title: Lack of invariant natural killer T cells affects lipid metabolism in adipose tissue of diet-induced obese mice.
abstract: OBJECTIVE
  Obesity promotes a chronic inflammatory condition in adipose tissue (AT). Impairment of insulin sensitivity coincides with infiltration of T cells into AT in early stages of obesity, when macrophages are not yet present. Here, we examine the role of invariant natural killer T (iNKT) cells, a subtype of T cells activated by lipid antigens, on glucose and lipid metabolism in obesity.
  
  
  RESULTS
  Jα18(-/-) mice, specifically lacking iNKT cells, and wild-type mice consumed a chow or high-fat diet for 10 weeks. One third of all T lymphocytes in the liver of wild-type mice were iNKT cells, whereas few were detected in AT. Diet-induced obesity increased blood glucose in both genotypes of mice, whereas glucose tolerance test revealed similar kinetics of glucose clearance in Jα18(-/-) and wild-type mice. Under obese conditions, expression of inflammatory cytokines in AT did not differ between the groups, although the number of T cells and macrophages was lower in Jα18(-/-) mice. Nonetheless, AT homeostasis in Jα18(-/-) mice was altered evidenced by lower AT weight, smaller adipocytes, accelerated lipogenesis, increased expression of hormone-sensitive lipase, and accelerated basal lipolysis.
  
  
  CONCLUSIONS
  iNKT cells do not affect glucose clearance but rather modulate lipid metabolism in both liver and AT. Only few iNKT cells are found in AT under lean and obese conditions, suggesting that their effects on lipid metabolism are mainly mediated in the liver, their primary host organ.
authors.affiliation: Department of Medicine, Center for Molecular Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.
authors.forename: Daniela
authors.initials: D
authors.lastname: Strodthoff
authors.forename: Anna M
authors.initials: AM
authors.lastname: Lundberg
authors.forename: Hanna E
authors.initials: HE
authors.lastname: Agardh
authors.forename: Daniel F J
authors.initials: DF
authors.lastname: Ketelhuth
authors.forename: Gabrielle
authors.initials: G
authors.lastname: Paulsson-Berne
authors.forename: Peter
authors.initials: P
authors.lastname: Arner
authors.forename: Göran K
authors.initials: GK
authors.lastname: Hansson
authors.forename: Norbert
authors.initials: N
authors.lastname: Gerdes
mesh_terms: D000273:Adipose Tissue / Q000276:immunology / Q000378:metabolism*; D000818:Animals; D055610:Antigens, CD1d / Q000276:immunology / Q000378:metabolism; D001786:Blood Glucose / Q000032:analysis; D059305:Diet, High-Fat; D004195:Disease Models, Animal; D005234:Fatty Liver / Q000276:immunology / Q000503:physiopathology; D005947:Glucose / Q000378:metabolism*; D007333:Insulin Resistance; D050356:Lipid Metabolism / Q000276:immunology / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008820:Mice, Obese; D055611:Natural Killer T-Cells / Q000276:immunology / Q000378:metabolism*; D011897:Random Allocation; D012016:Reference Values; D012680:Sensitivity and Specificity; D002787:Sterol Esterase / Q000276:immunology / Q000378:metabolism*
chemical_list: D055610:Antigens, CD1d; D001786:Blood Glucose; D002787:Sterol Esterase; D005947:Glucose
keywords: NKT cells; immune system; leukocytes; lipases; obesity