Abstract 651: Phenotype Shifts in Vascular Smooth Muscle Cells Induced by a Low-Carbohydrate High-Protein Diet

Abstract

The growing rate of obesity is of concern as the condition is associated with increased risk for cardiovascular disease (CVD). Diets that reduce or eliminate carbohydrates, while increasing fat and/or protein intake (Atkin’s Diet) are growing in popularity for rapid weight loss. Despite their effectiveness, recent studies have implicated these low-carbohydrate high-protein (LCHP) diets with an increased incidence of CVD and greater fatty deposits in the aortic wall than a traditional western diet (WD). We assessed the hypothesis that LCHP diets result in greater vascular smooth muscle cell (VSMC) dedifferentiation and a more pro-atherosclerotic environment when compared to a control diet (CON) or WD. Experiments were performed on aorta and plasma obtained from male Apolipoprotein E-knockout mice that were fed either regular chow (CON), WD or LCHP diet for 6 weeks. Immunoblotting was used to determine VSMC dedifferentiation as a marker of disease stage in isolated vessels using proteins calponin, alpha-actin, and TRPC1. Plasma lipid concentrations were obtained by liquid chromatography - mass spectrometry (LC-MS). Calponin was significantly downregulated in the LCHP diet versus both the WD and CON, with no difference detected between WD and CON. There was a trend towards a decreased level of alpha-actin and a higher TRPC1 level in the LCHP diet compared with CON (no differences between CON and WD). LC-MS data revealed significantly higher plasma levels of certain triglycerides in LCHP than WD. This data indicates that the LCHP diet results in a more synthetic phenotype of SMC as indicated by the diminished contractile protein expression (calponin and alpha-actin) and increased TRPC1, when compared to CON and WD. Additionally, the LCHP diet results in an abnormal lipid profile when compared to the WD; a traditional high-risk diet. Taken together, this data suggests that the LCHP diet results in an increased pro-atherosclerotic environment, even when equated to the WD in terms of cholesterol intake. This novel information may require attention from both clinicians and dieters when evaluating diet choices.