Physical exercise promotes memory capability by enhancing hippocampal mitochondrial functions and inhibiting apoptosis in obesity-induced insulin resistance by high fat diet

Nov 30, 2017Metabolic brain disease

Physical exercise may improve memory by boosting energy production and reducing cell death in the memory system of obese mice with insulin resistance caused by a high-fat diet

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Abstract

A high-fat diet induced obesity in mice, resulting in memory loss linked to insulin resistance and increased apoptosis in the hippocampus.

Obesity from a high-fat diet was associated with insulin resistance and decreased memory function.
Insulin resistance correlated with reduced mitochondrial function in the hippocampus, indicated by alterations in Caretention and Orespiration.
Increased apoptosis in the hippocampus was observed due to lower Bcl-2 levels and higher levels of Bax, cytochrome c, and caspase-3.
Physical exercise was linked to reduced insulin resistance and improved mitochondrial function in the hippocampus.
Exercise also resulted in decreased apoptosis in the hippocampus, which may help in preventing memory loss related to obesity-induced insulin resistance.

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A high-fat diet induces obesity in mice, leading to insulin resistance, decreased mitochondrial function, and increased apoptosis in the hippocampus, which eventually result in memory loss. The present study investigated the effect of physical exercise on memory, hippocampal mitochondrial function, and apoptosis in mice with in insulin resistance caused by obesity due to high-fat diet. Mice were randomly divided into four groups: control (CON), control and exercise (CON + EX), high fat diet (HFD), and high fat diet and exercise (HFD + EX). After receiving a high-fat (60%) diet for 20 weeks to induce obesity, the animals were subjected to an exercise routine 6 times per week, for 12 weeks. The exercise duration and intensity gradually increased over 4-week intervals. Hippocampal memory was examined using the step-down avoidance task. Mitochondrial function and apoptosis were also examined in the hippocampus and dentate gyrus. We found that obesity owing to a high-fat diet induced insulin resistance and caused a decrease in memory function. Insulin resistance also caused a decrease in mitochondrial function in the hippocampus by reducing Caretention and Orespiration, increasing the levels of HO, and Cyp-D, and mPTP opening. In addition, apoptosis in the hippocampus increased owing to decreased expression of Bcl-2 and increased expression of Bax, cytochrome c, and caspase-3 and TUNEL-positive cells. In contrast, physical exercise led to reduced insulin resistance, improved mitochondrial function, and reduced apoptosis in the hippocampus. The results suggest that physiological stimulations such as exercise improve hippocampal function and suppress apoptosis, potentially preventing the memory loss associated with obesity-induced insulin resistance. 2+ 2, 2 2

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Physical exercise promotes memory capability by enhancing hippocampal mitochondrial functions and inhibiting apoptosis in obesity-induced insulin resistance by high fat diet

Abstract

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