Maternal Obesity-Impaired Insulin Signaling in Sheep and Induced Lipid Accumulation and Fibrosis in Skeletal Muscle of Offspring

Xu Yan; YAN HUANG; Jun-Xing ZHAO; Nathan M LONG; Adam B UTHLAUT; Mei-Jun ZHU; Stephen P FORD; Peter W NATHANIELSZ; Min Du

doi:10.1095/biolreprod.110.089649

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Maternal Obesity-Impaired Insulin Signaling in Sheep and Induced Lipid Accumulation and Fibrosis in Skeletal Muscle of Offspring

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Maternal Obesity-Impaired Insulin Signaling in Sheep and Induced Lipid Accumulation and Fibrosis in Skeletal Muscle of Offspring

Xu Yan, YAN HUANG, Jun-Xing ZHAO, Nathan M LONG, Adam B UTHLAUT, Mei-Jun ZHU, Stephen P FORD, Peter W NATHANIELSZ and Min Du

Biology of reproduction, Vol.85(1), pp.172-178

2011

DOI: https://doi.org/10.1095/biolreprod.110.089649

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https://hdl.handle.net/2376/104356

PMID: 21349823

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Abstract

Fundamental and applied biological sciences. Psychology

Vertebrates: osteoarticular system, musculoskeletal system

Striated muscle. Tendons

Vertebrates: reproduction

Biological and medical sciences

Metabolic diseases

Medical sciences

Obesity

The prevalence of maternal obesity is increasing rapidly in recent decades. We previously showed that maternal obesity affected skeletal muscle development during the fetal stage. The objective of this study was to evaluate the effects of maternal obesity on the skeletal muscle properties of offspring. Ewes were fed a control diet (100% energy requirement, Con) or an obesogenic diet (150% energy requirement, OB) from 2 mo before pregnancy to weaning. After weaning, the offspring lambs were fed a maintenance diet until 19 mo of age and then ad libitum for 12 wk to measure feed intake. At 22 mo old, the longissimus dorsi (LD) muscle was biopsied. The downstream insulin signaling was lower in OB than Con lambs as shown by reduction in the phosphorylation of protein kinase B, mammalian target of rapamycin, and 4-E binding protein 1. On the other hand, the phosphorylation of protein kinase C and insulin receptor substrate 1 was higher in OB compared to Con lambs. More intramuscular adipocytes were observed in OB compared to Con offspring muscle, and the expression of peroxisome proliferator-activated receptor gamma, an adipocyte marker, was also higher, which was consistent with the higher intramuscular triglyceride content. Both fatty acid transport protein 1 and cluster of differentiation 36 (also known as fatty acid translocase) were increased in the OB group. In addition, higher collagen content was also detected in OB compared to Con offspring. In conclusion, our data show that offspring from obese mothers had impaired insulin signaling in muscle compared with control lambs, which correlates with increased intramuscular triglycerides and higher expression of fatty acid transporters. These data clearly show that maternal obesity impairs the function of the skeletal muscle of offspring, supporting the fetal programming of adult metabolic diseases.

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Title: Maternal Obesity-Impaired Insulin Signaling in Sheep and Induced Lipid Accumulation and Fibrosis in Skeletal Muscle of Offspring
Creators: Xu Yan - The Center for the Study of Fetal Programming,Department of Animal Science, University of Wyoming, Laramie, Wyoming, United States
YAN HUANG - The Center for the Study of Fetal Programming,Department of Animal Science, University of Wyoming, Laramie, Wyoming, United States
Jun-Xing ZHAO - The Center for the Study of Fetal Programming,Department of Animal Science, University of Wyoming, Laramie, Wyoming, United States
Nathan M LONG - The Center for the Study of Fetal Programming,Department of Animal Science, University of Wyoming, Laramie, Wyoming, United States
Adam B UTHLAUT - The Center for the Study of Fetal Programming,Department of Animal Science, University of Wyoming, Laramie, Wyoming, United States
Mei-Jun ZHU - University of Wyoming
Stephen P FORD - The Center for the Study of Fetal Programming,Department of Animal Science, University of Wyoming, Laramie, Wyoming, United States
Peter W NATHANIELSZ - Center for Pregnancy and Newborn Research,Department of Obstetrics and Gynecology, University of Texas Health Sciences Center, San Antonio, Texas, United States
Min Du - The Center for the Study of Fetal Programming,Department of Animal Science, University of Wyoming, Laramie, Wyoming, United States
Publication Details: Biology of reproduction, Vol.85(1), pp.172-178
Academic Unit: Department of Animal Sciences
Publisher: Society for the Study of Reproduction; Madison, WI
Number of pages: 7
Grant note: P20RR016474 / NATIONAL CENTER FOR RESEARCH RESOURCES; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Center for Research Resources (NCRR) 2008-35206-18826 / USDA National Institute of Food and Agriculture; United States Department of Agriculture (USDA) 1R01HD067449 / NIH; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA P20RR016474 / Wyoming INBRE R01HD067449 / EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Identifiers: 99900546773101842
Language: English
Resource Type: Journal article