4.7 Article

Effect of Antarctic krill phospholipid (KOPL) on high fat diet-induced obesity in mice

期刊

FOOD RESEARCH INTERNATIONAL
卷 148, 期 -, 页码 -

出版社

ELSEVIER
DOI: 10.1016/j.foodres.2021.110456

关键词

Antarctic krill phospholipid; Diet-induced obesity; Lipid metabolic; Intestinal damage; Inflammatory state; Microbiota

资金

  1. Zhejiang Provincial Key Research and Development Project of China [2019C02076, 2019C02075]
  2. Zhoushan Science and Technology Project of China [2018C21019]

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KOPL treatment effectively improves symptoms in HFD-induced obese mice by reducing weight gain and fat accumulation, protecting liver and intestinal tissues, regulating inflammation, and modulating intestinal microbiota diversity. It may be a promising dietary strategy for treating obesity and related metabolic diseases.
Phospholipids are the main lipid components in Antarctic krill oil, and the combination of n-3 polyunsaturated fatty acids (n-3 PUFAs) shows multiple nutritional advantages. At present, the research about Antarctic krill phospholipid (KOPL) mainly focuses on the purification, and there are few reports on the anti-obesity effect. Thus, this study aimed at evaluating the effect of KOPL on the high-fat diet (HFD)-induced obesity mice. All the mice were divided into five groups, which were fed chow diet, HFD, and different doses of KOPL + HFD, respectively. The results showed that KOPL treatment could reduce the weight gain, fat accumulation, and liver tissue damage in HFD-induced mice. KOPL treatment could reduce the levels of serum lipid (TC, TG, L-LDL) and fasting blood glucose in HFD-induced mice, and the inflammatory cytokines (IL-1 beta and TNF-alpha) in serum. Further analysis showed that KOPL could promote the normal expression of lipid-synthesis-related genes and proteins, including sterol regulatory element-binding protein-1c (SREBP-1c), fatty acid synthetase (FAS), and peroxisome proliferator-activated receptor alpha (PPAR-alpha) in liver tissue. Besides, it inhibited the overexpression of inflammatory cytokine genes (IL-1 beta and TNF-alpha), but increased the expression of tight junction genes (ZO-1 and Occludin) in the colon tissue. Additionally, KOPL improved the decrease of diversity and imbalance of intestinal microbiota, which could contribute to its beneficial effects. In summary, the KOPL treatment improves the effects of HFD-induced obese mice by maintaining normal lipid levels, protecting the liver tissue, reducing inflammation response and intestinal damage, and regulating intestinal microbiota abnormalities. It refer to KOPL could be a promising dietary strategy for treating obesity and improving its related metabolic diseases.

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