Journal
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
Volume 97, Issue -, Pages -Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jnutbio.2021.108799
Keywords
Sugar kelp; Inflammation; Liver fibrosis; NAFLD; NASH
Funding
- USDA Hatch [CONS00978]
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This study demonstrated that the consumption of U.S.-grown sugar kelp can prevent obesity-related metabolic abnormalities and NASH in a mouse model. Mice fed with sugar kelp showed lower body weight, increased metabolism, reduced fat accumulation, inflammation, and fibrosis in the liver and adipose tissue compared to the control group.
Nonalcoholic steatohepatitis (NASH), closely associated with obesity, is a health concern worldwide. We investigated whether the consumption of U.S.-grown sugar kelp (Saccharina latissima), an edible brown alga, can prevent obesity-associated metabolic disturbances and NASH in a mouse model of diet-induced NASH. Male C57BL/6J mice were fed a low-fat diet, a high-fat/high-sucrose/high-cholesterol diet (HF), or a HF diet containing sugar kelp (HF -Kelp) for 14 weeks. HF-Kelp group showed lower body weight with increased O-2 consumption, CO2 production, physical activity, and energy expenditure compared with the HF. In the liver, there were significant decreases in weight, triglycerides, total cholesterol, and steatosis with HF-Kelp. The HF-Kelp group decreased hepatic expression of a macrophage marker adhesion G protein-coupled receptor E1 (Adgre1) and an M1 macrophage marker integrin alpha x (Itgax). HF-Kelp group also exhibited decreased liver fibrosis, as evidenced by less expression of fibrogenic genes and collagen accumulation than those of HF group. In epididymal white adipose tissue (eWAT), HF-Kelp group exhibited decreases in eWAT weight and adipocyte size compared with those of the HF. HF-Kelp group showed decreased expression of collagen type VI alpha 1 chain, Adgre1, Itgax, and tumor necrosis factor alpha in eWAT. We demonstrated, for the first time, that the consumption of U.S-grown sugar kelp prevented the development of obesity and its associated metabolic disturbances, steatosis, inflammation, and fibrosis in the liver and eWAT of a diet-induced NASH mouse model. (C) 2021 Elsevier Inc. All rights reserved.
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