title: Circulating vaspin and visfatin are not affected by acute or chronic energy deficiency or leptin administration in humans.
abstract: OBJECTIVE
  Animal and in vitro studies indicate that leptin alleviates starvation-induced reduction in circulating vaspin and stimulates the production of visfatin. We thus examined whether vaspin and visfatin are affected by short- and long-term energy deprivation and leptin administration in human subjects in vivo.
  
  
  METHODS
  We measured circulating levels of vaspin and visfatin i) before and after 72 h of starvation (leading to severe hypoleptinemia) with or without leptin administration in replacement doses in 13 normal-weight subjects, ii) before and after 72 h of starvation with leptin administration in pharmacological doses in 13 lean and obese subjects, iii) during chronic energy deficiency in eight women with hypothalamic amenorrhea on leptin replacement for 3 months, and iv) during chronic energy deficiency in 18 women with hypothalamic amenorrhea on leptin replacement or placebo for 3 months.
  
  
  RESULTS
  Acute starvation decreased serum leptin to 21% of baseline values, (P=0.002) but had no significant effect on vaspin and visfatin concentrations (P>0.05). Nor did normalization of leptin levels affect the concentrations of these two adipokines (P>0.9). Leptin replacement in women with hypothalamic amenorrhea did not significantly alter vaspin and visfatin concentrations, whether relative to baseline or placebo administration (P>0.25). Pharmacological doses of leptin did not affect circulating vaspin and visfatin concentrations (P>0.9).
  
  
  CONCLUSIONS
  Circulating vaspin and visfatin are not affected by acute or chronic energy deficiency leading to hypoleptinemia and are not regulated by leptin in human subjects, indicating that these adipocyte-secreted hormonal regulators of metabolism are independently regulated in humans.
authors.affiliation: Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, SL Room 412, Boston, Massachusetts 02215, USA. ekang@bidmc.harvard.edu
authors.forename: Eun Seok
authors.initials: ES
authors.lastname: Kang
authors.forename: Faidon
authors.initials: F
authors.lastname: Magkos
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Sienkiewicz
authors.forename: Christos S
authors.initials: CS
authors.lastname: Mantzoros
mesh_terms: D000328:Adult; D000568:Amenorrhea / Q000097:blood; D004311:Double-Blind Method; D002149:Energy Intake / Q000502:physiology*; D004797:Enzyme-Linked Immunosorbent Assay; D015444:Exercise / Q000502:physiology; D005215:Fasting / Q000502:physiology; D005260:Female; D020249:Hormone Replacement Therapy; D006801:Humans; D007027:Hypothalamic Diseases / Q000097:blood; D020738:Leptin / Q000097:blood / Q000494:pharmacology* / Q000627:therapeutic use; D008297:Male; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood*; D015843:Serpins / Q000097:blood*; D055815:Young Adult
chemical_list: D020738:Leptin; C507339:SERPINA12 protein, human; D015843:Serpins; D054409:Nicotinamide Phosphoribosyltransferase