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Inhibition of the beta-1 adrenergic receptor does not potentiate mirabegron-stimulated human brown adipose tissue thermogenesis.

Dumont, L.; Caron, A.; Richard, G.; Croteau, E.; Fortin, M.; Frisch, F.; Phoenix, S.; Dubreuil, S.; Guerin, B.; Turcotte, E. E.; Carpentier, A. C.; Blondin, D. P.

2023-03-28 pharmacology and therapeutics
10.1101/2023.03.22.23287600 medRxiv
Show abstract

Pharmacological stimulation of human brown adipose tissue (BAT) has been hindered by either ineffective activation or undesirable off-target secondary effects. Oral administration of the maximal allowable dose of mirabegron (200 mg), a {beta}3-adrenergic receptor ({beta}3-AR) agonist, has been effective in stimulating BAT thermogenesis and whole-body energy expenditure. However, this too has been accompanied by undesirable cardiovascular effects. Combining mirabegron with a cardio-selective {beta}1-AR antagonist could not only suppress these unwanted effects, but potentially increase the sensitivity of the {beta}3-AR and {beta}2-AR in WAT and BAT. Here we report that co-ingesting a high dose of the {beta}1-AR antagonist bisoprolol with mirabegron suppresses the increase in heart rate, systolic blood pressure and myocardial oxygen consumption. However, it also blunted the mirabegron-stimulated increase in BAT lipolysis, thermogenesis and glucose uptake. Whether the attenuation in BAT blood flow induced by the large dose of bisoprolol limited BAT thermogenesis remains to be determined. clinicaltrials.gov (NCT04823442)

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