Insulin Induces Upregulation of Vascular AT ₁ Receptor Gene Expression by Posttranscriptional Mechanisms

Abstract

Insulin-induced upregulation of the AT1 receptor by posttranscriptional mechanisms may explain the association of hyperinsulinemia with hypertension and arteriosclerosis, because activation of the AT1 receptor plays a key role in the regulation of blood pressure and fluid homeostasis.

The increased angiotensin II (type 1) receptor density in myocardium of type 2 diabetic patients is prevented by blockade of the renin–angiotensin system

“…In each panel the blots are representative of two individual experiments. *p<0.05 vs ND of insulin on AT1 receptor gene expression, but showed a prolonged mRNA half-life, indicating that overexpression of the receptor may be caused by stabilisation of AT1 receptor mRNA [1]. In the present study, levels of AT1 receptor mRNA correlated well with the percentage levels of HbA 1c in the serum of diabetic patients (Fig.…”

“…In cultured vascular smooth muscle cells both high glucose as well as insulin induced an upregulation of AT1 receptor expression [1,29]. The pathway for the insulin-driven upregulation of the AT1 receptor is dependent on tyrosine kinases and presumably involves the p42/44 mitogen-activated protein kinase, suggesting in this case a post-transcriptional regulation of receptor expression.…”

“…In contrast, type 1 diabetic individuals (the remaining 5%) typically show no signs of metabolic syndrome and have low levels of insulin due to the destruction of pancreatic beta cells. Both, glucose and insulin have been implicated in gene regulation that may promote the development of cardiovascular disease in diabetic patients [1,2].…”

The effect of a rapid weight loss induced by laparoscopic adjustable gastric banding on arterial stiffness, metabolic and inflammatory parameters in patients with morbid obesity

“…There are a number of mechanisms by which increasing adiposity and obesity might contribute to arterial stiffening, both in short and in long term. First, the state of insulin resistance that commonly accompanies obesity impairs endothelium-dependent vasodilatation 24 and increases the local activity of a variety of growth factors in vascular tissue, 25,26 promoting collagen production and the development of vascular smooth muscle cell (VSMC) hypertrophy. 27 In addition, the pro-inflammatory state typical of obesity may promote free radical formation, leading to the development of oxidative stress.…”

Effect of ID ACE gene polymorphism on dietary composition and obesity-related anthropometric parameters in the Czech adult population

“…Several lines of evidence have previously suggested that angiotensin II, the direct consequence of ACE activity, impairs insulin sensitivity [22,24], and insulin resistance promotes the development of various co-morbidities by upregulating the number and activity of angiotensin II receptors [20]. In several other studies, insulin resistance has been improved in response to treatment with angiotensin I-converting enzyme inhibitors (ACEIs) [12,13].…”