ABSTRACT. An absolute reduction of the plasma cortisol levels and a delay of the peak concentrations were recorded in 10 healthy subjects, when a bile‐sequestering anionic exchange resin, cholestyramine, was given prior to a single oral hydrocortisone dose, indicating that the resin interferes with the uptake of a neutral sterol in the human gastrointestinal tract. The possibility of a direct binding of drug to resin is supported by the affinity of hydrocortisone to cholestyramine in vitro, which was uninfluenced by the presence of sodium taurocholate. Cholestyramine significantly delayed the gastric emptying of a glucose solution, indicating that the resin not only decreases but also delays hydrocortisone absorption. Careful supervision is recommended when treatment with cholestyramine is given concomitant to neutral sterol drugs.
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 less than 0.05), and to epinephrine in the presence of yohimbine (P less than 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)-benzimidazole- -2-one-hydrochloride (3H-CGP) was markedly exaggerated (P less than 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.
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