Polysaccharides from Enteromorpha prolifera improves insulin sensitivity and promotes adipose thermogenesis in diet-induced obese mice associated with activation of PGC-1α-FNDC5/irisin pathway

Polysaccharide from Enteromorpha prolifera (EPP) has therapeutic and nutraceutical potential for obesity management due to its high hypolipidaemic activity. However, the metabolic mechanism by which EPP mediates anti-adiposity effects are not fully understood. This study aimed to evaluate the effects of EPP on insulin signaling and adaptive thermogenesis in high-fat diet (HFD)-fed obese mice, and further explore the underlying mechanisms. C57BL/6 male mice were fed a control diet or an HFD diet with or without 5% EPP for 12 weeks. The insulin signaling and thermogenic program in adipose tissue, and energy expenditure, as well as involvement of PPAR gamma( )coactivator-1 alpha (PGC-1 alpha)-fibronectin type 3 domain-containing protein 5 (FNDC5)/irisin pathway were assessed. EPP alleviated diet-induced adiposity, and decreased inflammatory response and improved insulin signaling in white adipose tissue (WAT) of HFD mice. Moreover, EPP administration increased oxygen consumption, carbon dioxide production and heat production in HFD mice, as reflected by the increased thermogenesis observed in brown fat and inguinal WAT. Meanwhile, EPP increased serum irisin concentration and activated PGC-1 alpha/FNDC5/adenosine monophosphate-activated protein kinase alpha (AMPK alpha) pathway. These results suggested that dietary EPP improved insulin signaling and whole-body energy metabolism in obese mice, likely by activating the PGC-1 alpha-FNDC5/irisin pathways.

Automated summary

The polysaccharide from Enteromorpha prolifera (EPP) has been found to improve insulin signaling and whole-body energy metabolism in high-fat diet-induced obese mice. It alleviates diet-induced adiposity and inflammatory response, and increases thermogenesis. These effects are likely mediated by the activation of the PGC-1 alpha-FNDC5/irisin pathways.