Background:Obesity is associated with gut microbiota dysbiosis, disrupted intestinal barrier and chronic inflammation. Given the high and increasing prevalence of obesity worldwide, anti-obesity treatments that are safe, effective and widely available would be beneficial. We examined whether the medicinal mushroom Antrodia cinnamomea may reduce obesity in mice fed with a high-fat diet (HFD).Methods:Male C57BL/6J mice were fed a HFD for 8 weeks to induce obesity and chronic inflammation. The mice were treated with a water extract of A. cinnamomea (WEAC), and body weight, fat accumulation, inflammation markers, insulin sensitivity and the gut microbiota were monitored.Results:After 8 weeks, the mean body weight of HFD-fed mice was 39.8±1.2 g compared with 35.8±1.3 g for the HFD+1% WEAC group, corresponding to a reduction of 4 g or 10% of body weight (P<0.0001). WEAC supplementation reduced fat accumulation and serum triglycerides in a statistically significant manner in HFD-fed mice. WEAC also reversed the effects of HFD on inflammation markers (interleukin-1β, interleukin-6, tumor necrosis factor-α), insulin resistance and adipokine production (leptin and adiponectin). Notably, WEAC increased the expression of intestinal tight junctions (zonula occludens-1 and occludin) and antimicrobial proteins (Reg3g and lysozyme C) in the small intestine, leading to reduced blood endotoxemia. Finally, WEAC modulated the composition of the gut microbiota, reducing the Firmicutes/Bacteroidetes ratio and increasing the level of Akkermansia muciniphila and other bacterial species associated with anti-inflammatory properties.Conclusions:Supplementation with A. cinnamomea produces anti-obesogenic, anti-inflammatory and antidiabetic effects in HFD-fed mice by maintaining intestinal integrity and modulating the gut microbiota.

Previous studies of the pancreatic exocrine response to intraduodenal glucose administration have not demonstrated the release of secretin; consequently, the importance of secretin in the enteric insulin release mechanism has been questioned.In tbis study, serum levels of secretin were estimated by radioimmunoassay in three normal subjects after oral, intravenous or intraduodenal administration of glucose (1 gm per Kg). No secretin response was recorded during the intravenous study but sirnilar peak levels (12 to 18 ng per ml) were observed with the oral and intraduodenal routes of administratioIL The initial response was rapid in both instances, but the effect was more prolonged after intraduodenal administration. As secretin is known to potentiate the glycaemic release of insulin, it is postulated that this hormone is a major factor in the augmented insulin response observed during both oral and intraduodenal studies.Horm. Metab. Res. 3: 180·183 (1971) K e y -W 0 r d s: Secretin Release -Insulin Release -Glu· cose Administration -Radioimmunoassay

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