High-carbohydrate diet-induced myocardial remodelling in rats

Abstract

BACKGROUND: A high-carbohydrate diet leads to the metabolic syndrome (MetS), which leads to an increased risk for cardiovascular dysfunction; however, the effect of high-carbohydrate diets on systemic metabolism has not yet been fully determined. It has been observed that abnormal fatty acid metabolism and increased oxidative stress play a role in the pathogenesis of MetS-related cardiovascular diseases. OBJECTIVE: To examine the effects of high sucrose intake on left ventricular contractility and structure of heart tissue. METHODS: MetS was induced in male rats with drinking water supplemented with 32% sucrose for 16 weeks. Oral glucose tolerance test results and parameters related to insulin resistance were used to validate MetS. RESULTS: Body weight and blood glucose levels were higher in the MetS group compared with age-matched controls. The increased serum leptin and triglyceride levels and decreased ghrelin levels further supported the existence of MetS in the MetS group. The ratio of total oxidant status to total antioxidant status measured in serum was also higher in the MetS group compared with the control group. The hemodynamic parameters of the MetS group, such as heart rate, and systolic and diastolic blood pressure levels, were markedly higher in the MetS group, while left ventricular developed pressure was significantly diminished with prolonged time course. Moreover, these functional alterations in cardiac preparations were further supported with structural changes such as significant increases in myofibril undulation and increased lipid droplets. CONCLUSIONS: These data highlight the link between high carbohydrate intake, MetS and cardiac dysfunction, in part due to increased systemic oxidative stress and lipid deposition in the heart tissue.

Effects of metabolic syndrome on masseter muscle of male Wistar rats

“…Metabolic syndrome was induced by a method previously described by Okatan et al . . Rats in the MetS group were fed with standard rat chow and 32% sucrose solution (instead of drinking water) ad libitum for 16 wk.…”

Tale of two kinases: Protein kinase A and Ca2+/calmodulin-dependent protein kinase II in pre-diabetic cardiomyopathy

“…The regulation of cardiac function by the sympathetic nervous system via β-ARs is of particular interest because dysregulation of this system has been reported in HF and metabolic disorders such as DM2 and MetS[ 27 - 29 ].…”

“…Most studies addressing diet-induced cardiometabolic alterations have been performed with laboratory animals under either carbohydrate- or fat and carbohydrate-enriched diets to emulate the Western diet, characterized by the ingestion of refined sugar and high caloric food. However, not all models — indeed, only eight[ 27 , 51 - 57 ] of those considered in this work — fulfill the requirement of at least three of the aforementioned criteria to be considered experimental models of MetS (Table 1 ).…”

“…Importantly, despite the discrepancies in metabolic alterations all these animal models developed pre-diabetic cardiomyopathy, characterized by several cardiac alterations. For instance, increased heart rate was reported in five models[ 27 , 48 , 51 , 56 , 63 ]; however, other studies in which this parameter was evaluated did not report changes[ 60 , 62 , 65 , 66 ]. Systolic dysfunction has also been observed, including decreased heart contractility, ventricular pressure, and intracellular Ca 2+ transient amplitude[ 27 , 55 , 60 , 67 - 71 ], along with reduced fractional shortening[ 55 , 65 - 67 , 70 - 72 ] (Table 1 ).…”

“…For instance, increased heart rate was reported in five models[ 27 , 48 , 51 , 56 , 63 ]; however, other studies in which this parameter was evaluated did not report changes[ 60 , 62 , 65 , 66 ]. Systolic dysfunction has also been observed, including decreased heart contractility, ventricular pressure, and intracellular Ca 2+ transient amplitude[ 27 , 55 , 60 , 67 - 71 ], along with reduced fractional shortening[ 55 , 65 - 67 , 70 - 72 ] (Table 1 ). Diastolic dysfunction is also manifested by increased diastolic Ca 2+ leak in the form of Ca 2+ waves, without altering cytoplasmic Ca 2+ levels[ 48 , 55 , 62 ].…”