title: Determinants of increased energy expenditure in HIV-infected women.
abstract: BACKGROUND
  Little is known about sex-specific effects of HIV infection on energy expenditure.
  
  
  OBJECTIVE
  We investigated the determinants of energy expenditure in HIV-infected women.
  
  
  METHODS
  Resting energy expenditure (REE), body composition, and hormonal and nutritional indexes were compared in 33 ambulatory, premenopausal HIV-infected women and 26 weight-matched, healthy premenopausal control subjects. REE was determined by indirect calorimetry and body composition by dual-energy X-ray absorptiometry (DXA), bioelectrical impedance analysis, and skinfold-thickness analysis. Hormonal indexes included leptin, testosterone, estradiol, and insulin-like growth factor I.
  
  
  RESULTS
  HIV-infected subjects had a higher REE than control subjects [6794 +/- 1374 compared with 6011 +/- 607 kJ/d (1624 +/- 329 compared with 1437 +/- 145 kcal/d), P = 0.0096]. On average, REE was 119 +/- 23% of Harris-Benedict predictions in HIV-infected subjects compared with 102 +/- 9% for control subjects (P = 0.0007). In HIV-infected subjects, REE was highly correlated with fat-free mass (FFM) by DXA (R = 0.641, P < 0.001), but not with weight or disease status. The slope of the regression equation for REE and FFM was significantly greater (P = 0.027, analysis of covariance) for HIV-infected subjects [REE (kJ/d) = 203.5 (kg FFM) - 1237] than for control subjects [REE (kJ/d) = 77.4 (kg FFM) + 2923]. In a stepwise regression analysis, FFM was the most significant variable (P = 0.005), followed by free testosterone (P = 0.029), which together explained 49% of the variation in REE. The final equation was REE (kJ/d) = 230.8 (kg FFM) + 395.9 (free testosterone, pmol/L) - 3304.
  
  
  CONCLUSIONS
  Energy expenditure was higher in HIV-infected women than in control women. FFM is the primary determinant of REE in HIV-infected women, but energy expenditure is greater per kg FFM in HIV-infected subjects than in control subjects, which may contribute to the wasting syndrome.
authors.affiliation: Neuroendocrine Unit, General Clinical Research Center, Massachusetts General Hospital and Harvard Medical School, Boston 02114, USA. Grinspoons@A1.mgh.harvard.edu
authors.forename: S
authors.initials: S
authors.lastname: Grinspoon
authors.forename: C
authors.initials: C
authors.lastname: Corcoran
authors.forename: K
authors.initials: K
authors.lastname: Miller
authors.forename: E
authors.initials: E
authors.lastname: Wang
authors.forename: J
authors.initials: J
authors.lastname: Hubbard
authors.forename: D
authors.initials: D
authors.lastname: Schoenfeld
authors.forename: E
authors.initials: E
authors.lastname: Anderson
authors.forename: N
authors.initials: N
authors.lastname: Basgoz
authors.forename: A
authors.initials: A
authors.lastname: Klibanski
mesh_terms: D015502:Absorptiometry, Photon; D000328:Adult; D001481:Basal Metabolism; D001823:Body Composition; D015992:Body Mass Index; D002153:Calorimetry, Indirect; D016022:Case-Control Studies; D017097:Electric Impedance; D002149:Energy Intake; D005260:Female; D012739:Gonadal Steroid Hormones / Q000097:blood; D015658:HIV Infections / Q000378:metabolism*; D006801:Humans; D020738:Leptin; D017697:Premenopause / Q000378:metabolism; D011506:Proteins / Q000378:metabolism; D012044:Regression Analysis
chemical_list: D012739:Gonadal Steroid Hormones; D020738:Leptin; D011506:Proteins