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- Title
Interleukin-7 Regulates Adipose Tissue Mass and Insulin Sensitivity in High-Fat Diet-Fed Mice through Lymphocyte-Dependent and Independent Mechanisms.
- Authors
Lucas, Stéphanie; Taront, Solenne; Magnan, Christophe; Fauconnier, Laurence; Delacre, Myriam; Macia, Laurence; Delanoye, Anne; Verwaerde, Claudie; Spriet, Corentin; Saule, Pasquine; Goormachtigh, Gautier; Héliot, Laurent; Ktorza, Alain; Movassat, Jamileh; Polakowska, Renata; Auriault, Claude; Poulain-Godefroy, Odile; Di Santo, James; Froguel, Philippe; Wolowczuk, Isabelle
- Abstract
Although interleukin (IL)-7 is mostly known as a key regulator of lymphocyte homeostasis, we recently demonstrated that it also contributes to body weight regulation through a hypothalamic control. Previous studies have shown that IL-7 is produced by the human obese white adipose tissue (WAT) yet its potential role on WAT development and function in obesity remains unknown. Here, we first show that transgenic mice overexpressing IL-7 have reduced adipose tissue mass associated with glucose and insulin resistance. Moreover, in the high-fat diet (HFD)-induced obesity model, a single administration of IL-7 to C57BL/6 mice is sufficient to prevent HFD-induced WAT mass increase and glucose intolerance. This metabolic protective effect is accompanied by a significant decreased inflammation in WAT. In lymphocyte-deficient HFDfed SCID mice, IL-7 injection still protects from WAT mass gain. However, IL-7-triggered resistance against WAT inflammation and glucose intolerance is lost in SCID mice. These results suggest that IL-7 regulates adipose tissue mass through a lymphocyte-independent mechanism while its protective role on glucose homeostasis would be relayed by immune cells that participate to WAT inflammation. Our observations establish a key role for IL-7 in the complex mechanisms by which immune mediators modulate metabolic functions.
- Subjects
INTERLEUKINS; LYMPHOCYTES; HOMEOSTASIS; HYPOTHALAMIC hormones; ADIPOSE tissues; INSULIN
- Publication
PLoS ONE, 2012, Vol 7, Issue 6, p1
- ISSN
1932-6203
- Publication type
Article
- DOI
10.1371/journal.pone.0040351