Evaluation of the Effects of Chia (Salvia hispanica L.) Leaves Ethanolic Extracts Supplementation on Biochemical and Hepatic Markers on Diet-Induced Obese Mice.

Obesity is a significant health concern affecting 13% of the world's population. It is often associated with insulin resistance and metabolic-associated fatty liver disease (MAFLD), which can cause chronic inflammation in the liver and adipose tissue. Obese hepatocytes show increased lipid droplets and lipid peroxidation, which can lead to the progression of liver damage. Polyphenols have been shown to have the ability to reduce lipid peroxidation, thereby promoting hepatocyte health. Chia leaves, a by-product of chia seed production, are a natural source of bioactive antioxidant compounds, such as cinnamic acids and flavonoids, which have antioxidant and anti-inflammatory properties. In this study, chia leaves' ethanolic extracts of two seed phenotypes were tested on diet-induced obese mice to evaluate their therapeutic potential. Results show that the chia leaf extract positively affected insulin resistance and lipid peroxidation in the liver. In addition, the extract improved the HOMA-IR index compared to the obese control group, reducing the number and size of lipid droplets and lipid peroxidation. These results suggest that chia leaf extract may help treat insulin resistance and liver damage associated with MAFLD.

EPA/DHA Concentrate by Urea Complexation Decreases Hyperinsulinemia and Increases Plin5 in the Liver of Mice Fed a High-Fat Diet.

Dietary intake of eicosapentaenoic/docosahexaenoic acid (EPA/DHA) reduces insulin resistance and hepatic manifestations through the regulation of metabolism in the liver. Obese mice present insulin resistance and lipid accumulation in intracellular lipid droplets (LDs). LD-associated proteins perilipin (Plin) have an essential role in both adipogenesis and lipolysis; Plin5 regulates lipolysis and thus contributes to fat oxidation. The purpose of this study was to compare the effects of deodorized refined salmon oil (DSO) and its polyunsaturated fatty acids concentrate (CPUFA) containing EPA and DHA, obtained by complexing with urea, on obesity-induced metabolic alteration. CPUFA maximum content was determined using the Box-Behnken experimental design based on Surface Response Methodology. The optimized CPUFA was administered to high-fat diet (HFD)-fed mice (200 mg/kg/day of EPA + DHA) for 8 weeks. No significant differences (p > 0.05) in cholesterol, glycemia, LDs or transaminase content were found. Fasting insulin and hepatic Plin5 protein level increased in the group supplemented with the EPA + DHA optimized product (38.35 g/100 g total fatty acids) compared to obese mice without fish oil supplementation. The results suggest that processing salmon oil by urea concentration can generate an EPA+DHA dose useful to prevent the increase of fasting insulin and the decrease of Plin5 in the liver of insulin-resistant mice.