Chronic high fat feeding attenuates load-induced hypertrophy in mice

Mitchell Sitnick, Sue C. Bodine, John C. Rutledge

Research output: Contribution to journalArticle

63 Citations (Scopus)

Abstract

The incidence of obesity and obesity-related conditions, such as metabolic syndrome and insulin resistance, is on the increase. The effect of obesity on skeletal muscle function, especially the regulation of muscle mass, is poorly understood. In this study we investigated the effect of diet-induced obesity on the ability of skeletal muscle to respond to an imposed growth stimulus, such as increased load. Male C57BL/6 mice were randomized into two diet groups: a low fat, high carbohydrate diet (LFD) and a high fat, low carbohydrate diet (HFD) fed ad libitum for 14 weeks. Mice from each diet group were divided into two treatment groups: sedentary control or bilateral functional overload (FO) of the plantaris muscle. Mice were evaluated at 3, 7, 14 or 30 days following FO. By 14 days of FO, there was a 10% reduction (P < 0.05) in absolute growth of the plantaris in response to overload in HFD mice vs. LFD mice. By 30 days the attenuation in growth increased to 16% in HFD mice compared to LFD mice. Following FO, there was a reduction in the formation of polysomes in the HFD mice relative to the LFD mice, suggesting a decrease in protein translation. Further, activation of Akt and S6K1, in response to increased mechanical loading, was significantly attenuated in the HFD mice relative to the LFD mice. In conclusion, chronic high fat feeding impairs the ability of skeletal muscle to hypertrophy in response to increased mechanical load. This failure coincided with a failure to activate key members of the Akt/mTOR signalling pathway and increase protein translation.

Original languageEnglish
Pages (from-to)5753-5765
Number of pages13
JournalJournal of Physiology
Volume587
Issue number23
DOIs
StatePublished - 1 Dec 2009

Fingerprint

Hypertrophy
Fats
Skeletal Muscle
Obesity
Protein Biosynthesis
Diet
Growth
Carbohydrate-Restricted Diet
Polyribosomes
High Fat Diet
Inbred C57BL Mouse
Insulin Resistance
Carbohydrates
Muscles
Control Groups
Incidence

Cite this

Sitnick, Mitchell ; Bodine, Sue C. ; Rutledge, John C. / Chronic high fat feeding attenuates load-induced hypertrophy in mice. In: Journal of Physiology. 2009 ; Vol. 587, No. 23. pp. 5753-5765.
@article{0ba90e42219d4630a0de2439339f290d,
title = "Chronic high fat feeding attenuates load-induced hypertrophy in mice",
abstract = "The incidence of obesity and obesity-related conditions, such as metabolic syndrome and insulin resistance, is on the increase. The effect of obesity on skeletal muscle function, especially the regulation of muscle mass, is poorly understood. In this study we investigated the effect of diet-induced obesity on the ability of skeletal muscle to respond to an imposed growth stimulus, such as increased load. Male C57BL/6 mice were randomized into two diet groups: a low fat, high carbohydrate diet (LFD) and a high fat, low carbohydrate diet (HFD) fed ad libitum for 14 weeks. Mice from each diet group were divided into two treatment groups: sedentary control or bilateral functional overload (FO) of the plantaris muscle. Mice were evaluated at 3, 7, 14 or 30 days following FO. By 14 days of FO, there was a 10{\%} reduction (P < 0.05) in absolute growth of the plantaris in response to overload in HFD mice vs. LFD mice. By 30 days the attenuation in growth increased to 16{\%} in HFD mice compared to LFD mice. Following FO, there was a reduction in the formation of polysomes in the HFD mice relative to the LFD mice, suggesting a decrease in protein translation. Further, activation of Akt and S6K1, in response to increased mechanical loading, was significantly attenuated in the HFD mice relative to the LFD mice. In conclusion, chronic high fat feeding impairs the ability of skeletal muscle to hypertrophy in response to increased mechanical load. This failure coincided with a failure to activate key members of the Akt/mTOR signalling pathway and increase protein translation.",
author = "Mitchell Sitnick and Bodine, {Sue C.} and Rutledge, {John C.}",
year = "2009",
month = "12",
day = "1",
doi = "10.1113/jphysiol.2009.180174",
language = "English",
volume = "587",
pages = "5753--5765",
journal = "Journal of Physiology",
issn = "0022-3751",
publisher = "Wiley-Blackwell Publishing Ltd",
number = "23",

}

Chronic high fat feeding attenuates load-induced hypertrophy in mice. / Sitnick, Mitchell; Bodine, Sue C.; Rutledge, John C.

In: Journal of Physiology, Vol. 587, No. 23, 01.12.2009, p. 5753-5765.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Chronic high fat feeding attenuates load-induced hypertrophy in mice

AU - Sitnick, Mitchell

AU - Bodine, Sue C.

AU - Rutledge, John C.

PY - 2009/12/1

Y1 - 2009/12/1

N2 - The incidence of obesity and obesity-related conditions, such as metabolic syndrome and insulin resistance, is on the increase. The effect of obesity on skeletal muscle function, especially the regulation of muscle mass, is poorly understood. In this study we investigated the effect of diet-induced obesity on the ability of skeletal muscle to respond to an imposed growth stimulus, such as increased load. Male C57BL/6 mice were randomized into two diet groups: a low fat, high carbohydrate diet (LFD) and a high fat, low carbohydrate diet (HFD) fed ad libitum for 14 weeks. Mice from each diet group were divided into two treatment groups: sedentary control or bilateral functional overload (FO) of the plantaris muscle. Mice were evaluated at 3, 7, 14 or 30 days following FO. By 14 days of FO, there was a 10% reduction (P < 0.05) in absolute growth of the plantaris in response to overload in HFD mice vs. LFD mice. By 30 days the attenuation in growth increased to 16% in HFD mice compared to LFD mice. Following FO, there was a reduction in the formation of polysomes in the HFD mice relative to the LFD mice, suggesting a decrease in protein translation. Further, activation of Akt and S6K1, in response to increased mechanical loading, was significantly attenuated in the HFD mice relative to the LFD mice. In conclusion, chronic high fat feeding impairs the ability of skeletal muscle to hypertrophy in response to increased mechanical load. This failure coincided with a failure to activate key members of the Akt/mTOR signalling pathway and increase protein translation.

AB - The incidence of obesity and obesity-related conditions, such as metabolic syndrome and insulin resistance, is on the increase. The effect of obesity on skeletal muscle function, especially the regulation of muscle mass, is poorly understood. In this study we investigated the effect of diet-induced obesity on the ability of skeletal muscle to respond to an imposed growth stimulus, such as increased load. Male C57BL/6 mice were randomized into two diet groups: a low fat, high carbohydrate diet (LFD) and a high fat, low carbohydrate diet (HFD) fed ad libitum for 14 weeks. Mice from each diet group were divided into two treatment groups: sedentary control or bilateral functional overload (FO) of the plantaris muscle. Mice were evaluated at 3, 7, 14 or 30 days following FO. By 14 days of FO, there was a 10% reduction (P < 0.05) in absolute growth of the plantaris in response to overload in HFD mice vs. LFD mice. By 30 days the attenuation in growth increased to 16% in HFD mice compared to LFD mice. Following FO, there was a reduction in the formation of polysomes in the HFD mice relative to the LFD mice, suggesting a decrease in protein translation. Further, activation of Akt and S6K1, in response to increased mechanical loading, was significantly attenuated in the HFD mice relative to the LFD mice. In conclusion, chronic high fat feeding impairs the ability of skeletal muscle to hypertrophy in response to increased mechanical load. This failure coincided with a failure to activate key members of the Akt/mTOR signalling pathway and increase protein translation.

UR - http://www.scopus.com/inward/record.url?scp=71249106254&partnerID=8YFLogxK

U2 - 10.1113/jphysiol.2009.180174

DO - 10.1113/jphysiol.2009.180174

M3 - Article

C2 - 19822547

AN - SCOPUS:71249106254

VL - 587

SP - 5753

EP - 5765

JO - Journal of Physiology

JF - Journal of Physiology

SN - 0022-3751

IS - 23

ER -