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Insulin Resistance and Other Mechanisms of Obesity Hypertension

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Pediatric Hypertension

Abstract

Insulin exerts important biological effects on the metabolic regulation of carbohydrates, lipids, and proteins. In addition, it has important influences on the vasculature, kidneys, and the sympathetic nervous system. Insulin resistance (or loss of insulin sensitivity) is typically defined as decreased insulin-mediated glucose disposal in the body in response to physiological (endogenous or exogenous) insulin concentrations. Insulin resistance is commonly associated with obesity, although not all individuals with obesity have insulin resistance, and insulin resistance may be present in persons without obesity. Insulin resistance can have important adverse consequences on the vasculature and blood pressure, thought to be mediated via vascular inflammation, nitric oxide action, sympathetic nervous system, and renal sodium retention. The “gold standard” for measurement of insulin sensitivity is glucose clamp studies, and the most widely used index for insulin resistance is the homeostasis model for insulin resistance (HOMA-IR). The prevalence of insulin resistance and its adverse effects has been found to be higher in children and adolescents with obesity, diabetes, chronic kidney disease, and in those with low birth weight. Modifications in diet, especially the use of DASH diet, physical activity, and drugs such as metformin and liraglutide, have been found to be effective in improving insulin resistance. Surgical treatment has been shown to be effective in youth with severe obesity and diabetes to improve metabolic consequences and should be offered to patients. Genetic and epigenetic mechanisms likely influence insulin resistance and are an active area of research.

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Thaker, V., Falkner, B. (2023). Insulin Resistance and Other Mechanisms of Obesity Hypertension. In: Flynn, J.T., Ingelfinger, J.R., Brady, T.M. (eds) Pediatric Hypertension. Springer, Cham. https://doi.org/10.1007/978-3-031-06231-5_39

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