Abstract
Current changes in diet, characterized by an increase in the intake of sweetened beverages, are heavily related to metabolic disorders such as non-alcoholic fatty liver. This condition can produce simple steatosis and, in worse cases, potentially result in steatohepatitis, fibrosis, and cirrhosis, comparable to the damage caused by the consumption of more or less 20–30 g of alcohol per day. The main objective of this research was to evaluate the effect of curcumin (Curcuma longa) nanoemulsions, using mono- and diacylglycerides medium chain fatty acids as stabilizers in an in vivo hepatic steatosis rat model. Pathology was induced by providing 30% fructose intake in the drinking water. Globule sizes under 200 nm that were stable for 4 weeks were obtained; curcumin encapsulated in the nanoemulsion was >70%. The results revealed an improvement regarding body and liver weight in the animals treated with curcumin nanoemulsions. A decrease in total cholesterol, LDL, AST/ALT, and HDL in serum was observed; however, no apparent improvement regarding serum glucose or triacylglycerides values was noted. Histological analysis showed a significant decrease in the extent of steatosis, inflammation, and brown adipose tissue in the treated animals.
Highlights
Introduction published maps and institutional affilHepatic steatosis is characterized by an accumulation of over 5% triacylglycerides in hepatocyte vesicles; this is a consequence of the increased uptake of fatty acids by the liver [1]
The reaction mixture was concentrated by rotary evaporation to obtain only the emulsifier; headspace was saturated with nitrogen to avoid fatty acid oxidation
According to results obtained by gas chromatography analysis, a mean of 81.85% of the MAG and DAG mixture was obtained after 30 min of reaction (Figure 1b)
Summary
Hepatic steatosis is characterized by an accumulation of over 5% triacylglycerides in hepatocyte vesicles; this is a consequence of the increased uptake of fatty acids by the liver [1]. Triacylglycerides originate from dietary sources or by de novo lipogenesis. It has been shown that hepatic lipids in patients, with non-alcoholic fatty liver disease (NAFLD), originate in 14.9% of cases from inadequate diets, 26.1% from de novo synthesis, and. NAFLD is considered the hepatic manifestation of metabolic syndrome, a serious health problem that affects between 30–40% of the male population and 15–20% of the female population worldwide with an increasing prevalence in people with obesity up to 60–80% [3,4,5].
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