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

BURGUEÑO A; CARABELLI J; SOOKOIAN S; PIROLA CJ,

HEPATOLOGY (BALTIMORE, MD.)

JOHN WILEY & SONS INC

Lugar: United States ; Año: 2010 p. 1 - 2

0270-9139

We read with great interest the article by Bruce KD et al. regarding the effect in a mice model 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 contributes toward the NAFLD progression in adult offspring, which is mediated through impaired hepatic mitochondrial metabolism. Although the authors reported only female mice data as their data from males and females showed the same pattern, we consider that some issues deserve further discussion. We evaluated in a rat model the impact of developmental and long-term adult nutritional insult of high fat diet (HFD) on liver steatosis and abdominal fat accumulation, and compared males and females offspring of dams exposed to different nutrition treatments (HFD vs. standard chow diet, SCD) to contrast the hypothesis of nutritional insults during fetal development can result in a fatty liver phenotype in adulthood. Interestingly, we replicated the findings of Bruce et al., and additionally observed that maternal HFD feeding modified sexual dimorphic effect of HFD on liver steatosis and abdominal fat content observed 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. The seventeen?week-old offspring were assigned either ad libitum HFD or SCD for a 18?week period, generating 8 experimental groups (Figure 1). At the completion of the study, animals were sacrificed and abdominal fat tissue (intra and retroperitoneal) was measured by direct weighting; 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 dimorphic effect of HFD feeding as female rats developed a significantly greater degree of fatty change than male rats; this finding was similar when we analyzed abdominal fat content (Figure 1). However, in the group of HFD-fed offspring of HFD-fed dams the sexual differences in both fatty liver degree and abdominal fat content were not observed, although the degree of liver steatosis was lower in female offspring of HFD-fed dams vs. those of SCD-fed dams (Figure 1). Interestingly, these effects were independent of dam body weight suggesting a specific effect of the diet. In conclusion, the female-specific consequences of feeding HFD (a finding previously reported in other rat models of NAFLD 4) deserves further investigations as the underlying mechanism involved in the gender difference are not clear. Otherwise, our study provides additional evidence of the effect of maternal HF nutrition on the liver and abdominal fat accumulation in either male or female HFD-fed offspring, thus suggesting the importance of the developmental programming that can induce the NAFLD phenotype completely independent of gender differences. This finding strongly supports the hypothesis of Bruce et al. about the ?priming? effect of maternal mitochondria on metabolic pathways associated with NAFLD, which is compatible with our recent findings of a decrease in mitochondrial DNA copy number in adolescents with insulin resistance 5 and in newborns with abnormal birth weight 6- two well known risk factors for Metabolic Syndrome in adult life.