GSE200749
Effect of depletion of succinate receptor 1 (SUCNR1) on the gene expression of mouse adipose tissue
The concept of “signaling metabolites” in the control of metabolic homeostasis is gaining traction. The Krebs cycle substrate succinate, a pleiotropic metabolite that acts akin to hormones and cytokines through succinate receptor 1 (SUCNR1, also known as GPR91), is one example of this new class of metabolites. SUCNR1 has a broad expression and is highly abundant in white adipose tissue. It was a general assumption that SUCNR1 is functionally inactive in healthy tissues, and for many years, SUCNR1 was explored from an immune perspective, mainly in inflammatory-related conditions, particularly those associated with chronic hypersuccinemia. Recent studies, however, indicate that extracellular levels of succinate transiently increase in response to physiological changes such as exercise, cold exposure, or food ingestion. Succinate thus emerges as a reporter of both tissue stress and metabolism, raising the possibility of its involvement in additional metabolic functions as a hormone-like metabolite. Indeed, it is conceivable that "succinate sensing" by SUCNR1 may be part of the metabolite-sensing machinery that governs energy homeostasis. To better understand the effect of the adipocyte Sucnr1 deletion on adipose tissue, we selectively inactivated Sucnr1 in murine adipocytes and profiled the transcription state of epididymal white adipose tissue from adipocyte cell-specific Sucnr1 knockout mice (Ad-Sucnr1 KO) and control Sucnr1fl/fl mice. Overall design: Comparative gene expression profiling analysis of RNA-seq data for  epididymal white adipose tissue from Ad-Sucnr1 KO (n=5) and  Sucnr1fl/fl (n=5) mice.