Affiliation:
1. Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, California;
2. Neurosciences Graduate Program, University of California, San Diego, La Jolla, California;
3. Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, Alabama;
4. Neurology Service, VA Medical Center, East Orange, New Jersey; and
5. Department of Neurology, Rutgers, New Jersey Medical School, Newark, New Jersey
Abstract
Maternal overnutrition or associated complications putatively mediate the obesogenic effects of perinatal high-fat diet on developing offspring. Here, we tested the hypothesis that a Western diet developmental environment increases adiposity not only in male offspring from obesity-prone (DIO) mothers, but also in those from obesity-resistant (DR) dams, implicating a deleterious role for the Western diet per se. Selectively bred DIO and DR female rats were fed chow (17% kcal fat) or Western diet (32%) for 54 days before mating and, thereafter, through weaning. As intended, despite chow-like caloric intake, Western diet increased prepregnancy weight gain and circulating leptin levels in DIO, but not DR, dams. Yet, in both genotypes, maternal Western diet increased the weight and adiposity of preweanlings, as early as in DR offspring, and increased plasma leptin, insulin, and adiponectin of weanlings. Although body weight normalized with chow feeding during adolescence, young adult Western diet offspring subsequently showed decreased energy expenditure and, in DR offspring, decreased lipid utilization as a fuel substrate. By mid-adulthood, maternal Western diet DR offspring ate more chow, weighed more, and were fatter than controls. Thus, maternal Western diet covertly programmed increased adiposity in childhood and adulthood, disrupted relations of energy regulatory hormones with body fat, and decreased energy expenditure in offspring of lean, genetically obesity-resistant mothers. Maternal Western diet exposure alone, without maternal obesity or overnutrition, can promote offspring weight gain.
Funder
HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
HHS | NIH | National Institute on Drug Abuse (NIDA)
Publisher
American Physiological Society
Subject
Physiology (medical),Physiology