title: Decrease in hepatic very-low-density lipoprotein-triglyceride secretion after weight loss is inversely associated with changes in circulating leptin.
abstract: OBJECTIVE
  Although weight loss usually decreases very-low-density lipoprotein-triglyceride (VLDL-TG) secretion rate, the change in VLDL-TG kinetics is not directly related to the change in body weight. Circulating leptin also declines with weight loss and can affect hepatic lipid metabolism. The aim of this study was to determine whether circulating leptin is associated with weight loss-induced changes in VLDL-TG secretion.
  
  
  METHODS
  Ten extremely obese subjects were studied. VLDL-TG secretion rate and the contribution of systemic (derived from lipolysis of subcutaneous adipose tissue TG) and non-systemic fatty acids (derived primarily from lipolysis of intrahepatic and intraperitoneal TG, and de novo lipogenesis) to VLDL-TG production were determined by using stable isotopically labelled tracer methods before and 1 year after gastric bypass surgery.
  
  
  RESULTS
  Subjects lost 33 +/- 12% of body weight, and VLDL-TG secretion rate decreased by 46 +/- 23% (p = 0.001), primarily because of a decrease in the secretion of VLDL-TG from non-systemic fatty acids (p = 0.002). Changes in VLDL-TG secretion rates were not significantly related to reductions in body weight, body mass index, plasma palmitate flux, free fatty acid or insulin concentrations. The change in VLDL-TG secretion was inversely correlated with the change in plasma leptin concentration (r = -0.72, p = 0.013), because of a negative association between changes in leptin and VLDL-TG secretion from non-systemic fatty acids (r = -0.95, p < 0.001).
  
  
  CONCLUSIONS
  Weight loss-induced changes in plasma leptin concentration are inversely associated with changes in VLDL-TG secretion rate. Additional studies are needed to determine whether the correlation between circulating leptin and VLDL-TG secretion represents a cause-and-effect relationship.
authors.affiliation: Center for Human Nutrition, Washington University School of Medicine, St Louis, MO 63110, USA.
authors.forename: F
authors.initials: F
authors.lastname: Magkos
authors.forename: E
authors.initials: E
authors.lastname: Fabbrini
authors.forename: J
authors.initials: J
authors.lastname: McCrea
authors.forename: B W
authors.initials: BW
authors.lastname: Patterson
authors.forename: J C
authors.initials: JC
authors.lastname: Eagon
authors.forename: S
authors.initials: S
authors.lastname: Klein
mesh_terms: D000328:Adult; D015992:Body Mass Index; D005260:Female; D015390:Gastric Bypass; D006801:Humans; D020738:Leptin / Q000378:metabolism; D050356:Lipid Metabolism / Q000187:drug effects* / Q000502:physiology; D008079:Lipoproteins, VLDL / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D009767:Obesity, Morbid / Q000188:drug therapy* / Q000503:physiopathology / Q000601:surgery; D014280:Triglycerides / Q000378:metabolism; D015431:Weight Loss / Q000187:drug effects* / Q000502:physiology
chemical_list: D020738:Leptin; D008079:Lipoproteins, VLDL; D014280:Triglycerides; C030106:very low density lipoprotein triglyceride