title: Peripubertal-onset but not adult-onset obesity increases IGF-I and drives development of lean mass, which may lessen the metabolic impairment in adult obesity.
abstract: It has been suggested that adult metabolic dysfunction may be more severe in individuals who become obese as children compared with those who become obese later in life. To determine whether adult metabolic function differs if diet-induced weight gain occurs during the peripubertal age vs. if excess weight gain occurs after puberty, male C57Bl/6J mice were fed a low-fat (LF; 10% kcal from fat) or high-fat (HF; 60% kcal from fat) diet starting during the peripubertal period (pHF; 4 wk of age) or as adults (aHF; 12 wk of age). Both pHF and aHF mice were hyperinsulinemic and hyperglycemic, and both showed impaired glucose tolerance and insulin resistance compared with their LF-fed controls. However, despite a longer time on diet, pHF mice were relatively more insulin sensitive than aHF mice, which was associated with higher lean mass and circulating IGF-I levels. In addition, HF feeding had an overall stimulatory effect on circulating corticosterone levels; however, this rise was associated only with elevated plasma ACTH in the aHF mice. Despite the belief that adult metabolic dysfunction may be more severe in individuals who become obese as children, data generated using a diet-induced obese mouse model suggest that adult metabolic dysfunction associated with peripubertal onset of obesity is not worse than that associated with adult-onset obesity.
authors.affiliation: Department of Cell Biology, Physiology, and Immunology, Instituto Maimónides de Investigación Biomédica de Córdoba/Hospital Universitario Reina Sofia, University of Cordoba Centro de Investigacion Biomedica en Red Fisiopatologia de Obesidad y Nutricion, Córdoba, Spain.
authors.forename: Jose
authors.initials: J
authors.lastname: Cordoba-Chacon
authors.forename: Manuel D
authors.initials: MD
authors.lastname: Gahete
authors.forename: Ana I
authors.initials: AI
authors.lastname: Pozo-Salas
authors.forename: Antonio
authors.initials: A
authors.lastname: Moreno-Herrera
authors.forename: Justo P
authors.initials: JP
authors.lastname: Castaño
authors.forename: Rhonda D
authors.initials: RD
authors.lastname: Kineman
authors.forename: Raúl M
authors.initials: RM
authors.lastname: Luque
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000375:Aging; D000818:Animals; D001823:Body Composition; D003345:Corticosterone / Q000097:blood; D059305:Diet, High-Fat / Q000009:adverse effects; D004195:Disease Models, Animal; D018149:Glucose Intolerance / Q000209:etiology; D006943:Hyperglycemia / Q000209:etiology; D006946:Hyperinsulinism / Q000209:etiology; D007333:Insulin Resistance; D007334:Insulin-Like Growth Factor I / Q000032:analysis*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D024510:Muscle Development; D009765:Obesity / Q000097:blood / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology*; D011897:Random Allocation; D012720:Severity of Illness Index; D046468:Sexual Development
chemical_list: D007334:Insulin-Like Growth Factor I; D000324:Adrenocorticotropic Hormone; D003345:Corticosterone