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We studied the effect of the external addition of noradrenaline (NA) on the electrical activity of white adipocytes from rat epididymal tissue. NA modified the active voltage response recorded by the current clamp technique, and decreased the macroscopic membrane potassium currents measured by a whole-cell configuration patch-clamp technique in cells obtained by culturing differentiating preadipocytes. To analyse if cAMP is implicated in the effect of this hormone on potassium conductances, the changes in electrical activity caused by an increase in the intracellular concentration of cAMP were studied using intracellular recording. The addition of forskolin, or NN-dibutyryl cAMP plus 3-isobutyl-1-methylxanthine to the bath reduced active changes in membrane voltage responses to hyperpolarizing and depolarizing pulses. A similar effect was observed when vasoactive intestinal peptide was added to the superfusion chamber. These results suggest that NA could modulate K+ conductances in white adipocytes, mediated by cAMP.
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Abstract
Pancreastatin is a regulatory peptide known to inhibit insulin secretion and insulin action with a glycogenolytic effect in the liver. This peptide is present in and secreted by many endocrine and chromaffin cells. Abnormalities of glucose, insulin and lipoprotein metabolism are common in patients with hypertension, as well as their first-degree relatives. We have recently studied a group of non-obese hypertensive subjects in which pancreastatin-like levels were increased compared with controls, and correlated with norepinephrine levels. We hypothesized that pancreastatin alongside the sympathoadrenal system might have a part in the insulin resistance of these patients, and this metabolic syndrome could play a role in the pathogenesis and complications of hypertension. In this article, we studied the normotensive offspring of these non-obese hypertensive patients and looked for metabolic abnormalities as well as plasma pancreastatin, glucagon and catecholamine levels. The subjects were separated into two groups: (1) offspring from non-insulin-resistant patients and (2) offspring from insulin-resistant patients. We found that after an intravenous glucose load, offspring from insulin-resistant patients were already hyperinsulinemic, although glucose clearance was normal, suggesting an early alteration in insulin sensitivity, whereas pancreastatin and catecholamine levels were normal compared with matched controls. However, offspring from non-insulin-resistant patients had no differences with controls. These results suggest that pancreastatin and catecholamines may not play an important role in triggering insulin resistance, although they may be important once the syndrome is established.
Journal of Endocrinology (1997) 153, 313–318
