Abstract

ObjectivesWe have previously shown that sugar kelp (Saccharina latissima), a brown seaweed, decreased serum triglycerides (TG) and total cholesterol (TC), and prevented adipose tissue inflammation and fibrosis in male diet-induced obesity mice. In this study, we investigated whether the consumption of sugar kelp can prevent metabolic and inflammatory features in low-density lipoprotein receptor knockout (Ldlr KO) mice fed a diet high in fat and cholesterol. MethodsMale Ldlr KO mice at the age of 7 weeks from the Jackson laboratory were randomly assigned to a high-fat/high-cholesterol control (HF/HC; 16% fat, 0.25% cholesterol, w/w, n = 12), or a HF/HC supplemented with sugar kelp (HF/HC-SK; 6.0% dried sugar kelp power, w/w, n = 12). Mice were fed the experimental diets for 16 weeks and then serum and tissue samples were collected to measure blood and liver lipids, serum alanine aminotransferase, and hepatic gene expression. ResultsMice fed HF/HC-SK diet showed a trend towards an increase in final body weight compared to HF/HC control. Serum TG and TC concentrations were not significantly different between control and sugar kelp-fed mice. In the liver, sugar kelp consumption did not alter weights, TG, TC, and lipogenic gene expression. However, the expression of macrophage markers, such as adhesion G protein-coupled receptor E1 and cluster of differentiation 68, and M1 macrophage markers, including tumor necrosis factor, and integrin subunit alpha X, were significantly higher in HF/HC-SK group than HF/HC control mice. Despite the increases in inflammatory markers in the liver of the HF/HC-SK group, serum ALT activity was not different between the two groups. ConclusionsSugar kelp consumption did not alter circulating and hepatic TC and TG, and serum liver injury marker in HF/HC-fed Ldlr KO mice. Further study is warranted to determine whether sugar kelp can impact the development of atherosclerosis in this mouse model. Funding SourcesUSDA Hatch CONS00993.

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