| Literature DB >> 26690975 |
Jinhui Wang1, Shiwei Hu2, Wei Jiang3, Wendong Song1, Lu Cai1, Jingfeng Wang4.
Abstract
Nutrition excess-induced inflammation positively contributed to insulin resistance. Fucoidan from sea cucumber can increase glucose translocation in skeletal muscle. However, its effects on inflammation-associated insulin resistance are not understood. We investigated fucoidan from Isostichopus badionotus (Ib-FUC)-alleviated inflammatory response and signaling as well as -improved insulin resistance in the liver of obesity mice. The results showed that Ib-FUC reduced body weight and glucose levels, increased insulin sensitivity, and inhibited serum lipid concentrations. Meanwhile, Hepatic glycogen synthesis was promoted by Ib-FUC via activation of the PI3K/PKB/GSK-3β signaling and regulation of glucose metabolism-related enzymatic activities. Ib-FUC regulated serum inflammatory cytokines and their mRNA expression in the liver. Ib-FUC-induced inactivation of the JNK and IKKβ/NFκB pathways was involved in the activation of insulin signal cascade and inflammatory factor production. These findings suggested that Ib-FUC supplementary-induced alleviation of inflammatory response could be a mechanism responsible for its beneficial effects against hepatic insulin resistance.Entities:
Keywords: Fucoidan; Inflammatory response; Insulin resistance; Sea cucumber
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Year: 2015 PMID: 26690975 DOI: 10.1016/j.intimp.2015.12.009
Source DB: PubMed Journal: Int Immunopharmacol ISSN: 1567-5769 Impact factor: 4.932