Altering Muscle Hypertrophy and Fat Accumulation in Myostatin Null Mice
type: CreativeWork
description: Myostatin is a negative regulator of muscle growth. Loss of myostatin function results in a dramatic phenotype in several species including cattle, mice, dogs and humans. Myostatin mutants exhibit wide-spread hypermuscularity and decreased fat accumulation. Though the phenotype of myostatin mutant animals is very striking, the question remains whether the loss of myostatin function fundamentally changes growth potential, metabolism, or inherent regulation in tissues, or if it is simply an effect independent of other factors. To that end, we sought to increase muscle growth even further in myostatin null mice through the use of the β-adrenergic agonist clenbuterol. The effects of clenbuterol treatment and the loss of myostatin function are quite similar and, in this study, were completely additive. Clenbuterol treatment increased muscle weights and protein accretion and reduced fat accumulation in both wild type and myostatin null mice. There was a significant interaction of genotype and clenbuterol treatment for gastrocnemius muscle weight, but the magnitude of the differences in weight gain between myostatin null and wild type was very small. We also aimed to alter fat accumulation and metabolism in myostatin null mice by feeding diets high in fat. Other research indicated that myostatin null mice were resistant to fat accumulation induced by high-fat feeding. In our study, fat accumulation was increased in both wild type and myostatin null mice fed high-fat diets, but the magnitude of the increase in myostatin null mice was less than that of wild type mice. This suggests that myostatin null mice are partially resistant to high-fat diet-induced obesity. Markers of metabolic syndrome often induced by high-fat feeding in mice were also improved in myostatin null compared with wild type mice. Liver fat content, serum triglycerides and serum leptin levels were lower in high-fat fed myostatin null mice than similarly fed wild type mice. Glucose tolerance, however, was a…
abstract: Myostatin is a negative regulator of muscle growth. Loss of myostatin function results in a dramatic phenotype in several species including cattle, mice, dogs and humans. Myostatin mutants exhibit wide-spread hypermuscularity and decreased fat accumulation. Though the phenotype of myostatin mutant animals is very striking, the question remains whether the loss of myostatin function fundamentally changes growth potential, metabolism, or inherent regulation in tissues, or if it is simply an effect independent of other factors. To that end, we sought to increase muscle growth even further in myostatin null mice through the use of the β-adrenergic agonist clenbuterol. The effects of clenbuterol treatment and the loss of myostatin function are quite similar and, in this study, were completely additive. Clenbuterol treatment increased muscle weights and protein accretion and reduced fat accumulation in both wild type and myostatin null mice. There was a significant interaction of genotype and clenbuterol treatment for gastrocnemius muscle weight, but the magnitude of the differences in weight gain between myostatin null and wild type was very small. We also aimed to alter fat accumulation and metabolism in myostatin null mice by feeding diets high in fat. Other research indicated that myostatin null mice were resistant to fat accumulation induced by high-fat feeding. In our study, fat accumulation was increased in both wild type and myostatin null mice fed high-fat diets, but the magnitude of the increase in myostatin null mice was less than that of wild type mice. This suggests that myostatin null mice are partially resistant to high-fat diet-induced obesity. Markers of metabolic syndrome often induced by high-fat feeding in mice were also improved in myostatin null compared with wild type mice. Liver fat content, serum triglycerides and serum leptin levels were lower in high-fat fed myostatin null mice than similarly fed wild type mice. Glucose tolerance, however, was a…
author: Dilger, Anna C.
language: eng
keywords: muscle, Fat, myostatin, mice
date published: 2010-01-06T16:12:00Z
date modified: 2026-07-22T22:25:07Z
provider: University of Illinois - Urbana-Champaign
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: University of Illinois at Urbana-Champaign

PropertyValue
property ID: Handle
value: http://hdl.handle.net/2142/14555