In addition, excessive secretion of insulin tends to produce hyperinsulinemia, which becomes a potential disease hazard (44, 45); hyperinsulinemia can contribute to increased renal tubular sodium reabsorption, sympathetic excitation, accelerated heart rate, increased vascular resistance, dyslipidemia, and narrowing of atherosclerosis, which in turn can increase intracellular calcium ion concentration and sensitivity to elevating substances, leading to the development of HTN (16, 46). Here, INS is linked to hyperinsulinism.