Growth hormone reverses dyslipidemia in adult offspring after maternal undernutrition

Wei-Fen Zhu1,2, Sheng-Jie Tang2, Zheng Shen3

  • 1Department of Pediatrics, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.

Scientific Reports
|July 22, 2017
PubMed

Insights

Growth hormone therapy in adulthood can reverse metabolic issues in individuals born small for gestational age (SGA). This treatment normalized lipid levels and improved gene expression related to metabolism in SGA rats.

Area of Science:

  • Endocrinology
  • Metabolic Research
  • Developmental Biology

Background:

  • Intrauterine growth restriction can lead to adult dyslipidemia.
  • Growth hormone (GH) therapy shows promise for improving metabolic parameters in children born small for gestational age (SGA).

Purpose of the Study:

  • To investigate if GH treatment during adolescence can reverse adult-onset dyslipidemia in SGA rats.
  • To explore the molecular mechanisms underlying GH's effects on lipid metabolism in SGA adults.

Main Methods:

  • Established an SGA rat model via maternal semi-starvation.
  • Administered GH or saline to SGA and appropriate for gestational age (AGA) rats from day 21 to 35.
  • Assessed body weight, length, serum triglycerides, hepatic gene expression (AMPK-α1, SREBP-1c, ACC-1), and histone acetylation in adulthood.

Main Results:

  • SGA rats exhibited reduced body size, elevated triglycerides, and altered hepatic gene expression (decreased AMPK-α1, increased SREBP-1c and ACC-1) compared to AGA rats.
  • GH treatment in adult SGA rats restored body size and normalized triglyceride levels.
  • GH administration reversed the expression changes of AMPK-α1, SREBP-1c, and ACC-1, accompanied by increased histone H3 acetylation at the AMPK-α1 promoter.

Conclusions:

  • A short course of GH treatment in adult SGA rats can effectively reverse dyslipidemia.
  • GH therapy normalizes lipid metabolism by modulating hepatic gene expression and epigenetic modifications at the AMPK-α1 promoter.