title: Serum leptin levels in acute protein deprivation.
abstract: BACKGROUND
  Protein energy malnutrition (PEM) induces a host neuroendocrine response, reflected by significant elevations in circulating glucocorticoid levels and associated with metabolic and immune dysfunction. Leptin regulates food intake and body mass and has a significant impact on the hypothalamic-pituitary-adrenal axis (HPA). We hypothesized that leptin may be altered by and may play an important role in regulating the effects of PEM.
  
  
  METHODS
  Female Balb/c mice were used. In experiment 1, mice were pair-fed either a protein-free (0% casein) or control (24% casein) diet for 7 days. In experiment 2, mice were implanted with either a placebo or corticosterone-releasing pellet and fed the control diet for 7 days. In experiment 3, adrenalectomized mice were pair-fed either the protein-free or control diet for 7 days. Serum corticosterone and leptin levels were measured in all experiments.
  
  
  RESULTS
  PEM caused significant reductions in food intake, body weight, and total body fat, but not lean body mass. Serum corticosterone and leptin levels were significantly greater in mice fed the protein-free diet. Subcutaneous implantation of a corticosterone pellet in mice fed the control diet resulted in a significantly elevated serum leptin level compared with placebo-implanted controls. Bilateral adrenalectomy partially blunted the increased serum leptin in PEM.
  
  
  CONCLUSIONS
  Leptin may be an important mediator of weight loss and decreased food intake in PEM. Elevated serum leptin in PEM may be secondary to elevated serum corticosterone, with other factors inherent in the host response to protein restriction also contributing to elevated serum leptin.
authors.affiliation: Department of Surgery, New York Presbyterian Hospital-Weill Medical College of Cornell University, USA. ppstap@temple.edu
authors.forename: Philip P
authors.initials: PP
authors.lastname: Stapleton
authors.forename: Catherine B
authors.initials: CB
authors.lastname: Barden
authors.forename: Martin D
authors.initials: MD
authors.lastname: McCarter
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Mackrell
authors.forename: Tracy A
authors.initials: TA
authors.lastname: Freeman
authors.forename: Hassan A
authors.initials: HA
authors.lastname: Naama
authors.forename: John M
authors.initials: JM
authors.lastname: Daly
mesh_terms: D000208:Acute Disease; D000315:Adrenalectomy; D000818:Animals; D001069:Appetite Regulation; D001823:Body Composition; D001835:Body Weight; D003345:Corticosterone / Q000008:administration & dosage / Q000097:blood*; D004044:Dietary Proteins / Q000008:administration & dosage*; D004343:Drug Implants; D004435:Eating / Q000187:drug effects; D005260:Female; D020738:Leptin / Q000097:blood*; D051379:Mice; D008807:Mice, Inbred BALB C; D011502:Protein-Energy Malnutrition / Q000097:blood*; D011897:Random Allocation; D013047:Specific Pathogen-Free Organisms
chemical_list: D004044:Dietary Proteins; D004343:Drug Implants; D020738:Leptin; D003345:Corticosterone