In vitro, Sirt1 overexpression in primary murine brown adipocytes exposed to a macrophage-derived pro-inflammatory conditioned medium consistently promoted mitochondrial respiration, fatty acid oxidation, and norepinephrine-mediated UCP-1 expression, indicating that targeting SIRT1 may have a therapeutic value in the treatment of inflammation-induced thermogenesis deficiency (63). Here, SIRT1 is linked to hyperinsulinemic hypoglycemia, familial, 4.