Abstract
Inflammation plays an important role in the pathophysiology of the metabolic syndrome (MS). We determined whether the overexpression of interleukin (IL)-18 could aggravate left ventricular (LV) remodeling and diastolic dysfunction in fructose-fed rats (FFRs). To create an animal model for MS, male Wistar rats received 10% fructose in water for 8 months. We used an adenovirus encoding rat IL-18 to overexpress IL-18 in FFRs by intravenous administration. IL-18 overexpression led to increases in collagen volume fraction and collagen deposition. LV systolic function was unaltered. But the LV end-diastolic pressure and the time constant of isovolumic relaxation (tau) were increased. Peak negative value of time derivative of LV pressure (-dp/dt) was decreased. Isovolumic relaxation time and myocardial index, as assessed by echocardiography, were increased. Overexpression of IL-18 leads to aggravated LV remodeling and dysfunction in FFRs. Attenuation of the inflammatory process may provide a novel therapeutic strategy in treating metabolic cardiomyopathy.
Highlights
Presence of obesity, non-insulindependent diabetes mellitus and hypertension is an essential feature of the metabolic syndrome (MS), which is associated with the development and progression of cardiovascular disease [1]
Clinical studies demonstrate that serum interleukin (IL)-18 is elevated in patients with MS, and IL-18 levels are associated with MS independent of obesity and insulin resistance, suggesting that activation of IL-18 is involved in the pathogenesis of MS [4]
The E wave and the Ea wave were significantly lower, and isovolumic relaxation time was significantly elevated in fructose-fed rats (FFRs)
Summary
Non-insulindependent diabetes mellitus and hypertension is an essential feature of the metabolic syndrome (MS), which is associated with the development and progression of cardiovascular disease [1]. Population-based studies report that MS patients present mild but significant left ventricular (LV) diastolic dysfunction [2,3]. A major cause of diastolic dysfunction, is prevalent in these MS patients. Collagen type I and collagen type III are the major fibrillar collagens present in the adult heart. Excessive interstitial collagens in the myocardium are associated with organ stiffness and result in diastolic dysfunction leading to heart failure. Clinical studies demonstrate that serum interleukin (IL)-18 is elevated in patients with MS, and IL-18 levels are associated with MS independent of obesity and insulin resistance, suggesting that activation of IL-18 is involved in the pathogenesis of MS [4]. The effect of IL-18 on MS remains obscure
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