Increased maternal fat consumption during pregnancy alters body composition in neonatal mice

Abstract

Krasnow SM, Nguyen MT, Marks DL. Increased maternal fat consumption during pregnancy alters body composition in neonatal mice. Am J Physiol Endocrinol Metab 301: E1243-E1253, 2011. First published September 6, 2011 doi:10.1152/ajpendo.00261.2011Maternal overnutrition prior to and during gestation causes pronounced metabolic dysfunction in the adult offspring. However, less is known about metabolic adaptations in the offspring that occur independently of postnatal growth and nutrition. Therefore, we evaluated the impact of excess maternal dietary lipid intake on the in utero programming of body composition, hepatic function, and hypothalamic development in newborn (P0) offspring. Female mice were fed a low-fat (LF) or high-fat (HF) diet and were mated after 4, 12, and 23 wk. A subset of the obese HF dams was switched to the LF diet during the second (DR2) or third (DR3) pregnancies. The HF offspring accrued more fat mass than the LF pups, regardless of duration of maternal HF diet consumption or prepregnancy maternal adiposity. Increased neonatal adiposity was not observed in the DR3 pups. Liver weights were reduced in the HF offspring but not in the DR2 or DR3 pups. Offspring hepatic triglyceride content was reduced in the HF pups, but hepatic inflammation and expression of lipid metabolism genes were largely unaffected by maternal diet. Maternal diet did not alter the hypothalamic expression of orexigenic and anorexigenic neuropeptides in the offspring. Thus, the intrauterine programming of increased neonatal adiposity and reduced liver size by maternal overnutrition is evident in mice at birth and occurs prior to the development of maternal obesity. These observations demonstrate that dietary intervention during pregnancy minimizes the deleterious effects of maternal obesity on offspring body composition, potentially reducing the offsprings' risk of developing obesity and related diseases later in life. metabolic programming; liver; hypothalamus; inflammation; obesity THE GLOBAL PREVALENCE OF OBESITY has reached epidemic proportions in recent years, not only threatening the health and well-being of affected individuals but also imposing a considerable burden on the economic and health care systems of developed and developing nations (33). In the US, the prevalence of obesity has more than doubled in adults and more than tripled in children and adolescents since the 1970s. According to estimates from the 2007-2008 National Health and Nutrition Examination Survey, 33.8% of adults and 16.9% of children aged 2-19 are obese, and 9.5% of infants and toddlers are at or above the 95th percentile of the weight-for-length growth charts (23,24,45,46). Obese individuals have an increased risk of developing type 2 diabetes mellitus, hypertension, dyslipidemia, and nonalcoholic fatty liver disease. Once restricted to adults, these metabolic diseases and conditions are now being diagnosed in children and adolescents at alarming rates, mirroring the rising rates of juvenile obesity (34,39,47,52,55).The etiology of obesity is...

High-saturated fat-sucrose feeding affects lactation energetics in control mice and mice selectively bred for high wheel-running behavior

“…This can be associated with increased body length (8); however, increases in lean mass are less obvious (24). The HFS-induced pup growth and development may be dampened by intense behavioral and metabolic activities (37).…”

Early growth response protein-1 mediates lipotoxicity-associated placental inflammation: role in maternal obesity

“…Recent evidence has emerged from studies on the independent effects of maternal high-fat feeding that support the hypothesis that increased circulating lipids, as opposed to maternal obesity per se, are the mediator of fetal programming (36,43,65). Importantly, gestational exposure to high-fat diets has been associated with epigenetic changes (histone acetylation and methylation) in adipokine genes (43) and genes regulating glucose metabolism (65) in offspring tissues.…”

Nutritional manipulations in the perinatal period program adipose tissue in offspring

“…Models of maternal overnutrition and obesity rely on feeding the dams a high-fat (HF) or highenergy/cafeteria (fat and sugar) diet before (preconceptional period) and/or during gestation and/or lactation. In rodents, studies on maternal overfeeding have reported variable effects on birth weight, ranging from low to normal to high values (51,67,80). The discrepancy between these studies may be related to the complex interaction between maternal diet composition and genotypic susceptibility of individual rodent strains.…”