Association between specific adipose tissue CD4+ T-cell populations and insulin resistance in obese individuals

Caterina Conte, Elisa Fabbrini, Marina Cella, Steve A. Mccartney, Anja Fuchs, Nada A. Abumrad, Terri A. Pietka, Zhouji Chen, Brian N. Finck, Dong Ho Han, Faidon Magkos, David Bradley, Gemma Fraterrigo, J. Christopher Eagon, Bruce W. Patterson, Marco Colonna, Samuel Klein

Risultato della ricerca: Contributo in rivistaArticolo in rivista

156 Citazioni (Scopus)

Abstract

BACKGROUND & AIMS: An increased number of macrophages in adipose tissue is associated with insulin resistance and metabolic dysfunction in obese people. However, little is known about other immune cells in adipose tissue from obese people, and whether they contribute to insulin resistance. We investigated the characteristics of T cells in adipose tissue from metabolically abnormal insulin-resistant obese (MAO) subjects, metabolically normal insulin-sensitive obese (MNO) subjects, and lean subjects. Insulin sensitivity was determined by using the hyperinsulinemic euglycemic clamp procedure. METHODS: We assessed plasma cytokine concentrations and subcutaneous adipose tissue CD4(+) T-cell populations in 9 lean, 12 MNO, and 13 MAO subjects. Skeletal muscle and liver samples were collected from 19 additional obese patients undergoing bariatric surgery to determine the presence of selected cytokine receptors. RESULTS: Adipose tissue from MAO subjects had 3- to 10-fold increases in numbers of CD4(+) T cells that produce interleukin (IL)-22 and IL-17 (a T-helper [Th] 17 and Th22 phenotype) compared with MNO and lean subjects. MAO subjects also had increased plasma concentrations of IL-22 and IL-6. Receptors for IL-17 and IL-22 were expressed in human liver and skeletal muscle samples. IL-17 and IL-22 inhibited uptake of glucose in skeletal muscle isolated from rats and reduced insulin sensitivity in cultured human hepatocytes. CONCLUSIONS: Adipose tissue from MAO individuals contains increased numbers of Th17 and Th22 cells, which produce cytokines that cause metabolic dysfunction in liver and muscle in vitro. Additional studies are needed to determine whether these alterations in adipose tissue T cells contribute to the pathogenesis of insulin resistance in obese people.
Lingua originaleEnglish
pagine (da-a)366-366-74.e1-3
RivistaGastroenterology
Volume145
DOI
Stato di pubblicazionePubblicato - 2013

Keywords

  • Adult
  • Animals
  • Body Mass Index
  • CD4-Positive T-Lymphocytes
  • Case-Control Studies
  • Cytokines
  • FFM
  • Female
  • GIF
  • Glucose
  • Glucose Clamp Technique
  • Hepatocytes
  • Humans
  • IFN
  • IL
  • Insulin Resistance
  • Interleukin-17
  • Interleukin-6
  • Interleukins
  • JNK
  • Liver
  • Lymphocytes
  • MAO
  • MNO
  • Male
  • Metabolically Abnormal Obesity
  • Metabolically Normal Obesity
  • Middle Aged
  • Muscle, Skeletal
  • NAFLD
  • Obesity
  • Rats
  • Receptors, Interleukin
  • Receptors, Interleukin-17
  • Subcutaneous Fat
  • T-Lymphocyte Subsets
  • Th17 Cells
  • c-Jun kinase
  • fat free mass
  • glucose infusion rate
  • interferon
  • interleukin
  • metabolically abnormal insulin-resistant obese
  • metabolically normal insulin-sensitive obese
  • nonalcoholic fatty liver disease

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