurs when pancreatic beta-cells fail to compensate for reduced insulin sensitivity.
- The precise mechanisms by which excessive caloric intake and weight gain induce insulin resistance remain incompletely understood.
Purpose of the Study:
- To investigate the role of skeletal muscle mitochondrial dysfunction in the development of insulin resistance.
- To clarify the relationship between skeletal muscle mitochondrial function and insulin resistance in human subjects.
- To address the inconclusive findings in previous research regarding skeletal muscle mitochondria and insulin resistance.
Main Methods:
- Review and synthesis of existing literature on skeletal muscle mitochondrial function and insulin resistance.
- Analysis of factors contributing to variability in study findings, including techniques, populations, and physiological parameters.
- Examination of the potential impact of mitochondrial capacity on fatty acid oxidation and its relation to insulin sensitivity.
Main Results:
- Findings on skeletal muscle mitochondrial function in relation to insulin resistance in humans are currently inconclusive.
- Variability in results may stem from differences in mitochondrial density, insulin-stimulated respiration, energy demand, perfusion, or intrinsic mitochondrial defects.
- The capacity of mitochondria often exceeds energy requirements, questioning whether reduced capacity limits fatty acid oxidation.
Conclusions:
- The causal relationship between reduced skeletal muscle mitochondrial function and insulin resistance requires further elucidation.
- It remains uncertain whether impaired mitochondrial function is a cause or a consequence of insulin resistance, potentially influenced by sedentary lifestyles.
More Related Videos
Related Concept Videos
01:28Insulin: 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...
01:24Type 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.
01:26Type 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...
01:37Mitochondria
Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
01:28The Inner Mitochondrial Membrane
The inner mitochondrial membrane is the primary site of ATP synthesis. The inner membrane domain that forms a smooth layer adjacent to the outer membrane is called the inner boundary membrane. This domain contains membrane transporters that drive metabolites in and out of the mitochondria. In contrast, the inner membrane network that invaginates into the matrix space is called the cristae membrane. This domain accounts for principle mitochondrial function as it accommodates the protein...
01:46Electron Transport Chain: Complex I and II
The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
ROS generation is regulated and maintained at moderate levels necessary...