Sánchez-Margalet V, Ramos E, Mateo J, Oliván J, Pérez-Cano R, Goberna R
Departamento de Bioquímica Clínica, Hospital Virgen Macarena, Facultad de Medicina, Universidad de Sevilla, Spain.
J Endocrinol. 1997 May;153(2):313-8. doi: 10.1677/joe.0.1530313.
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 nonobese 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.
胰抑制素是一种调节肽，已知它可抑制胰岛素分泌和胰岛素作用，并对肝脏有糖原分解作用。这种肽存在于许多内分泌细胞和嗜铬细胞中，并由它们分泌。高血压患者及其一级亲属中，葡萄糖、胰岛素和脂蛋白代谢异常很常见。我们最近研究了一组非肥胖高血压患者，他们的胰抑制素样水平相比对照组有所升高，且与去甲肾上腺素水平相关。我们推测，胰抑制素与交感肾上腺系统一起，可能在这些患者的胰岛素抵抗中起作用，而这种代谢综合征可能在高血压的发病机制和并发症中发挥作用。在本文中，我们研究了这些非肥胖高血压患者的血压正常的后代，并寻找代谢异常以及血浆胰抑制素、胰高血糖素和儿茶酚胺水平。受试者被分为两组：（1）非胰岛素抵抗患者的后代和（2）胰岛素抵抗患者的后代。我们发现，静脉注射葡萄糖负荷后，胰岛素抵抗患者的后代虽然葡萄糖清除正常，但已经出现高胰岛素血症，这表明胰岛素敏感性早期发生了改变，而与匹配的对照组相比，胰抑制素和儿茶酚胺水平正常。然而，非胰岛素抵抗患者的后代与对照组没有差异。这些结果表明，胰抑制素和儿茶酚胺在引发胰岛素抵抗方面可能不起重要作用，尽管它们在综合征确立后可能很重要。
