title: Maternal Western diet increases adiposity even in male offspring of obesity-resistant rat dams: early endocrine risk markers.
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.
authors.affiliation: Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, California.|Neurosciences Graduate Program, University of California, San Diego, La Jolla, California.
authors.forename: Jennifer B
authors.initials: JB
authors.lastname: Frihauf
authors.affiliation: Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, California.
authors.forename: Éva M
authors.initials: ÉM
authors.lastname: Fekete
authors.affiliation: Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, Alabama.
authors.forename: Tim R
authors.initials: TR
authors.lastname: Nagy
authors.affiliation: Neurology Service, VA Medical Center, East Orange, New Jersey; and.|Department of Neurology, Rutgers, New Jersey Medical School, Newark, New Jersey.
authors.forename: Barry E
authors.initials: BE
authors.lastname: Levin
authors.affiliation: Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, California; ezorrilla@scripps.edu.|Neurosciences Graduate Program, University of California, San Diego, La Jolla, California.
authors.forename: Eric P
authors.initials: EP
authors.lastname: Zorrilla
mesh_terms: D050154:Adiposity / Q000502:physiology; D000818:Animals; D021461:Animals, Outbred Strains; D015415:Biomarkers / Q000097:blood; D066273:Diet, Western; D060467:Disease Resistance / Q000502:physiology*; D002149:Energy Intake; D005260:Female; D006728:Hormones / Q000097:blood*; D008297:Male; D039382:Maternal Nutritional Physiological Phenomena / Q000502:physiology*; D009765:Obesity / Q000097:blood / Q000175:diagnosis / Q000503:physiopathology*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012307:Risk Factors
chemical_list: D015415:Biomarkers; D006728:Hormones
keywords: diet-induced obesity; endocrine hormone; energy expenditure; environmental programming; heritable obesity