Article Text

Investigation into peroxisome proliferator activated receptor α and γ hepatic mRNA levels in diet induced obesity: a potential mechanism for fetal programming
  1. M Godfrey,
  2. J McConnell,
  3. N Igosheva
  1. King's College London, London, UK

Abstract

Introduction Fetal programming is a potentially maladaptive response to the nutritional environment during gestation, and may be responsive for the development of the metabolic syndrome in adult life. Changes in maternal peroxisome proliferator activated receptor-α (PPARα) and PPARγ expression have be implicated in fetal programming of the metabolic syndrome.

Methods Virgin female C57BL/6J mice were fed either an obesogenic (high fat/high carbohydrate) diet or control diet (standard mouse chow) for 8 weeks prior to liver collection and RNA extraction. Hepatic PPARα and PPARγ mRNA copy numbers were quantified for the two groups using reverse transcription and real-time PCR techniques.

Results Hepatic mRNA levels of PPARα was significantly decreased in mice fed the obesogenic diet compared with the control diet (p=0.018). PPARγ expression also decreased (p=0.089).

Conclusion This study aimed to assess the effects of an obesogenic diet similar to that prevalent in the developed world on the gene expression of PPARα and PPARγ in a mouse model of obesity. The motivation for this work was to incorporate the results into an improved understanding of the mechanism by which over-nutrition affects maternal and fetal metabolic pathways to program the fetus for chronic disease in later life.

The authors found the obesogenic diet significantly decreased PPARα expression, which may be caused by raised plasma glucose and insulin levels, which can downregulate PPARα expression. Changes in PPARα expression in obesity alter the maternal environment for conception and fetal development, potentially mediating fetal programming for the metabolic syndrome in adult life.

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