Figure 1.

Global ATGL Deficiency Causes Cold-Induced Hypothermia and BAT Hypertrophy, but Does Not Alter Mitochondrial Function in BAT

(A) TG hydrolase activities of BAT infranatants in the absence or presence of HSL inhibitor (HSLi) from mice housed at 22°C–23°C (n = 3).

(B) Body temperature in ad libitum-fed mice upon acute cold exposure at 5°C for 3–6 hr (n = 6).

(C) BAT weight (n = 7).

(D) Histology of BAT. Scale bar, 100 μm.

(E) Relative mRNA expression of classical brown fat genes upon acute cold exposure (n = 6).

(F) UCP-1 immunoblot of isolated BAT mitochondria upon acute cold exposure.

(G) Total DNA content in whole BAT depots (n = 6).

(H) DNA content in isolated brown adipocytes (adi) and stroma-vascular fraction (SVF; n = 3).

(I) Total protein content in isolated mitochondria from whole BAT depots (n = 10).

(J) Relative mtDNA content in BAT assessed by qPCR and calculated from copy numbers of the mtDNA-encoded MtCO1 gene and the nuclear DNA-encoded Ndufv1 gene (n = 6).

(K) Representative transmission electron micrographs from BAT. Scale bar, 0.5 μm.

(L) Oxygen consumption rates (OCRs) in BAT homogenates (hom) using pyruvate (pyr), glycerol-3-P (G3P) in the absence or presence of rotenone (R, G3P/R), and guanosine 5′-diphosphate (GDP). OCRs were calculated for whole BAT depots (n = 6–7).

Analyses were performed in male mice, except for (H), which used female mice, aged 9–10 weeks. Data are presented as means ± SD. Statistical significance was evaluated by unpaired two-tailed Student’s t test. ^∗p < 0.05, ^∗∗p < 0.01, and ^∗∗∗p < 0.001. See also Figure S1.