Protein carbonylation, mitochondrial dysfunction, and insulin resistance
Brigitte I Frohnert1, David A Bernlohr
1Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, MN, USA.
Advances in Nutrition (Bethesda, Md.)
|March 16, 2013
Summary
Oxidative stress, particularly protein carbonylation, contributes to mitochondrial dysfunction and insulin resistance in obesity. This review explores the link between protein carbonylation and mitochondrial health in metabolic diseases.
Area of Science:
- Biochemistry
- Cellular Biology
- Metabolic Diseases
Background:
- Oxidative stress is a key mechanism in cellular damage across diseases.
- Obesity and insulin resistance involve oxidative stress and inflammation.
- Mitochondrial dysfunction is linked to metabolic defects and oxidative stress.
Purpose of the Study:
- To review the relationship between protein carbonylation and mitochondrial biology.
- To investigate protein carbonylation as a mechanism for mitochondrial dysfunction in obesity-related insulin resistance.
Main Methods:
- Literature review focusing on oxidative stress, protein carbonylation, and mitochondrial function.
- Analysis of studies linking lipid peroxidation to protein carbonylation and mitochondrial defects.
Main Results:
- Protein carbonylation is a significant effect of oxidative stress.
- Lipid peroxidation-induced protein carbonylation may determine mitochondrial dysfunction.
- This process is implicated in insulin resistance in adipocytes and myocytes.
Conclusions:
- Protein carbonylation is a critical factor in mitochondrial dysfunction.
- Understanding this link is crucial for metabolic disease research.
- Further investigation into the causal role of protein carbonylation is warranted.
More Related Videos
12:32High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds
Published on: January 23, 2018
08:12Measurement of Mitochondrial Respiration in Human and Mouse Skeletal Muscle Fibers by High-Resolution Respirometry
Published on: October 4, 2024
Related Concept Videos
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.
01:19Overview of Carbohydrate Metabolism
Carbohydrate metabolism is a fundamental biochemical process that ensures a constant supply of energy to living cells. The most important carbohydrate is glucose, which can be broken down via glycolysis to enter into the Krebs cycle and eventually lead to the production of ATP through oxidative phosphorylation.
Glucose transport into cells is facilitated by a family of transport proteins called GLUT (Glucose Transporters). GLUT4 is the primary glucose transporter for insulin-stimulated glucose...
Glucose transport into cells is facilitated by a family of transport proteins called GLUT (Glucose Transporters). GLUT4 is the primary glucose transporter for insulin-stimulated glucose...
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...
01:22Diabetic Ketoacidosis ll: Pathophysiology
Diabetic ketoacidosis (DKA) is a metabolic emergency characterized by hyperglycemia, ketonemia, and metabolic acidosis. It results from severe insulin deficiency and an excess of counterregulatory hormones, leading to uncontrolled lipolysis, ketogenesis, and widespread electrolyte and fluid disturbances.Pathophysiology The central event in DKA is a profound loss of insulin action. Without insulin, glucose uptake in insulin-dependent tissues is impaired, while hepatic glucose production...
01:26Type 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...
01:26Diabetes Mellitus: Introduction
Diabetes mellitus consists of chronic metabolic disorders characterized by persistent hyperglycemia. This elevated blood glucose results from defects in insulin secretion, impaired insulin action, or both. Insulin, produced by pancreatic β-cells, is essential for maintaining glucose homeostasis by facilitating cellular glucose uptake for energy or storage. Disruptions in insulin production or function lead to glucose accumulation in the bloodstream, causing the clinical features and long-term...