Related Experiment Video
Updated: Feb 5, 2026
09:48
Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance
Published on: February 17, 2023
3.5K
Altered mitochondrial function in insulin-deficient and insulin-resistant states
The Journal of Clinical Investigation
|September 1, 2018
Summary
Diabetes disrupts mitochondrial function, leading to inefficient energy production and increased oxidative stress. Correcting amino acid levels and exercise can improve mitochondrial health and insulin action in diabetic individuals.
Area of Science:
- Mitochondrial biology
- Metabolic disorders
- Cellular physiology
Background:
- Diabetes mellitus, characterized by insulin deficiency or resistance, profoundly impacts cellular fuel metabolism.
- Mitochondrial dysfunction, including inefficient coupling and excessive reactive oxygen species (ROS) production, is a hallmark of diabetes.
- Insulin plays a critical role in maintaining mitochondrial proteome homeostasis, influencing biogenesis and preventing damage.
Purpose of the Study:
- To review the association between diabetes and alterations in mitochondrial proteome homeostasis and function.
- To discuss how these mitochondrial changes contribute to diabetic complications.
- To highlight the role of nutrient excess and exercise in modulating mitochondrial function in diabetes.
Main Methods:
- Literature review focusing on the role of insulin in mitochondrial regulation.
- Analysis of studies examining mitochondrial function in various tissues in diabetes models.
- Examination of the impact of nutrient excess and aerobic exercise on mitochondrial physiology.
Main Results:
- Insulin deficiency and resistance are linked to impaired mitochondrial coupling and increased ROS production.
- Nutrient excess, particularly fat, exacerbates mitochondrial dysfunction and impairs insulin action via ROS.
- Aerobic exercise can enhance mitochondrial biogenesis and efficiency, improving insulin action in insulin-resistant individuals.
Conclusions:
- Alterations in mitochondrial proteome homeostasis and function are central to diabetes pathophysiology.
- Mitochondrial dysfunction contributes significantly to the development of diabetic complications.
- Strategies targeting mitochondrial health, such as exercise and nutritional management, hold therapeutic potential for diabetes.
Related Concept Videos
01:05Insulin Secretory Vesicles
7.0K
Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
7.0K
01:28Insulin: The Receptor and Signaling Pathways
3.3K
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...
3.3K
01:27Insulin Formulations: Types and Delivery
744
Insulin preparations are categorized by their duration of action into short-acting and long-acting types. Two strategies are used to modify insulin's absorption and pharmacokinetic profile: slowing the absorption post-subcutaneous injection, or altering human insulin's amino acid sequence or protein structure. These changes retain the insulin's ability to bind to the insulin receptor, but alter its behavior in solution or after injection.
Short-acting insulins are divided into...
Short-acting insulins are divided into...
744
01:25Insulin: Biosynthesis, Chemistry, and Preparation
1.4K
The endoplasmic reticulum (ER) of pancreatic β-cells synthesizes preproinsulin, which consists of a signal peptide, A and B chains, and a C-peptide. Preproinsulin is then cleaved and folded into proinsulin, which translocates to the Golgi apparatus for sorting and packaging into secretory granules. In these granules, enzymatic clipping generates insulin and C-peptide.
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment...
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment...
1.4K
01:16Insulin: Dosing Regimen and Adverse Effects
788
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...
The basal dose constitutes about 40%-50% of the total daily dose, with the rest as premeal insulin. The mealtime insulin dose should mirror...
788
01:27Glucose Homeostasis: Pancreatic Islets and Insulin Secretion
2.6K
The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are...
Insulin and C-peptide are...
2.6K