Sarcolipin knockout mice fed a high‐fat diet exhibit altered indices of adipose tissue inflammation and remodeling. Issue 7 (July 2016)

• Record Type: Journal Article
• Authors: MacPherson, Rebecca E.K.; Gamu, Daniel; Frendo‐Cumbo, Scott; Castellani, Laura; Kwon, Frenk; Tupling, A. Russell; Wright, David C.
• Is Part Of: Obesity. Volume 24:Issue 7(2016)
• Page Start: 1499
• Page End: 1505
• Publication Date: 2016-07
• Subjects: Obesity -- Periodicals; 616.398005
• DOI: 10.1002/oby.21521
• Languages: English
• ISSNs: 1930-7381

Abstract

Abstract : Objective: To investigate indices of adipose tissue inflammation and remodeling in high‐fat diet (HFD) sarcolipin‐knockout ( SLN − /− ) mice. SLN regulates muscle‐based nonshivering thermogenesis and is up‐regulated with HFD. SLN − /− mice develop greater diet‐induced obesity and glucose intolerance. This is accompanied by increases in circulating catecholamines and fatty acids. Catecholamines and fatty acids play a role in the pathology of adipose tissue inflammation. Methods: Male mice (wild type and SLN − /− ) were fed a HFD (42% kcal from fat) for 8 weeks. Results: SLN − /− mice displayed greater obesity and glucose intolerance. This was accompanied by higher circulating epinephrine and nonesterified fatty acids. Epididymal but not inguinal subcutaneous adipose tissue from SLN − /− mice displayed higher interleukin‐6, suppressor of cytokine signaling 3, interleukin‐1β, and tumor necrosis factor‐α mRNA expression, and this was associated with increased markers of macrophage infiltration (F4/80 expression and crown‐like structures) and M1 polarization (higher CD11c expression and CD11c/MGL1). Interestingly, this occurred despite SLN − /− mice having smaller adipocytes. Conclusions: In conditions of nutrient excess, SLN − /− mice display depot‐specific increases in indices of adipose tissue inflammation and remodeling. This could be a compensatory response to reductions in muscle‐based thermogenesis.