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Impact of abnormal nutrition during pregnancy on the offspring hormone resistance

W W Song1, S M Zhang, H B Liu

  • 1Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, 110004 Shenyang, China. songww@cmu2h.com

Journal of Endocrinological Investigation
|October 15, 2008
PubMed

Insights

Maternal nutrition impacts offspring health. Both low and high birth weights in offspring are linked to adult obesity and resistance to insulin and leptin, driven by distinct mechanisms.

Area of Science:

  • Reproductive biology and developmental origins of health and disease (DOHaD).

Background:

  • Maternal nutrition during pregnancy is crucial for fetal development.
  • Nutritional insults can have long-term consequences on offspring metabolic health.

Purpose of the Study:

  • To investigate the effects of abnormal maternal nutrition on insulin and leptin resistance in adult offspring.
  • To determine if abnormal birth weight, resulting from maternal dietary imbalances, influences metabolic syndrome markers.

Main Methods:

  • Established a rat model of abnormal pregnancy nutrition (low-protein or high-energy diets).
  • Categorized offspring into small for gestational age (SGA), large for gestational age (LGA), and control groups based on birth weight.
  • Measured body weight, fat weight, insulin and leptin levels, and insulin sensitivity index (ISI) at 4 and 12 weeks post-birth.

Main Results:

  • Low-protein diet resulted in SGA offspring; high-energy diet resulted in LGA offspring.
  • SGA and LGA offspring exhibited increased abdominal fat accumulation and elevated body weight by 12 weeks.
  • Both SGA and LGA offspring developed insulin and leptin resistance, indicated by increased hormone levels and decreased ISI.

Conclusions:

  • Abnormal maternal nutrition during pregnancy leads to abnormal offspring birth weight.
  • Both low (SGA) and high (LGA) birth weights are associated with adult-onset abdominal obesity and metabolic dysfunction, including insulin and leptin resistance.
  • The mechanisms underlying these metabolic disturbances may differ between SGA and LGA individuals.
Abstract

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