title: Leptin and insulin response to long-term total parenteral nutrition depends on body fat mass.
abstract: OBJECTIVE
  Circulating leptin and insulin concentrations are physiologically representing energy homeostasis. However, the artificial situation of long-term total parenteral nutrition (TPN) and its effects on serum leptin and insulin is not fully understood.
  
  
  METHODS
  We studied 42 gastroenterological patients who received TPN for 19+/-11 days. Serum leptin and insulin levels as well as body composition assessed by bioelectrical impedance analysis were evaluated on days 0, 7 and 14. Insulin sensitivity was estimated by calculating the QUICKI.
  
  
  RESULTS
  Before the start of TPN, leptin correlated positively with female gender (P<0.03), BMI (P<0.02), fat mass (P<0.02), insulin levels (P<0.001) and QUICKI (P<0.001). Within the first week of TPN, an increase of leptin levels was found only in patients with a body fat mass of >30% (P<0.02). As these were predominantly women, their leptin levels increased likewise (P<0.003). In regression analysis, fat mass (P<0.001), female gender (P<0.04), insulin levels (P<0.03), and i.v. glucose supply rates (P<0.05) were independently associated to leptin levels.
  
  
  CONCLUSIONS
  TPN-especially glucose-induces a neurohumoral response as shown here for leptin and insulin that is mainly depending on the fat mass. Better understanding of this regulatory mechanism during artificial nutrition could offer a new approach to improve its therapeutic effects.
authors.affiliation: Department of Gastroenterology, Hepatology and Endocrinology, Medical School Hannover, Carl Neuberg Strasse 1, 30625 Hannover, Germany.
authors.forename: Kinan
authors.initials: K
authors.lastname: Rifai
authors.forename: Stephan C
authors.initials: SC
authors.lastname: Bischoff
authors.forename: Adji
authors.initials: A
authors.lastname: Widjaja
authors.forename: Georg
authors.initials: G
authors.lastname: Brabant
authors.forename: Michael P
authors.initials: MP
authors.lastname: Manns
authors.forename: Johann
authors.initials: J
authors.lastname: Ockenga
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D050154:Adiposity / Q000502:physiology*; D001786:Blood Glucose / Q000378:metabolism; D001823:Body Composition / Q000502:physiology*; D015992:Body Mass Index; D005260:Female; D006801:Humans; D007328:Insulin / Q000097:blood*; D020738:Leptin / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009748:Nutrition Disorders / Q000097:blood / Q000628:therapy*; D010289:Parenteral Nutrition, Total; D012737:Sex Factors
chemical_list: D001786:Blood Glucose; D007328:Insulin; D020738:Leptin