(PO07-28-22) Sugar Kelp Consumption Did Not Alter Circulating and Hepatic Lipids in Low-Density Lipoprotein Receptor Knockout Mice Fed a Diet High in Fat and Cholesterol

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Presenting Author(s)

HJ

Hyungryun Jang, Bachelor
– PhD student, University of Connecticut, Storrs, Connecticut, United States

Co-Author(s)

OC

Olivia Corvino
– University of Connecticut
HK

Hyunju Kang, PhD
– University of Connecticut, Current Assistant Professor at Keimyung University, Storrs, Connecticut, United States
Mi-Bo Kim, PhD
– Postdoctoral researcher, University of Connecticut, Storrs, Connecticut, United States
WO

William Odell
– University of Connecticut
VK

Victoria Kostour
– University of Connecticut
Ji-Young Lee, Ph.D.
– Professor and Head, University of Connecticut, Storrs, Connecticut, United States
YP

Young-Ki Park, Ph.D.
– University of Connecticut, Storrs, Connecticut, United States

Disclosure(s):

Hyungryun Jang, Bachelor: No relevant financial relationship(s) with ineligible companies to disclose.

Hyunju Kang, PhD: No relevant financial relationship(s) with ineligible companies to disclose.

Objectives: We 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.

Methods: Male 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.

Results: Mice 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.

Conclusions: Sugar 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 Sources: USDA Hatch CONS00993