Heart Smart Insulin-Like Growth Factor 1

Abstract

See related article, pp 680–693 The prevalence of obesity, metabolic syndrome, and type 2 diabetes mellitus, and the associated cardiac pathologies are rising to alarming levels. Conventional medical therapies for the prevention and treatment of cardiomyopathy are less effective in patients with these metabolic disorders, and this is attributed, at least in part, to a limited understanding of the cellular and genetic mechanisms responsible for the pathology in the heart. The cause(s) underlying the development of obesity and metabolic syndrome have been attributed to several factors including, but not limited to, consumption of a high-fat diet and are often associated with myocardial contractile and metabolic dysfunction.1 The detrimental effects of high-fat diets on the heart are likely to be multifactorial and include lipotoxicity, abnormal fatty acid metabolism, endothelial dysfunction, impaired calcium handling, mitochondrial dysfunction, and disruption of the insulin signaling pathway. Recent evidence also suggests that a high-fat diet induces epigenetic defects in the heart,2 which could potentially result in an increased risk of cardiac pathologies in offspring. A better understanding of the mechanisms underlying the increased propensity for high-fat diets to induce cardiac dysfunction is necessary to develop treatment strategies. Insulin-like growth factor-1 (IGF-1) plays a role in regulating cell proliferation, differentiation, survival, and metabolism and is produced in many tissues, including the heart. Reduced IGF-1 levels are associated with obesity, cardiovascular disease, atherosclerosis, and diabetes mellitus, whereas elevated IGF-1 has been associated with longevity in humans.3 …