Increased lipolytic sensitivity to catecholamines in diabetic patients with severe autonomic neuropathy

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Abstract
Lipolytic sensitivity to catecholamines was studied in gluteal adipocytes from diabetic subjects with severe (n = 3), mild (n = 6) or no autonomic neuropathy (n = 8). Two of the three patients with severe autonomic neuropathy had a completely abolished plasma epinephrine response to insulin‐induced hypoglycaemia, whereas the third patient showed a reduced and delayed plasma epinephrine response. Lipolytic sensitivity to isoprenaline (P < 0.05), and to epinephrine in the presence of yohimbine (P < 0.0001), was significantly increased in the diabetic subjects with severe autonomic neuropathy, compared to the other study groups. Moreover, the specific binding of the beta‐adrenoceptor antagonist (±)‐4‐(3‐butylamino‐2‐hydroxypropoxyl)‐(5.7‐3H)‐benzimida‐zole‐2‐one‐hydrochloride (3H‐CGP) was markedly exaggerated (P < 0.05) in the patients with severe autonomic neuropathy. These findings demonstrate that the lipolytic sensitivity to catecholamines in adipose tissue was increased only in patients with severe autonomic neuropathy and impaired epinephrine response to insulin‐induced hypoglycaemia. This increased beta‐adrenergic sensitivity could, at least in part, be attributed to an increased density of beta‐adrenergic receptors in the adipocytes.