Maternal High-Fat Diet Modulates Hepatic Glucose, Lipid Homeostasis and Gene Expression in the PPAR Pathway in the Early Life of Offspring

Abstract

Maternal dietary modifications determine the susceptibility to metabolic diseases in adult life. However, whether maternal high-fat feeding can modulate glucose and lipid metabolism in the early life of offspring is less understood. Furthermore, we explored the underlying mechanisms that influence the phenotype. Using C57BL/6J mice, we examined the effects on the offspring at weaning from dams fed with a high-fat diet or normal chow diet throughout pregnancy and lactation. Gene array experiments and quantitative real-time PCR were performed in the liver tissues of the offspring mice. The offspring of the dams fed the high-fat diet had a heavier body weight, impaired glucose tolerance, decreased insulin sensitivity, increased serum cholesterol and hepatic steatosis at weaning. Bioinformatic analyses indicated that all differentially expressed genes of the offspring between the two groups were mapped to nine pathways. Genes in the peroxisome proliferator-activated receptor (PPAR) signaling pathway were verified by quantitative real-time PCR and these genes were significantly up-regulated in the high-fat diet offspring. A maternal high-fat diet during pregnancy and lactation can modulate hepatic glucose, lipid homeostasis, and gene expression in the PPAR signaling in the early life of offspring, and our results suggested that potential mechanisms that influences this phenotype may be related partially to up-regulate some gene expression in the PPAR signalling pathway.

Maternal Diet Enriched with α-Linolenic or Saturated Fatty Acids Differentially Regulates Gene Expression in the Liver of Mouse Offspring

“…In line with this, we have previously shown that maternal SFA-enriched diet promoted the human symptoms of metabolic syndrome in mice, including diet-induced obesity, fatty liver and insulin resistance in adult mice exposed to an HFD. Interestingly, a similar offspring phenotype has been shown in mice by others, but subsequent to maternal HFD [16]. These findings enhance the relevance of our results, pointing to the maternal SFA ‘per se' independent of excess fat, in the programming of chronic disease in the offspring.…”

Maternal Low-Protein Diet Modulates Glucose Metabolism and Hepatic MicroRNAs Expression in the Early Life of Offspring †

“…The tolerance test was performed as described previously [16]. Mice were overnight-fasted (12–16 h) and fasted blood glucose was measured in tail vein blood samples.…”

Perinatal maternal high‐fat diet promotes alterations in hepatic lipid metabolism and resistance to the hypolipidemic effect of fish oil in adolescent rat offspring

“…Female Wistar rats, 60 days old, received a standard diet (STD) for rodents (9% of the calories as fat) or a HFD (28,6% of the calories as fat) for eight weeks before mating and during gestation and lactation . Our HFD is moderately high fat compared to most experimental models, which generally use diets with 50% of the calories as fat . This is an important aspect, because the diet was formulated to obtain an increased percent of lipid without characteristics of low‐protein or low‐carbohydrate diet, and conserving equal calories with standard diet.…”