title: Percentage extremity fat, but not percentage trunk fat, is lower in adolescent boys with anorexia nervosa than in healthy adolescents.
abstract: BACKGROUND
  Anorexia nervosa (AN) is a condition of severe undernutrition associated with altered regional fat distribution in females. Although primarily a disease of females, AN is increasingly being recognized in males and is associated with hypogonadism. Testosterone is a major regulator of body composition in males, and testosterone administration in adults decreases visceral fat. However, the effect of low testosterone and other hormonal alterations on body composition in boys with AN is not known.
  
  
  OBJECTIVE
  We hypothesized that testosterone deficiency in boys with AN is associated with higher trunk fat, as opposed to extremity fat, compared with control subjects.
  
  
  METHODS
  We assessed body composition using dual-energy X-ray absorptiometry and measured fasting testosterone, estradiol, insulin- like growth factor-1, leptin, and active ghrelin concentrations in 15 boys with AN and in 15 control subjects of comparable maturity aged 12-19 y.
  
  
  RESULTS
  Fat and lean mass in AN boys was 69% and 86% of that in control subjects. Percentage extremity fat and extremity lean mass were lower in boys with AN (P = 0.003 and 0.0008); however, percentage trunk fat and the trunk to extremity fat ratio were higher after weight was adjusted for (P = 0.005 and 0.003). Testosterone concentrations were lower in boys with AN, and, on regression modeling, positively predicted percentage extremity lean mass and inversely predicted percentage trunk fat and trunk to extremity fat ratio. Other independent predictors of regional body composition were bone age and weight.
  
  
  CONCLUSIONS
  In adolescent boys with AN, higher percentage trunk fat, higher trunk to extremity fat ratio, lower percentage extremity fat, and lower extremity lean mass (adjusted for weight) are related to the hypogonadal state.
authors.affiliation: Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. mmisra@partners.org
authors.forename: Madhusmita
authors.initials: M
authors.lastname: Misra
authors.forename: Debra K
authors.initials: DK
authors.lastname: Katzman
authors.forename: Jennalee
authors.initials: J
authors.lastname: Cord
authors.forename: Stephanie J
authors.initials: SJ
authors.lastname: Manning
authors.forename: Diane
authors.initials: D
authors.lastname: Mickley
authors.forename: David B
authors.initials: DB
authors.lastname: Herzog
authors.forename: Karen K
authors.initials: KK
authors.lastname: Miller
authors.forename: Anne
authors.initials: A
authors.lastname: Klibanski
mesh_terms: D015502:Absorptiometry, Photon; D000273:Adipose Tissue / Q000033:anatomy & histology* / Q000473:pathology; D000293:Adolescent; D000856:Anorexia Nervosa / Q000503:physiopathology*; D001823:Body Composition / Q000502:physiology*; D016022:Case-Control Studies; D002648:Child; D004958:Estradiol / Q000097:blood; D005121:Extremities; D054439:Ghrelin / Q000097:blood; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D020738:Leptin / Q000097:blood; D008297:Male; D013739:Testosterone / Q000097:blood / Q000172:deficiency*; D013909:Thorax; D055815:Young Adult
chemical_list: D054439:Ghrelin; D020738:Leptin; D013739:Testosterone; D004958:Estradiol; D007334:Insulin-Like Growth Factor I