NORMAL PANCREASTATIN-LIKE AND INCREASED POST-GLUCOSE INSULIN LEVELS IN YOUNG OFFSPRING OF INSULIN-RESISTANT NONOBESE ESSENTIAL HYPERTENSIVEPATIENTS

Citation
V. Sanchezmargalet et al., NORMAL PANCREASTATIN-LIKE AND INCREASED POST-GLUCOSE INSULIN LEVELS IN YOUNG OFFSPRING OF INSULIN-RESISTANT NONOBESE ESSENTIAL HYPERTENSIVEPATIENTS, Journal of Endocrinology, 153(2), 1997, pp. 313-318
Citations number
39
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
00220795
Volume
153
Issue
2
Year of publication
1997
Pages
313 - 318
Database
ISI
SICI code
0022-0795(1997)153:2<313:NPAIPI>2.0.ZU;2-U
Abstract
Pancreastatin is a regulatory peptide known to inhibit insulin secreti on and insulin action with a glycogenolytic effect in the liver. This peptide is present in and secreted by many endocrine and chromaffin ce lls. Abnormalities of glucose, insulin and lipoprotein metabolism are common in patients with hypertension, as well as their first-degree re latives. We have recently studied a group of non-obese hypertensive su bjects 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 p art in the insulin resistance of these patients, and this metabolic sy ndrome could play a role in the pathogenesis and complications of hype rtension. In this article, we studied the normotensive offspring of th ese nonobese hypertensive patients and looked for metabolic abnormalit ies 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 pa tients. We found that after an intravenous glucose load, offspring fro m insulin-resistant patients were already hyperinsulinemic, although g lucose clearance was normal, suggesting an early alteration in insulin sensitivity, whereas pancreastatin and catecholamine levels were norm al compared with matched controls. However, offspring from non-insulin -resistant patients had no differences with controls. These results su ggest that pancreastatin and catecholamines may not play an important role in triggering insulin resistance, although they may be important once the syndrome is established.