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Altered adipocyte structure and function in nutritionally programmed microswine offspring.

E A DuPriest1, P Kupfer1, B Lin1

  • 11Department of Medicine, Oregon Health & Science University, Portland, OR, USA.

Journal of Developmental Origins of Health and Disease
|August 8, 2014
PubMed
Summary
This summary is machine-generated.

Early-life protein restriction programs adipocyte dysfunction, altering adiponectin levels and glucose homeostasis independently of obesity. This nutritional programming in young swine suggests increased future disease risk.

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Area of Science:

  • Developmental Biology
  • Nutritional Science
  • Endocrinology

Background:

  • Adipose tissue (AT) dysfunction is linked to obesity and cardiometabolic disease.
  • The impact of early-life nutritional deficiency on adipocyte function, independent of obesity, remains largely untested.

Purpose of the Study:

  • To investigate if perinatal maternal protein restriction (MPR) programs adipocyte dysfunction in juvenile offspring.
  • To assess adipocyte size, gene expression (adiponectin, TNF-α mRNA), and plasma hormone levels in response to MPR, independent of obesity.

Main Methods:

  • Juvenile microswine offspring from mothers fed either a normal or protein-restricted diet were studied.
  • Measurements included adipocyte size in intra-abdominal (ABD-AT) and subcutaneous (SC-AT) adipose tissues.
  • Assessed adiponectin and tumor necrosis factor (TNF)-α messenger ribonucleic acid (mRNA) levels, plasma cortisol, leptin, insulin, and glucose.

Main Results:

  • Low-protein offspring (LPO) exhibited reduced adipocyte size in ABD-AT and altered SC-AT adipocyte size in females.
  • Adiponectin mRNA levels were significantly lower in LPO regardless of depot or sex.
  • Correlations between body fat and adipokine levels, significant in controls, were absent in LPO, indicating dysregulation.

Conclusions:

  • Perinatal protein restriction can program adipocyte structure and adipokine gene expression independently of obesity.
  • This early-life nutritional programming leads to altered adiponectin levels and subtle glucose homeostasis changes.
  • These metabolic alterations in juvenile offspring suggest an increased risk for future cardiometabolic disease.