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Transgenic expression of myostatin propeptide prevents diet-induced obesity and insulin resistance
Baoping Zhao1, Robert J Wall, Jinzeng Yang
1Department of Human Nutrition, Food and Animal Sciences, University of Hawaii, Honolulu, HI 96822, USA.
Abstract:
Obesity and insulin resistance cause serious consequences to human health. To study effects of skeletal muscle growth on obesity prevention, we focused on a key gene of skeletal muscle named myostatin, which plays an inhibitory role in muscle growth and development. We generated transgenic mice through muscle-specific expression of the cDNA sequence (5'-region 886 nucleotides) encoding for the propeptide of myostatin. The transgene effectively depressed myostatin function. Transgenic mice showed dramatic growth and muscle mass by 9 weeks of age. Here we reported that individual major muscles of transgenic mice were 45-115% heavier than those of wild-type mice, maintained normal blood glucose, insulin sensitivity, and fat mass after a 2-month regimen with a high-fat diet (45% kcal fat). In contrast, high-fat diet induced wild-type mice with 170-214% more fat mass than transgenic mice and developed impaired glucose tolerance and insulin resistance. Insulin signaling, measured by Akt phosphorylation, was significantly elevated by 144% in transgenic mice over wild-type mice fed a high-fat diet. Interestingly, high-fat diet significantly increased adiponectin secretion while blood insulin, resistin, and leptin levels remained normal in the transgenic mice. The results suggest that disruption of myostatin function by its propeptide favours dietary fat utilization for muscle growth and maintenance. An increased secretion of adiponectin may promote energy partition toward skeletal muscles, suggesting that a beneficial interaction between muscle and adipose tissue play a role in preventing obesity and insulin resistance.
Insights
Inhibiting myostatin in mice promotes skeletal muscle growth and enhances fat utilization. This genetic modification prevents diet-induced obesity and insulin resistance, highlighting muscle
Area of Science:
- Molecular Biology
- Metabolic Diseases
- Genetics
Background:
- Obesity and insulin resistance pose significant global health challenges.
- Myostatin is a key negative regulator of skeletal muscle growth and development.
- Understanding skeletal muscle's role in metabolic health is crucial for obesity prevention.
Purpose of the Study:
- To investigate the impact of inhibiting myostatin on obesity and insulin resistance.
- To explore the potential of skeletal muscle growth as a strategy for metabolic disease prevention.
- To analyze the effects of myostatin propeptide expression on metabolic parameters in mice.
Main Methods:
- Generation of transgenic mice with muscle-specific expression of the myostatin propeptide cDNA.
- Assessment of muscle mass, body composition, and metabolic parameters (glucose tolerance, insulin sensitivity) after high-fat diet feeding.
- Measurement of insulin signaling pathway activation (Akt phosphorylation) and adipokine levels.
Main Results:
- Transgenic mice exhibited significantly increased muscle mass (45-115% heavier) compared to wild-type controls.
- Transgenic mice maintained normal blood glucose, insulin sensitivity, and fat mass on a high-fat diet.
- Wild-type mice on a high-fat diet developed increased fat mass (170-214%) and insulin resistance, unlike transgenic mice.
Conclusions:
- Disrupting myostatin function via its propeptide promotes dietary fat utilization for muscle growth.
- Increased adiponectin secretion in transgenic mice may enhance energy partitioning towards skeletal muscles.
- Targeting myostatin offers a potential therapeutic strategy for preventing obesity and insulin resistance through muscle-adipose tissue crosstalk.
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