title: Normal insulin sensitivity and IMCL content in overweight humans are associated with higher fasting lipid oxidation.
abstract: Intramyocellular lipid (IMCL) storage is considered a local marker of whole body insulin resistance; because increments of body weight are supposed to impair insulin sensitivity, this study was designed to assess IMCL content, lipid oxidation, and insulin action in individuals with a moderate increment of body fat mass and no family history of diabetes. We studied 14 young, nonobese women with body fat <30% (n = 7) or >30% (n = 7) and 14 young, nonobese men with body fat <25% (n = 7) or >25% (n = 7) by means of the euglycemic-insulin clamp to assess whole body glucose metabolism, with indirect calorimetry to assess lipid oxidation, by localized (1)H NMR spectroscopy of the calf muscles to assess IMCL content, and with dual-energy X-ray absorptiometry to assess body composition. Subjects with higher body fat had normal insulin-stimulated glucose disposal (P = 0.80), IMCL content in both soleus (P = 0.22) and tibialis anterior (P = 0.75) muscles, and plasma free fatty acid levels (P = 0.075) compared with leaner subjects in association with increased lipid oxidation (P < 0.05), resting energy expenditure (P = 0.046), resting oxygen consumption (P = 0.049), and plasma leptin levels (P < 0.01) in the postabsorptive condition. In conclusion, in overweight subjects, preservation of insulin sensitivity was combined with increased lipid oxidation and maintenance of normal IMCL content, suggesting that abnormalities of these factors may mutually determine the development of insulin resistance associated with weight gain.
authors.affiliation: Division of Nutrition/Metabolism, Università Vita e Salute San Raffaele, Istituto Scientifico H San Raffaele, 20132 Milan, Italy. perseghin.gianluca@hsr.it
authors.forename: Gianluca
authors.initials: G
authors.lastname: Perseghin
authors.forename: Paola
authors.initials: P
authors.lastname: Scifo
authors.forename: Massimo
authors.initials: M
authors.lastname: Danna
authors.forename: Alberto
authors.initials: A
authors.lastname: Battezzati
authors.forename: Stefano
authors.initials: S
authors.lastname: Benedini
authors.forename: Elena
authors.initials: E
authors.lastname: Meneghini
authors.forename: Alessandro
authors.initials: A
authors.lastname: Del Maschio
authors.forename: Livio
authors.initials: L
authors.lastname: Luzi
mesh_terms: D000328:Adult; D000886:Anthropometry; D015703:Antigens, CD / Q000097:blood; D001835:Body Weight / Q000502:physiology*; D002096:C-Peptide / Q000097:blood; D004734:Energy Metabolism; D005215:Fasting / Q000502:physiology*; D005260:Female; D005947:Glucose / Q000378:metabolism; D006706:Homeostasis; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007328:Insulin / Q000502:physiology*; D020738:Leptin / Q000097:blood; D050356:Lipid Metabolism; D008055:Lipids / Q000097:blood; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism*; D010084:Oxidation-Reduction; D019518:Postprandial Period; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood; D047889:Receptors, Tumor Necrosis Factor, Type II; D012016:Reference Values
chemical_list: D015703:Antigens, CD; D002096:C-Peptide; D007328:Insulin; D020738:Leptin; D008055:Lipids; D018124:Receptors, Tumor Necrosis Factor; D047889:Receptors, Tumor Necrosis Factor, Type II; D005947:Glucose; D006854:Hydrocortisone