TY - JOUR

T1 - Contribution of β3-adrenoceptor activation to ephedrine induced thermogenesis in humans

AU - Liu, Y. L.

AU - Toubro, S.

AU - Astrup, Arne

AU - Stock, M. J.

PY - 1995

Y1 - 1995

N2 - OBJECTIVE: To investigate the contribution of β3-adrenoceptor activation to sympathetic stimulation of thermogenesis in humans using a sympathomimetic (ephedrine) in combination with a non-selective β-adrenoceptor antagonist (nadolol). DESIGN: Three doses (2.5, 5 and 10 mg) of nadolol were used to estimate what fraction of the thermogenic response to ephedrine (30 mg) remained after inhibition of β1- and β2-adrenoceptor mediated responses. SUBJECTS: Nine healthy, young male volunteers at rest after an overnight fast. MEASUREMENTS: Energy expenditure, respiratory quotient, heart rate, blood pressure and plasma potassium, glucose, lactate, glycerol, NEFA and triglycerides were measured before, and for 3 h after treatment with placebo, ephedrine and ephedrine plus three doses of nadolol. RESULTS: Ephedrine produced significant increases in energy expenditure (thermogenesis), heart rate, systolic blood pressure and plasma glucose; the other parameters measured did not change significantly. Nadolol caused significant inhibition of all responses, but 43% of the thermogenic response to ephedrine remained after the 2.5 mg dose of nadolol, whereas the same dose completely inhibited the heart rate and plasma glucose responses. CONCLUSION: All three β-adrenoceptor subtypes (β1, β2 and β3) may be involved in ephedrine-induced thermogenesis, but the resistance to complete inhibition by the non-selective antagonist nadolol indicates that at least 40% of the response is mediated by an atypical receptor, which is presumed to be the β3-adrenoceptor.

AB - OBJECTIVE: To investigate the contribution of β3-adrenoceptor activation to sympathetic stimulation of thermogenesis in humans using a sympathomimetic (ephedrine) in combination with a non-selective β-adrenoceptor antagonist (nadolol). DESIGN: Three doses (2.5, 5 and 10 mg) of nadolol were used to estimate what fraction of the thermogenic response to ephedrine (30 mg) remained after inhibition of β1- and β2-adrenoceptor mediated responses. SUBJECTS: Nine healthy, young male volunteers at rest after an overnight fast. MEASUREMENTS: Energy expenditure, respiratory quotient, heart rate, blood pressure and plasma potassium, glucose, lactate, glycerol, NEFA and triglycerides were measured before, and for 3 h after treatment with placebo, ephedrine and ephedrine plus three doses of nadolol. RESULTS: Ephedrine produced significant increases in energy expenditure (thermogenesis), heart rate, systolic blood pressure and plasma glucose; the other parameters measured did not change significantly. Nadolol caused significant inhibition of all responses, but 43% of the thermogenic response to ephedrine remained after the 2.5 mg dose of nadolol, whereas the same dose completely inhibited the heart rate and plasma glucose responses. CONCLUSION: All three β-adrenoceptor subtypes (β1, β2 and β3) may be involved in ephedrine-induced thermogenesis, but the resistance to complete inhibition by the non-selective antagonist nadolol indicates that at least 40% of the response is mediated by an atypical receptor, which is presumed to be the β3-adrenoceptor.

KW - β-adrenoceptors

KW - Ephedrine

KW - Human

KW - Nadolol

KW - Sympathetic

KW - Thermogenesis

UR - http://www.scopus.com/inward/record.url?scp=0029132152&partnerID=8YFLogxK

M3 - Journal article

C2 - 8574280

AN - SCOPUS:0029132152

VL - 19

SP - 678

EP - 685

JO - International Journal of Obesity

JF - International Journal of Obesity

SN - 0307-0565

IS - 9

ER -