FIG. 6.

GLP-1R signaling is not critical for the control of BAT thermogenesis in response to changes in ambient temperature. WT and Glp1r^−/− mice implanted with a telemeter temperature transmitter in the iBAT were exposed to decreasing ambient temperature from 24 to 14°C in decrements of 2°C per day. The decrease in ambient temperature led to a similar increase in food intake (A) in both WT and Glp1r^−/− mice paralleled by an increase in locomotor activity (Loc. Act) (B) and energy expenditure (EE) (C). Both WT and knockout mice maintained similar iBAT temperature, including circadian-dependent oscillations (D). E–J: Response to an acute cold exposure: WT and Glp1r^−/− mice fed with standard chow ad libitum and housed always at room temperature were singly housed and exposed to 4°C for 8 h. BCT was measured using a rectal probe (E). Another set of mice was exposed to 4°C for 2 h before euthanasia, while the corresponding control groups were maintained at room temperature. UCP-1 (F), PGC1a (G), and DIO2 (H) gene expression was assessed in BAT. Fat mass was measured using nuclear magnetic resonance to calculate adiposity (I). iBAT was carefully dissected and weighed (J). Food was removed at the beginning of the cold exposure, which started 2 h after the onset of the light phase. Data are expressed as means ± SE (A–E, n = 8; F–J, n = 5–6). ##P < 0.01 Glp1r^−/− vs. WT; ***P < 0.001 vs. corresponding vehicle; two-way ANOVA with Bonferroni post hoc test. Temp, temperature; cnts, counts; KO, knockout.