title: IL-7 receptor deletion ameliorates diet-induced obesity and insulin resistance in mice.
abstract: OBJECTIVE
  Obesity-induced inflammation plays an important role in the development of insulin resistance and type 2 diabetes. Recent studies have demonstrated that adiposity can be improved by ablating certain inflammatory signalling pathways. Although the IL-7 receptor (IL-7R) is mostly known as a key regulator of T lymphocyte development and homeostasis, its role in obesity and metabolic diseases is unknown. Because IL-7 is markedly increased in the serum of obese individuals and IL-7R (also known as IL7R) is overexpressed in white adipose tissue (WAT) in obesity, we studied the metabolic consequences of genetic Il-7r ablation in mice.
  
  
  METHODS
  Age-matched Il-7r-deficient (Il-7r KO) and wild-type (WT) littermates were fed a standard chow or high-fat diet (HFD) for 14 weeks. Their serum metabolic variables were measured. The expression of genes and proteins related to insulin resistance and inflammation was evaluated in WAT.
  
  
  RESULTS
  We demonstrated that Il-7r KO mice exhibited significantly reduced body weight gain and visceral adiposity compared with WT controls on both chow and HFD. The expression of signalling molecules involved in adipogenesis was reduced in the WAT of Il-7r KO mice. We also found that Il-7r KO mice had significantly enhanced glucose homeostasis and insulin sensitivity. Consistent with an improved metabolic phenotype, proinflammatory cytokine production and macrophage infiltration was attenuated in the WAT of Il-7r KO mice.
  
  
  CONCLUSIONS
  The IL-7R plays an important role in the induction of HFD-induced adipogenesis and insulin resistance in mice.
authors.affiliation: Department of Food and Nutrition, Brain Korea 21 Plus Project, Yonsei University, 50 Yonsei-ro, Seodaemun-gu, Seoul, 120-749, Republic of Korea.
authors.forename: Miyoung
authors.initials: M
authors.lastname: Lee
authors.affiliation: Department of Food and Nutrition, Brain Korea 21 Plus Project, Yonsei University, 50 Yonsei-ro, Seodaemun-gu, Seoul, 120-749, Republic of Korea.
authors.forename: Su Jin
authors.initials: SJ
authors.lastname: Song
authors.affiliation: Department of Food Science and Nutrition, Kyungpook National University, Daegu, Republic of Korea.
authors.forename: Myung-Sook
authors.initials: MS
authors.lastname: Choi
authors.affiliation: Department of Food Science and Nutrition, University of Ulsan, Mugeo-dong, Nam-ku, Ulsan, Republic of Korea.
authors.forename: Rina
authors.initials: R
authors.lastname: Yu
authors.affiliation: Department of Food and Nutrition, Brain Korea 21 Plus Project, Yonsei University, 50 Yonsei-ro, Seodaemun-gu, Seoul, 120-749, Republic of Korea. tspark@yonsei.ac.kr.
authors.forename: Taesun
authors.initials: T
authors.lastname: Park
mesh_terms: D050156:Adipogenesis / Q000235:genetics*; D000273:Adipose Tissue / Q000378:metabolism; D050154:Adiposity / Q000235:genetics*; D000818:Animals; D059305:Diet, High-Fat; D007249:Inflammation / Q000378:metabolism; D007333:Insulin Resistance / Q000235:genetics*; D051379:Mice; D018345:Mice, Knockout; D009765:Obesity / Q000235:genetics* / Q000378:metabolism; D020395:Receptors, Interleukin-7 / Q000235:genetics* / Q000378:metabolism
chemical_list: D020395:Receptors, Interleukin-7
keywords: Adipogenesis; Inflammation; Insulin resistance; Interleukin-7 receptor; Obesity