Altered adipocyte structure and function in nutritionally programmed microswine offspring

E. A. Dupriest, P. Kupfer, B. Lin, K. Sekiguchi, Terry Morgan, Kim Saunders, T. T. Chatkupt, O. N. Denisenko, Jonathan Purnell, Susan Bagby

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Adipose tissue (AT) dysfunction links obesity of any cause with cardiometabolic disease, but whether early-life nutritional deficiency can program adipocyte dysfunction independently of obesity is untested. In 35-month-old juvenile microswine offspring exposed to isocaloric perinatal maternal protein restriction (MPR) and exhibiting accelerated prepubertal fat accrual without obesity, we assessed markers of acquired obesity: adiponectin and tumor necrosis factor (TNF)-α messenger ribonucleic acid (mRNA) levels and adipocyte size in intra-abdominal (ABD-AT) and subcutaneous (SC-AT) adipose tissues. Plasma cortisol, leptin and insulin levels were measured in fetal, neonatal and juvenile offspring. In juvenile low-protein offspring (LPO), adipocyte size in ABD-AT was reduced 22% (P = 0.011 v. controls), whereas adipocyte size in SC-AT was increased in female LPO (P = 0.05) and normal in male LPO; yet, adiponectin mRNA in LPO was low in both sexes and in both depots (P <0.001). Plasma leptin (P = 0.004) and cortisol (P <0.05) were reduced only in neonatal LPO during MPR. In juveniles, correlations between % body fat and adiponectin mRNA, TNF-α mRNA or plasma leptin were significant in normal-protein offspring (NPO) but absent in LPO. Plasma glucose in juvenile LPO was increased in males but decreased in females (interaction, P = 0.023); plasma insulin levels and insulin sensitivity were unaffected. Findings support nutritional programming of adipocyte size and gene expression and subtly altered glucose homeostasis. Reduced adiponectin mRNA and adipokine dysregulation in juvenile LPO following accelerated growth occurred independently of obesity, adipocyte hypertrophy or inflammatory markers; thus, perinatal MPR and/or growth acceleration can alter adipocyte structure and disturb adipokine homeostasis in metabolically adverse patterns predictive of enhanced disease risk.

Original languageEnglish (US)
Pages (from-to)198-209
Number of pages12
JournalJournal of Developmental Origins of Health and Disease
Volume3
Issue number3
DOIs
StatePublished - Jun 2012

Fingerprint

Adipocytes
Proteins
Adiponectin
Adipose Tissue
Obesity
RNA
Leptin
Adipokines
Mothers
Hydrocortisone
Homeostasis
Tumor Necrosis Factor-alpha
Insulin
Glucose
Intra-Abdominal Fat
Nutritional Support
Subcutaneous Fat
Growth
Malnutrition
Hypertrophy

Keywords

  • adipose tissue
  • catch-up growth
  • maternal protein restriction

ASJC Scopus subject areas

  • Medicine (miscellaneous)

Cite this

Altered adipocyte structure and function in nutritionally programmed microswine offspring. / Dupriest, E. A.; Kupfer, P.; Lin, B.; Sekiguchi, K.; Morgan, Terry; Saunders, Kim; Chatkupt, T. T.; Denisenko, O. N.; Purnell, Jonathan; Bagby, Susan.

In: Journal of Developmental Origins of Health and Disease, Vol. 3, No. 3, 06.2012, p. 198-209.

Research output: Contribution to journalArticle

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AU - Morgan, Terry

AU - Saunders, Kim

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