Catecholamine-induced lipolysis was investigated in adipocytes obtained before and after 30 min of exercise from 10 insulin-treated type I (insulin-dependent) diabetic men and 10 male matched control subjects. The α2-adrenoceptor-mediated antilipolytic effect of catecholamines was normal, but the β-adrenoceptor-mediated lipolytic sensitivity was increased 10-fold (P < .01) in diabetic subjects before and after exercise. The latter correlated inversely (r > .7) with the circulating norepinephrine level, which was significantly reduced in diabetic subjects. Basal lipolysis and lipolysis activated at different steps distal to the β-receptor were similar in the two groups. There was no major change in the total number of β- and α-adrenoceptors in the diabetic patients. However, the proportion of high-affinity β-adrenoceptors was significantly increased in these patients compared with control subjects. In the diabetic patients, ∼50% of the β-adrenoceptors were in a high-affinity state, compared to ∼30% in the control subjects (P < .025). In diabetic subjects there was an enhanced plasma glycerol response to exercise, despite a blunted plasma norepinephrine response. The data suggest enhanced sensitivity of catecholamine-induced lipolysis in type I diabetes due to an increase in the number of high-affinity (i.e., coupled) β-adrenoceptors in fat cells. This mechanism may be due to low levels of circulating norepinephrine and may also explain the exaggerated lipolytic response to exercise in the diabetic state.

This content is only available via PDF.