title: High-fat meals reduce 24-h circulating leptin concentrations in women.
abstract: Leptin induces weight loss in rodents via its effects on food intake and energy expenditure. High-fat diets induce weight gain, but the mechanism is not well understood. Previous studies have not found an effect of dietary fat content on fasting leptin. There is a nocturnal increase of leptin, however, which is related to insulin responses to meals. We have reported that adipocyte glucose utilization is involved in insulin-induced leptin secretion in vitro. Accordingly, high-fat, low-carbohydrate (HF/LC) meals, which induce smaller insulin and glucose responses, would produce lower leptin concentrations than low-fat, high-carbohydrate (LF/HC) meals. Blood samples were collected every 30-60 min for 24 h from 19 normal-weight (BMI, 24.2 +/- 0.7 kg/m2; percent body fat = 31 +/- 1%) women on 2 days (10 days apart) during which the subjects were randomized to consume three isocaloric 730-kcal meals containing either 60/20 or 20/60% of energy as fat/carbohydrate. Overall insulin and glycemic responses (24-h area under the curve [AUC]) were reduced by 55 and 61%, respectively, on the HF/LC day (P < 0.0001). During LF/HC feeding, there were larger increases of leptin 4-6 h after breakfast (38 +/- 7%, P < 0.001) and lunch (78 +/- 14%, P < 0.001) than after HF/LC meals (both P < 0.02). During LF/HC feeding, leptin increased from a morning baseline of 10.7 +/- 1.6 ng/ml to a nocturnal peak of 21.3 +/- 1.3 ng/ml (change, 10.6 +/- 1.3 ng/ml; percent change, 123 +/- 16%; P < 0.0001). The amplitudes of the nocturnal rise of leptin and the 24-h leptin AUC were 21 +/- 8% (P < 0.005) and 38 +/- 12% (P < 0.0025) larger, respectively, on the LF/HC day. In summary, consumption of HF/LC meals results in lowered 24-h circulating leptin concentrations. This result may be a consequence of decreased adipocyte glucose metabolism. Decreases of 24-h circulating leptin could contribute to the weight gain during consumption of high-fat diets.
authors.affiliation: Department of Nutrition, University of California, Davis 95616, USA. pjhavel@ucdavis.edu
authors.forename: P J
authors.initials: PJ
authors.lastname: Havel
authors.forename: R
authors.initials: R
authors.lastname: Townsend
authors.forename: L
authors.initials: L
authors.lastname: Chaump
authors.forename: K
authors.initials: K
authors.lastname: Teff
mesh_terms: D000273:Adipose Tissue / Q000033:anatomy & histology; D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D015992:Body Mass Index; D002940:Circadian Rhythm / Q000502:physiology*; D004041:Dietary Fats / Q000008:administration & dosage* / Q000494:pharmacology; D005260:Female; D005934:Glucagon / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007328:Insulin / Q000097:blood; D019344:Lactic Acid / Q000097:blood; D020738:Leptin; D009994:Osmolar Concentration; D011506:Proteins / Q000032:analysis*
chemical_list: D001786:Blood Glucose; D004041:Dietary Fats; D007328:Insulin; D020738:Leptin; D011506:Proteins; D019344:Lactic Acid; D005934:Glucagon; D006854:Hydrocortisone