Figure 2.

A lipolytic signal controls cold-induced expression of Gpr3

(A) Cold-induced Gpr3 expression in BAT.

(B) Lipolytic activity in ex vivo eWAT from wild-type control and β-less mice stimulated with either isoproterenol (ISO) or forskolin (Fsk).

(C–E) (C) Protein levels of adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) in BAT, (D) gene expression of Atgl and Hsl, and (E) lipolytic activity in primary subcutaneous white adipocytes following ISO treatment with or without lipase inhibitors (ATGL inhibitor, Atglistatin; HSL inhibitor, 76-0079).

(F and G) BAT Gpr3 expression in (F) acute cold-induced (RT, room temperature) and (G) 3-week cold-adapted DAKO mice and control littermates.

(H) Gpr3 expression in primary brown adipocytes following ISO treatment with or without lipase inhibitors (ATGL inhibitor, Atglistatin; HSL inhibitor, CAY10499).

(I) Regulation of brown adipocyte Gpr3 expression by the lipolytic activator, SR-3420, with or without lipase inhibitors (ATGL inhibitor, Atglistatin; HSL inhibitor, CAY10499).

(J) Gpr3 expression in brown adipocytes following SR-3420 treatment with or without lipid oxidation inhibitors.

(K) BAT gene expression from mice given PPARα (fenofibrate) or PPARγ (rosiglitazone) agonists for 2 weeks.

(L) Small interfering RNA (siRNA)-mediated knockdown of the lipid-activated nuclear receptors.

(M) Impact on norepinephrine (NE)-induced Gpr3 expression in brown adipocytes.

For all panels, error bars represent ±SEM, p ≤ 0.05 = ∗, p ≤ 0.01 = ∗∗, p ≤ 0.001 = ∗∗∗, p ≤ 0.0001 = ∗∗∗∗, t test (A, B, D, F–J, L, and M) or Bonferroni's multiple comparisons test (E and K). See also Figure S1.