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Obesity

Obesity

The Body Mass Index (BMI) is a numerical value derived from a person's weight and height, used to categorize individuals into weight ranges. It is calculated using the formula: weight in kilograms divided by height in meters squared. Obesity is a health condition characterized by excessive accumulation of adipose tissue that poses health risks, often diagnosed with a BMI ≥ 30. This excess fat storage occurs when surplus dietary calories are converted into triglycerides and stored in...

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Updated: Mar 24, 2026

A Chronic High-Intensity Interval Training and Diet-Induced Obesity Model to Maximize Exercise Effort and Induce Physiologic Changes in Rats

A Chronic High-Intensity Interval Training and Diet-Induced Obesity Model to Maximize Exercise Effort and Induce Physiologic Changes in Rats

Published on: April 28, 2023

Voluntary exercise improves hypothalamic and metabolic function in obese mice.

Brenton T Laing¹, Khoa Do¹, Tomoko Matsubara¹

¹Department of KinesiologyEast Carolina University, Greenville, North Carolina, USA East Carolina Diabetes and Obesity InstituteEast Carolina University, Greenville, North Carolina, USA.

The Journal of Endocrinology

|March 3, 2016

Summary

Voluntary exercise training in mice partially reversed high-fat diet-induced weight gain and improved metabolic function. Exercise protected pro-opiomelanocortin (POMC) neurons in the hypothalamus, enhancing leptin signaling and whole-body energy homeostasis.

Keywords:

exercise hypothalamus metabolism mouse obesity

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Area of Science:

Neuroscience
Metabolic Research
Exercise Physiology

Background:

Exercise is crucial for glucose homeostasis and body weight regulation.
Mechanisms linking exercise to central nervous system (CNS) metabolic functions require further elucidation.

Purpose of the Study:

To investigate the effects of voluntary exercise on metabolic functions in mice fed a high-fat diet (HFD).
To explore exercise-induced changes in hypothalamic pro-opiomelanocortin (POMC)-expressing neurons and associated signaling pathways.

Main Methods:

C57BL6 male mice were divided into normal chow, HFD, and HFD with exercise groups for 12 weeks.
Metabolic function assessed using Comprehensive Lab Animal Monitoring System, MRI, glucose/insulin tolerance tests, and insulin/leptin sensitivity studies.
Immunohistochemistry used to analyze POMC neurons, Ki67, and apoptosis markers in the hypothalamus.

Main Results:

Exercise partially attenuated HFD-induced body weight gain and adiposity.
Insulin and leptin sensitivity were significantly enhanced in the exercise group compared to the HFD group.
Exercise training restored HFD-impaired POMC-expressing neurons, suggesting neuroprotective effects involving altered proliferation and apoptosis.

Conclusions:

Voluntary exercise improves HFD-induced metabolic dysfunction.
Exercise exerts neuroprotective effects on hypothalamic POMC neurons, crucial for regulating energy homeostasis.
Enhanced leptin signaling in the hypothalamus contributes to exercise-mediated metabolic benefits.