Lutein ameliorates high‐fat diet‐induced obesity, fatty liver, and glucose intolerance in C57BL/6J mice

Abstract

Obesity is a multi‐factorial metabolic syndrome that increases the risk of cardiovascular diseases, diabetes, and cancer. We recently demonstrated the antiadipogenic efficacy of lutein using a 3 T3‐L1 cell culture model. This study aimed to examine the antiobesity efficacy of lutein on high‐fat (60% kcal fat) diet‐induced C57BL/6J obese mice model. Lutein (300 and 500 μM), Orlistat (30 mg/kg body weight ‐ positive control), and its combination (orlistat, 15 mg/kg body weight+lutein, 300 μM) were administered in high‐fat diet (HFD)‐fed mice every other day for 24 weeks. The effect on serum and hepatic lipid parameters was estimated using biochemical assay kits. The adipose tissue expression of adipocyte differentiation markers at gene and protein levels was analyzed by RT‐PCR and western blotting, respectively. The results showed that lutein administration and drug significantly reduced epididymal and abdominal adipose tissue weights. Further, lutein reduced the serum cholesterol and LDL‐C concentration compared to the HFD group. The HFD‐induced elevation in the hepatic triglycerides and cholesterol levels were significantly blocked by lutein and its combination with the drug. Similarly, lutein and its drug combination efficiently lowered the HFD‐mediated elevated blood glucose levels. Lutein downregulated the expression of CEBP‐α, PPAR‐γ, and FAS in the epididymal adipose tissue. Thus, supplementation of lutein may control diet‐induced obesity and associated complications in the human population.

Maternal Lutein Intake during Pregnancies with or without Gestational Diabetes Mellitus and Cognitive Development of Children at 2 Years of Age: A Prospective Observational Study

“…We previously found that GDM increased the incidence of large-for-gestational-age (LGA) births in this cohort [ 16 ]. There was evidence in animals that lutein supplementation alleviated obesity in rodents fed a high-fat diet [ 31 ]. We thus examined the association between maternal L + Z intake or status and neonatal length and weight, but did not identify any significant associations ( Supplementary Table S2 ).…”

“…While lutein levels may be impacted by lipid metabolism, recent research suggests that lutein intake may also affect lipid metabolism by serving as an antioxidant to prevent peroxidation of lipoproteins and increasing peroxisome proliferators activated receptors (PPAR)-α gene expression, which promotes fatty acid catabolism, thereby reducing adiposity and improving cardiometabolic health [ 53 , 54 ]. Lutein supplementation was found to reduce the risk of obesity and glucose intolerance in high-fat-diet-fed rodents [ 31 ]. A major adverse outcome of GDM is fetal overgrowth or macrosomia at birth due partly to the excess fat accretion of the fetus [ 55 ].…”

Nutritional Factors: Benefits in Glaucoma and Ophthalmologic Pathologies

“…Lutein is a powerful antioxidant that can neutralize free radicals and reactive oxygen species, which can cause oxidative damage to cells and tissues. It can help protect cells from oxidative stress and reduce the risk of chronic diseases such as cancer, cardiovascular disease, and neurodegenerative disorders [ 185 ]. Chronic inflammation is associated with numerous health problems, including arthritis, asthma, and heart disease.…”

Alanyl-Glutamine Dipeptide Attenuates Non-Alcoholic Fatty Liver Disease Induced by a High-Fat Diet in Mice by Improving Gut Microbiota Dysbiosis

“…The escalation of energy intake can precipitate a derangement in energy metabolism, ultimately fostering lipid accumulation within both adipose tissue and the liver, culminating in obesity [ 23 ]. Mice subjected to HFD, mirroring obesity and its concomitant disorders such as NAFLD, have become a frequently adopted animal model [ 24 ].…”