title: Sea cucumber cerebrosides and long-chain bases from Acaudina molpadioides protect against high fat diet-induced metabolic disorders in mice.
abstract: Metabolic syndrome (MS) is a cluster of metabolic disorders such as abdominal obesity, hypertension, glucose intolerance, dyslipidemia and hepatic steatosis that contribute to increased cardiovascular morbidity and mortality. There is an urgent need for strategies to prevent this emerging global epidemic. Recently, growing interest in discovering food functional nutrients for the prevention and treatment of MS has generated. In the present study, sea cucumber cerebrosides (SCC) and the main structural units, long-chain bases (LCB), were prepared from Acaudina molpadioides and then administered to high fat (HF) diet-induced obese C57BL/6J mice at a diet supplement dosage of 0.025% for 5 weeks to evaluate their effects on obesity-related metabolic disorders. SCC and LCB significantly decreased epididymal adipose tissue weights, lowered hepatic triacylglycerol levels, and reduced serum glucose, insulin levels and HOMA-IR index in mice. The activities of hepatic lipogenetic enzymes including FAS, ME and the mRNA levels of SREBP-1c and FAS were reduced by SCC and LCB treatment. However, SCC and LCB showed no effect on the hepatic lipolysis pathway. Besides, SCC and LCB also efficiently up-regulated the gene expression of SREBP-1c, FAS, ACC, ATGL and HSL, and down-regulated the gene expression of LPL and VLDL-r in the adipose tissue. These results demonstrated that SCC and LCB were efficacious in suppressing hepatic SREBP-1c mediated lipogenesis, inhibiting lipid uptake and increasing TG catabolism in the adipose tissue. The ameliorative degree and regulatory mechanisms of these two compounds were basically the same, suggesting that LCB are the key active structural units. Such findings would offer new insight into the application of SCC or LCB in the development of functional foods for preventing MS in humans.
authors.affiliation: Division of Food Engineering and Nutrition, Yellow Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, No. 106 Nanjing Road, Qingdao, Shandong Province 266071, P. R. China.
authors.forename: Xiaofang
authors.initials: X
authors.lastname: Liu
authors.forename: Jie
authors.initials: J
authors.lastname: Xu
authors.forename: Yong
authors.initials: Y
authors.lastname: Xue
authors.forename: Zhuang
authors.initials: Z
authors.lastname: Gao
authors.forename: Zhaojie
authors.initials: Z
authors.lastname: Li
authors.forename: Kailiang
authors.initials: K
authors.lastname: Leng
authors.forename: Jingfeng
authors.initials: J
authors.lastname: Wang
authors.forename: Changhu
authors.initials: C
authors.lastname: Xue
authors.forename: Yuming
authors.initials: Y
authors.lastname: Wang
mesh_terms: D050156:Adipogenesis / Q000187:drug effects; D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D001482:Base Composition; D001786:Blood Glucose / Q000187:drug effects; D002554:Cerebrosides / Q000737:chemistry / Q000494:pharmacology*; D059305:Diet, High-Fat / Q000009:adverse effects*; D004041:Dietary Fats / Q000009:adverse effects; D055951:Functional Food; D007328:Insulin / Q000097:blood; D008055:Lipids / Q000097:blood; D050155:Lipogenesis / Q000187:drug effects; D008066:Lipolysis / Q000187:drug effects; D008099:Liver / Q000378:metabolism; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000209:etiology / Q000517:prevention & control*; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000097:blood / Q000178:diet therapy; D020011:Protective Agents / Q000494:pharmacology*; D012333:RNA, Messenger / Q000378:metabolism; D012616:Sea Cucumbers / Q000737:chemistry*; D051780:Sterol Regulatory Element Binding Protein 1 / Q000235:genetics; D014280:Triglycerides / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D002554:Cerebrosides; D004041:Dietary Fats; D007328:Insulin; D008055:Lipids; D020011:Protective Agents; D012333:RNA, Messenger; D051780:Sterol Regulatory Element Binding Protein 1; D014280:Triglycerides