This study investigates how sympathetic nervous system activity influences the secretion of FABP4, independent of ATGL-mediated lipolysis, using adipocyte-specific ATGL Knockout (ATGL^AdpKO) mice.
Enhanced FABP4 secretion upon β-adrenergic stimulation in ATGL^AdpKO mice; sympathetic signaling influences FABP4 release; adipocytes are the primary source of circulating FABP4.
Adipocyte-specific ATGL Knockout (ATGL^AdpKO) mouse model developed by genOway, in which Pnpla2 (ATGL) is selectively deleted in adipocytes using the Cre-loxP system. This model allows for the study of lipolysis-independent regulation of FABP4 secretion.
Obesity, Metabolic disease, Sympathetic nervous system, Lipolysis, FABP4 secretion
Adipocyte-specific ATGL Knockout mouse model, Cre-loxP system, β-adrenergic stimulation, Sympathetic signaling inhibition, Thermoneutral housing, FABP4 secretion analysis
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