Maternal obesity heritably perturbs offspring metabolism for three generations without serial programming
S A Eaton1,2, A J Aiken1, P E Young1
1Molecular, Structural and Computational Biology Division, Victor Chang Cardiac Research Institute, Darlinghurst, New South Wales, Australia.
International Journal of Obesity (2005)
|October 7, 2017
Summary
Maternal obesity can induce a latent metabolic dysfunction in male descendants across generations. This predisposition is inherited via germline, not serial exposure, suggesting epigenetic inheritance.
Area of Science:
- Metabolic programming
- Developmental origins of health and disease
- Epigenetics
Background:
- Maternal obesity impacts offspring metabolism across generations.
- Distinguishing true inheritance from serial exposure is crucial.
Purpose of the Study:
- To investigate the inheritance pattern of metabolic dysfunction induced by maternal obesity.
- To differentiate between germline inheritance and serial programming in multigenerational effects.
Main Methods:
- Utilized the Avy mouse model of maternal obesity.
- Assessed metabolic health and phenotype latency in F1, F2, and F3 male descendants.
- Analyzed hepatic Apoa4 expression as a molecular marker.
Main Results:
- F2 grandsons and F3 great grandsons inherited a latent predisposition to metabolic dysfunction.
- Phenotype remained latent on a healthy diet, excluding serial programming.
- Upregulation of hepatic Apoa4 was a consistent signature across generations.
Conclusions:
- Multigenerational metabolic effects of maternal obesity are inherited via the germline.
- Serial programming through repeated gestational exposure is excluded.
- Evidence supports epigenetic inheritance of metabolic dysfunction.
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