Journal article
Maternal obesity, inflammation, and fetal skeletal muscle development
Biology of reproduction, Vol.82(1), pp.4-12
01/2010
Handle:
https://hdl.handle.net/2376/108413
PMID: 19516021
Abstract
Maternal obesity coupled with Western-style high-energy diets represents a special problem that can result in poor fetal development, leading to harmful, persistent effects on offspring, including predisposition to obesity and type 2 diabetes. Mechanisms linking maternal obesity to the increased incidence of obesity and other metabolic diseases in offspring remain poorly defined. Because skeletal muscle is the principal site for glucose and fatty acid utilization and composes 40%-50% of total body mass, changes in the properties of offspring skeletal muscle and its mass resulting from maternal obesity may be responsible for the increase in type 2 diabetes and obesity. Fetal stage is crucial for skeletal muscle development because there is no net increase in the muscle fiber number after birth. Fetal skeletal muscle development involves myogenesis, adipogenesis, and fibrogenesis, which are all derived from mesenchymal stem cells (MSCs). Shifting commitment of MSCs from myogenesis to adipogenesis and fibrogenesis will result in increased intramuscular fat and connective tissue, as well as reduced numbers of muscle fiber and/or diameter, all of which have lasting negative effects on offspring muscle function and properties. Maternal obesity leads to low-grade inflammation, which changes the commitment of MSCs in fetal muscle through several possible mechanisms: 1) inflammation downregulates wingless and int (WNT) signaling, which attenuates myogenesis; 2) inflammation inhibits AMP-activated protein kinase, which promotes adipogenesis; and 3) inflammation may induce epigenetic modification through polycomb group proteins. More studies are needed to further explore the underlying mechanisms associated with maternal obesity, inflammation, and the commitment of MSCs.
Metrics
7 Record Views
Details
- Title
- Maternal obesity, inflammation, and fetal skeletal muscle development
- Creators
- Min Du - Department of Animal Science, University of Wyoming, Laramie, Wyoming 82071, USA. mindu@uwyo.eduXu YanJun F TongJunxing ZhaoMei J Zhu
- Publication Details
- Biology of reproduction, Vol.82(1), pp.4-12
- Academic Unit
- Animal Sciences, Department of
- Publisher
- United States
- Grant note
- R01 HD067449 / NICHD NIH HHS R03HD060076-01 / NICHD NIH HHS R03 HD060076 / NICHD NIH HHS
- Identifiers
- 99900547172401842
- Language
- English
- Resource Type
- Journal article