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

Copyright © 2013 AGA Institute. Published by Elsevier Inc. All rights reserved..

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.

Errataetall:

CommentIn: Gastroenterology. 2013 Aug;145(2):282-5. - PMID 23806542

Medienart:

E-Artikel

Erscheinungsjahr:

2013

Erschienen:

2013

Enthalten in:

Zur Gesamtaufnahme - volume:145

Enthalten in:

Gastroenterology - 145(2013), 2 vom: 01. Aug., Seite 366-74.e1-3

Sprache:

Englisch

Beteiligte Personen:

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

Links:

Volltext

Themen:

C-Jun kinase
Cytokines
FFM
Fat free mass
GIF
Glucose
Glucose infusion rate
IFN
IL
IL17RA protein, human
IL6 protein, human
IY9XDZ35W2
Interferon
Interleukin
Interleukin-17
Interleukin-22 receptor
Interleukin-6
Interleukins
JNK
Journal Article
Lymphocytes
MAO
MNO
Metabolically Abnormal Obesity
Metabolically Normal Obesity
Metabolically abnormal insulin-resistant obese
Metabolically normal insulin-sensitive obese
NAFLD
Nonalcoholic fatty liver disease
Receptors, Interleukin
Receptors, Interleukin-17
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Anmerkungen:

Date Completed 27.09.2013

Date Revised 13.02.2024

published: Print-Electronic

CommentIn: Gastroenterology. 2013 Aug;145(2):282-5. - PMID 23806542

Citation Status MEDLINE

doi:

10.1053/j.gastro.2013.04.010

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM226789071