The impact of maternal high fat feeding on liver and abdominal fat accumulation in adult offspring under a long term high fat diet

BURGUEÑO AL; CARABELLI J; SOOKOIAN S; PIROLA CJ

HEPATOLOGY

Wiley

Año: 2010 vol. 51 p. 2234 - 2235

0171-6123

We read with great interest the article by Bruce KD et al. regarding the effect in a micemodel of maternal high fat feeding on the development of nonalcoholic fatty liver disease(NAFLD) in adult offspring 1. The authors observed that maternal fat intake contributestoward the NAFLD progression in adult offspring, which is mediated through impairedhepatic mitochondrial metabolism. Although the authors reported only female mice data astheir data from males and females showed the same pattern, we consider that some issuesdeserve further discussion.We evaluated in a rat model the impact of developmental and long-term adult nutritionalinsult of high fat diet (HFD) on liver steatosis and abdominal fat accumulation, andcompared males and females offspring of dams exposed to different nutrition treatments(HFD vs. standard chow diet, SCD) to contrast the hypothesis of nutritional insults duringfetal development can result in a fatty liver phenotype in adulthood. Interestingly, wereplicated the findings of Bruce et al., and additionally observed that maternal HFD feedingmodified sexual dimorphic effect of HFD on liver steatosis and abdominal fat contentobserved in offspring of mothers fed-SCD.Female Wistar rats were randomly assigned to either ad libitum HFD solid diet 2 or SCD.Dams were fed 15 days before conception and during gestation and lactation. Theseventeen–week-old offspring were assigned either ad libitum HFD or SCD for a 18–weekperiod, generating 8 experimental groups (Figure 1). At the completion of the study, animalswere sacrificed and abdominal fat tissue (intra and retroperitoneal) was measured by directweighting; the degree of liver steatosis was assessed as previously reported 3.In the group of HFD-fed offspring of SCD-fed dams we observed a clear sexually dimorphiceffect of HFD feeding as female rats developed a significantly greater degree of fatty changethan male rats; this finding was similar when we analyzed abdominal fat content (Figure 1). of feeding HFD (a finding previouslyreported in other rat models of NAFLD 4) deserves further investigations as the underlyingmechanism involved in the gender difference are not clear. Otherwise, our study providesadditional evidence of the effect of maternal HF nutrition on the liver and abdominal fataccumulation in either male or female HFD-fed offspring, thus suggesting the importance ofthe developmental programming that can induce the NAFLD phenotype completelyindependent of gender differences. This finding strongly supports the hypothesis of Bruce etal. about the “priming” effect of maternal mitochondria on metabolic pathways associatedwith NAFLD, which is compatible with our recent findings of a decrease in mitochondrialDNA copy number in adolescents with insulin resistance 5 and in newborns with abnormalbirth weight 6- two well known risk factors for Metabolic Syndrome in adult life.