Long-term sucrose solution consumption causes metabolic alterations and affects hepatic oxidative stress in wistar rats

Abstract

As the number of overweight and obese people has risen in recent years, there has been a parallel increase in the number of people with metabolic syndrome, diabetes and non-alcoholic fatty liver disease. The consumption of artificially sweetened beverages contributes to these epidemics. This study investigated the long-term effects of ingestion of a 40% sucrose solution on serum and hepatic parameters in male Wistar rats (Rattus norvegicus). After 180 days, the glycemic response, lipid profile and hepatic oxidative stress were compared to those of rats maintained on water. Sucrose ingestion led to higher body weight, increased fat deposits, reduced voluntary food intake and reduced feeding efficiency. Rats that received sucrose solution showed early signs of glucose intolerance and insulin resistance, such as hyperinsulinemia. Serum triacylglycerol (TG), very-low density lipoprotein (VLDL), cholesterol, ALT and AST levels increased after sucrose consumption. Elevated malondialdehyde and superoxide dismutase (SOD) levels and reduced glutathione levels characterize the hepatic oxidative stress due to sucrose ingestion. Liver sample histology showed vacuolar traces and increased fibrotic tissue. Our data showed the harmful effects of chronic consumption of sucrose solution, which can cause alterations that are found frequently in obesity, glucose intolerance and non-alcoholic hepatic disease, characteristics of metabolic syndrome.

Effects of Vanadium Inhalation and Sweetened Beverage Ingestion in Mice: Morphological and Biochemical Changes in the Liver

“…The nuclear and cellular changes increase with the simultaneous administration of V + S possibly as a result of the potentiating effect of V + S on oxidative stress as it was reported for the kidney. 11 It is also possible that the potentiated ROS/RNS production by the co-administration of sucrose and V has a major effect on cytoskeleton disruption favoring the presence of meganucleated and bi or three-nucleated cells, 27 assumptions that need further study. On the other hand, changes in nuclear ploidy (meganuclei) and in the number of nuclei (multinucleated) cells might be a regenerative response as it has been observed in mice models of NAFLD, partial hepatectomies, viral infections such as HBV and HCV, and in patients with non-alcoholic steatohepatitis (NASH) and in V inhalation.…”

The Intricate Relationship between Type 2 Diabetes Mellitus (T2DM), Insulin Resistance (IR), and Nonalcoholic Fatty Liver Disease (NAFLD)

“…High fructose intake is associated with increased risk of steatosis, liver fibrosis, obesity, and IR [148]. Long-term sucrose ingestion led to increased fat accumulation, glucose intolerance and hyperinsulinemia, and histological damage like increased hepatocyte size and ballooning [149]. Dietary intake of monosaturated FAs found in foods like olive oil and avocado has been shown to improve insulin sensitivity and hepatic fat in prediabetic [150] and in paediatric patients with NAFLD [151].…”

S-Nitrosoglutathione Reverts Dietary Sucrose-Induced Insulin Resistance

“…It is evident that impaired NO plays a role in insulin resistance and T2D in humans [57][58][59] and the negative impact of hypercaloric diets on GSH levels is documented, stressing the importance of GSH action to maintain a proper antioxidant system and whole-body homeostasis [60,61]. Here we show that dietary sucrose led to an increase in iNOS expression, which can account for the increase in hepatic NO.…”