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.
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.
Authors: Tara L MacDonald; Rebecca MacPherson; Laura Castellani; Daniel Cervone; Eoin Anderson; David C Wright; David J Dyck Journal: Adipocyte Date: 2017-01-27 Impact factor: 4.534
Authors: Santosh K Maurya; Jose L Herrera; Sanjaya K Sahoo; Felipe C G Reis; Rick B Vega; Daniel P Kelly; Muthu Periasamy Journal: Cell Rep Date: 2018-09-11 Impact factor: 9.423
Authors: Rebecca L Paszkiewicz; Richard N Bergman; Roberta S Santos; Aaron P Frank; Orison O Woolcott; Malini S Iyer; Darko Stefanovski; Deborah J Clegg; Morvarid Kabir Journal: Int J Mol Sci Date: 2020-09-10 Impact factor: 5.923