Obesity is a global health concern. An ideal drug would inhibit appetite and elevate energy expenditure (EE), but no currently available medication can safely do this. Glucagon elevates EE in humans, but the mechanism remains unknown.
To investigate, for a given energy expenditure rise, the differential effects of glucagon infusion and cold exposure on brown adipose tissue (BAT) activation in humans.
Indirect calorimetry and supraclavicular thermography was performed in 11 healthy male volunteers before and after cold exposure, glucagon infusion (at 23°C) and vehicle infusion (at 23°C). All volunteers underwent 18F-FDG PET/CT scanning with cold exposure. Subjects with cold-induced BAT activation on 18F-FDG PET/CT (n=8) underwent a randomly allocated second 18F-FDG PET/CT scan (at 23°C) either with glucagon infusion (n=4) or vehicle infusion (n=4).
EE increased by 14% following cold exposure and by 15% post-glucagon infusion (50 ng/kg/min) (P<0.05 vs control for both). Cold exposure produced an increase in neck temperature (+0.44°C; P<0.001 vs control), but glucagon infusion did not alter neck temperature. In subjects with cold-induced increase in the metabolic activity of supraclavicular BAT on 18F-FDG PET/CT, a significant rise in metabolic activity of BAT following glucagon infusion was not detected. Cold exposure increased sympathetic activation, as measured by circulating norepinephrine levels, but glucagon infusion did not.
Glucagon increases energy expenditure to a similar magnitude compared to cold activation, but independently of BAT thermogenesis. This finding is of importance for the development of safe treatments of obesity through upregulation of energy expenditure.
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