Carrot Juice Administration Decreases Liver Stearoyl-CoA Desaturase 1 and Improves Docosahexaenoic Acid Levels, but Not Steatosis in High Fructose Diet-Fed Weanling Wistar Rats

Abstract

Non-alcoholic fatty liver disease (NAFLD) is one of the most prevalent liver diseases associated with an altered lifestyle, besides genetic factors. The control and management of NAFLD mostly depend on lifestyle modifications, due to the lack of a specific therapeutic approach. In this context, we assessed the effect of carrot juice on the development of high fructose-induced hepatic steatosis. For this purpose, male weanling Wistar rats were divided into 4 groups, fed either a control (Con) or high fructose (HFr) diet of AIN93G composition, with or without carrot juice (CJ) for 8 weeks. At the end of the experimental period, plasma biochemical markers, such as triglycerides, alanine aminotransferase, and β-hydroxy butyrate levels were comparable among the 4 groups. Although, the liver injury marker, aspartate aminotransferase, levels in plasma showed a reduction, hepatic triglycerides levels were not significantly reduced by carrot juice ingestion in the HFr diet-fed rats (HFr-CJ). On the other hand, the key triglyceride synthesis pathway enzyme, hepatic stearoyl-CoA desaturase 1 (SCD1), expression at mRNA level was augmented by carrot juice ingestion, while their protein levels showed a significant reduction, which corroborated with decreased monounsaturated fatty acids (MUFA), particularly palmitoleic (C16:1) and oleic (C18:1) acids. Notably, it also improved the long chain n-3 polyunsaturated fatty acid, docosahexaenoic acid (DHA; C22:6) content of the liver in HFr-CJ. In conclusion, carrot juice ingestion decreased the SCD1-mediated production of MUFA and improved DHA levels in liver, under high fructose diet-fed conditions. However, these changes did not significantly lower the hepatic triglyceride levels.

Folic acid supplementation prevents high fructose-induced non-alcoholic fatty liver disease by activating the AMPK and LKB1 signaling pathways

“…The current study showed that the high-fructose diet did not change the liver and body weights, but significantly elevated hepatic TG, plasma TG, and plasma TC levels. Similar to our observation, in a study by Mahesh et al [ 29 ], a high-fructose diet induced fatty liver without significant differences in body or liver weight for 8 weeks. Similarly, Kawasaki et al [ 7 ] reported that, in a study of rats fed a high-fructose, high-fat, or high-sucrose diet for 6 weeks, there was no significant difference in the body weight or liver weight in the high-fructose or high-sucrose-diet groups compared to the control group.…”

Carrot juice ingestion attenuates high fructose‐induced circulatory pro‐inflammatory mediators in weanling Wistar rats

“…However, despite a significant increase in plasma FFA levels, which is known to be associated with the development of insulin resistance, high fructose diet‐fed animals did not display hyperinsulinemia and impaired glucose tolerance. In addition, although resistin and IGFBP levels increased in RPWAT owing to carrot juice feeding, it had no effect on insulin sensitivity, which is evident from the unaltered glucose uptake of skeletal muscle in these animals …”

Diabetogenic diet-induced insulin resistance associates with lipid droplet proteins and adipose tissue secretome, but not with sexual dimorphic adipose tissue fat accumulation in Wistar rats

“…Soleus muscles were excised immediately after the animals were sacrificed and processed for glucose uptake assay according to the previously described method [ 18 ].…”