Related Experiment Video
Updated: May 16, 2025
08:32
Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain
Published on: January 4, 2018
10.2K
Exercise-induced signalling in alleviating neuronal insulin resistance
Ishitha Reddy1, Chinmoy Sankar Dey1
1Kusuma School of Biological Sciences, Indian Institute of Technology-Delhi, Hauz Khas, New Delhi, India.
The Journal of Physiology
|April 2, 2025
Summary
Regular exercise improves brain health and combats metabolic disorders like type 2 diabetes. Exercise-induced signaling molecules enhance neuroprotection and insulin sensitivity, offering a non-pharmaceutical approach to conditions like Alzheimer's disease.
Area of Science:
- Neuroscience
- Metabolic Health
- Exercise Physiology
Background:
- Exercise positively impacts glucose homeostasis, insulin sensitivity, neuroprotection, and neurogenesis.
- Individuals with type 2 diabetes have an increased risk for Alzheimer's disease.
- Exercise offers a non-pharmaceutical strategy for managing metabolic disorders.
Purpose of the Study:
- To explore the molecular signaling pathways activated by exercise.
- To understand how exercise-induced signaling can improve neuronal insulin resistance.
- To investigate exercise's potential as a therapeutic intervention for Alzheimer's disease.
Main Methods:
- Review of molecular signaling pathways involved in exercise's effects on the brain.
- Analysis of cross-talk between various molecular cascades.
- Identification of key molecules and pathways mediating exercise benefits.
Main Results:
- Exercise evokes circulating molecules that transmit its benefits throughout the body and brain.
- Exercise signaling pathways, including SIRT1/PGC-1α and BDNF/TrkB, show promise in improving conditions associated with Alzheimer's disease.
- Exercise can act as a bypass mechanism to improve neuronal insulin resistance.
Conclusions:
- Exercise-induced molecular signaling is a critical area for future research.
- Understanding these pathways is crucial for developing therapeutic strategies for neurodegenerative and metabolic diseases.
- Further research into exercise's molecular mechanisms can lead to novel treatments for Alzheimer's disease and type 2 diabetes.
Related Concept Videos
01:28Insulin: The Receptor and Signaling Pathways
1.0K
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...
1.0K
01:16Hormones Regulating Blood Glucose
2.9K
Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
In addition to accelerating glucose uptake and utilization, insulin has...
In addition to accelerating glucose uptake and utilization, insulin has...
2.9K
01:27Glucose Homeostasis: Pancreatic Islets and Insulin Secretion
1.0K
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...
1.0K
01:24Glucagon-like Receptor Agonists
272
Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
272
01:05Insulin Secretory Vesicles
4.8K
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...
4.8K
01:15Hypoglycemia and Glucagon
143
Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
143