title: Leptin and energy metabolism in pulmonary tuberculosis.
abstract: BACKGROUND
  Pulmonary tuberculosis is the classic cause of "consumption," but the pathogenesis of such wasting is largely unknown. Animal studies in other conditions suggest that leptin may be a mediator between proinflammatory cytokine activity and wasting.
  
  
  OBJECTIVE
  We tested whether the leptin concentration, after control for body fat mass, is higher during active pulmonary tuberculosis than after recovery and whether it correlates with energy metabolism and proinflammatory cytokine activity.
  
  
  METHODS
  Nondiabetic adults with pulmonary tuberculosis (n = 32) were recruited into a prospective observational study. Patients found to be antibody positive for human immunodeficiency virus were excluded from the study. Dual-energy X-ray absorptiometry, indirect calorimetry, and food intake protocols were performed at baseline and after 1 and 6 mo of tuberculosis treatment. Fasting plasma leptin, tumor necrosis factor alpha and its soluble receptor, and interleukin 6 were measured by enzyme-linked immunosorbent assay.
  
  
  RESULTS
  Resting energy expenditure was close to Harris-Benedict predictions and did not change significantly during treatment, but energy intake increased. Leptin concentration was correlated in a log-linear fashion with percentage body fat but was independent of cytokines and energy intake. There was no significant difference in leptin, corrected for energy balance and fat mass, at baseline and after 1 and 6 mo of treatment.
  
  
  CONCLUSIONS
  These data are compatible with recovery from anorexia or starvation without discernible hyper- or hypometabolism. The close correlation of leptin with body fat mass is similar to observations in healthy subjects. No additional influence of disease state or proinflammatory cytokine activity was found. Leptin does not appear to be a component of the immune response to human pulmonary tuberculosis, and thus it cannot account for the weight loss and anorexia associated with tuberculosis.
authors.affiliation: Department of Infectious Diseases, St George's Hospital Medical School, London, United Kingdom. a.schwenk@doctors.org.uk
authors.forename: Achim
authors.initials: A
authors.lastname: Schwenk
authors.forename: Lisa
authors.initials: L
authors.lastname: Hodgson
authors.forename: Charlotte F J
authors.initials: CF
authors.lastname: Rayner
authors.forename: George E
authors.initials: GE
authors.lastname: Griffin
authors.forename: Derek C
authors.initials: DC
authors.lastname: Macallan
mesh_terms: D015502:Absorptiometry, Photon / Q000379:methods; D000273:Adipose Tissue / Q000378:metabolism; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001823:Body Composition; D001834:Body Water / Q000378:metabolism; D002153:Calorimetry, Indirect / Q000379:methods; D002908:Chronic Disease; D016207:Cytokines / Q000097:blood; D002149:Energy Intake; D004734:Energy Metabolism / Q000502:physiology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D020738:Leptin / Q000097:blood*; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D014397:Tuberculosis, Pulmonary / Q000097:blood / Q000378:metabolism* / Q000503:physiopathology; D015431:Weight Loss
chemical_list: D016207:Cytokines; D020738:Leptin