The intake of red raspberry fruit is inversely related to cardiac risk factors associated with metabolic syndrome

Abstract

The effect of red raspberry fruit (RSP) was assessed in obesity-prone, Zucker Fatty rats as a model of cardiometabolic risk. RSP reduced fasting triglycerides and fasting glucose but did not appear to affect fasting insulin, low-density lipoprotein, or body weight gain. RSP did significantly reduce heart rate relative to time-matched CON rats. Noteworthy, RSP reduced left ventricular enlargement and wall thickening as measured by echocardiography, without impacting ejection fraction. Cardiac tissue was also evaluated for relative gene expression of key genes impacted in non-insulin-dependent diabetes mellitus (NIDDM). RSP upregulated the expression of myocardial adiponectin receptor 1 and apolipoprotein E, which may impact plasma cholesterol and triglyceride homeostasis. The lipoprotein lipase (Lpl) gene was down-regulated. On the contrary, RSP did not alter PPAR and NF-kB-related mRNA in heart tissue, but did alter nicotinamide phosphoribosyltransferase (Nampt) mRNA. RSP intake impacted cardiometabolic pathophysiology in this model, and molecular mechanisms deserve further study.