Title:
The Role of Insulin Resistance in Congestive Heart Failure, Impaired Glucose Tolerance, and Hypertension
Aim:
The aim of this study was to explore the role of insulin resistance and compensatory hyperinsulinemia in glucose intolerance, hypertension, and CVD across conditions such as congestive heart failure (CHF) and non-insulin-dependent diabetes mellitus (NIDDM).
Background:
Insulin resistance is a characteristic feature of congestive heart failure (CHF), non-insulin-dependent diabetes mellitus (NIDDM), and essential hypertension. Hyperinsulinemia, increased plasma norepinephrine, and disturbed glucose metabolism contribute to these conditions. Although compensatory hyperinsulinemia maintains glucose homeostasis, it may enhance cardiovascular risks by promoting endothelial dysfunction and dyslipidaemia.
Methodology:
The analysis synthesizes findings from the following:
- A case–control study of congestive heart failure patients and controls, using oral glucose tolerance tests and euglycemic clamps.
- Longitudinal studies of insulin-mediated glucose uptake and β-cell function in NIDDM and hypertension.
- Population-based studies of fasting insulin, norepinephrine, and free fatty acids (FFA).
Results and Discussion:
CHF patients presented with increased levels of norepinephrine, insulin, and FFA. These resulted in impaired glucose clearance and hepatic glucose regulation via insulin. NIDDM required hyperinsulinemia to counteract insulin resistance and maintain glucose tolerance, ultimately failing as the function of the β-cells declined. Hypertension linked insulin resistance with dyslipidaemia and CVD, characterized by high triglycerides and low HDL cholesterol. Insulin resistance in CHF and hypertension further exacerbates metabolic derangement and increases CVD risk.
Conclusion:
The mechanisms of insulin resistance and compensatory hyperinsulinemia are central to the pathogenesis of glucose intolerance, hypertension, and CVD in CHF, NIDDM, and related disorders. Addressing these disturbances may help mitigate disease progression and improve cardiovascular outcomes.
