An extract from the Atlantic brown algae Saccorhiza polyschides counteracts diet-induced obesity in mice via a gut related multi-factorial mechanisms

作者：Huebbe Patricia^*; Nikolai Sibylle; Schloesser Anke; Herebian Diran; Campbell Graeme; Glueer Claus Christian; Zeyner Annette; Demetrowitsch Tobias; Schwarz Karin; Metges Cornelia C; Roeder Thomas; Schultheiss Gerhard; Ipharraguerre Ignacio R; Rimbach Gerald

来源：Oncotarget, 2017, 8(43): 73501-73515.

DOI：10.18632/oncotarget.18113

• circulating bile acids
• bile salt hydrolase activity
• intestinal gluconeogenesis
• life span
• mTOR activation
• Gerotarget

In this study we addressed the questions whether an Atlantic brown algae extract (BAE) affects diet induced obesity in mice and which would be the primary targets and underlying key mechanisms.
Male C57 BL/6 mice were fed a hypercaloric diet, referred to as high fat diet (HFD), supplemented with a freeze-dried aqueous BAE from Saccorhiza polyschides (5 %) for 8 months. Compared to the control group, dietary BAE supplementation significantly attenuated increase in body weight and fat mass. We observed apparent metabolic improvement including normalization of blood glucose, reduced plasma leptin, reduced fecal bile salt hydrolase activity with lower microbial production of toxic bile acid metabolites in the gut and increased systemic bile acid circulation in BAE-fed mice counteracting adverse effects of long term HFD feeding. Survival of mice receiving dietary BAE supplementation appeared slightly enhanced; however, median and maximal life spans as well as hepatic mTOR activation were not significantly different between BAE and control mice.
We suggest that the beneficial metabolic effects of our BAE are at least partly mediated by alterations in gut microbiota associated with fermentation of indigestible polysaccharides that are major components of brown algae such as alginates and fucoidans. We moreover propose a multi-factorial mechanism that involves profound alterations in bile acid homeostasis, changes in intestinal and systemic glucose metabolism likely including increased intestinal gluconeogenesis, increased activity of the intestinally derived hormone GLP-1 contributing to promote systemic insulin sensitivity, and inhibition of a-amylase activity, which expectably limits dietary carbohydrate digestion and glucose release.

• 出版日期2017-9-26