Puerarin improves hepatic glucose and lipid homeostasis in vitro and in vivo by regulating the AMPK pathway.

Obesity is an increasingly concerning global health issue, which is accompanied by disruption of glucose and lipid metabolisms. The aim of this study was to uncover the potential and molecular actions of puerarin, a phytochemical, for alleviating metabolic dysfunctions of glucose and lipid metabolisms. A rat model fed a high fat and high fructose diet and a HepG2 cell model challenged with fructose combined with free fatty acid were utilized to identify the effects of puerarin on obesity-associated insulin resistance and hepatic steatosis. The molecular mechanisms underlying puerarin treatment effects were further investigated using qRT-PCR and western blotting. Results show that puerarin significantly ameliorated features of obesity in rats, including bodyweight, hyperlipidemia, hyperglycemia, glucose/insulin intolerance, insulin resistance, hepatic steatosis, and oxidative stress, which are related to the activation of AMPK and PI3K/Akt pathways in the liver. Puerarin reduced lipid accumulation and caused a reduction of the mRNA expression of lipogenic genes such as SREBP-1c, FAS, SCD-1, and HMGCR, and an increment in the phosphorylation of AMPK and ACC in HepG2 cells. Moreover, puerarin ameliorated insulin resistance by increasing GLUT4 mRNA expression and activating the PI3K/Akt pathway. Treatment with the AMPK inhibitor compound C partially abolished the beneficial effects of puerarin on lipid accumulation and insulin resistance in HepG2 cells, which indicated that the protective effects of puerarin partially depend on the AMPK pathway. The present study indicates that puerarin shows potential as a functional food therapeutic for the treatment of obesity.

Isolation and characterization of sulfonamide-degrading bacteria Escherichia sp. HS21 and Acinetobacter sp. HS51.

With the intensive application of sulfonamides in aquaculture and animal husbandry and the increase of sulfonamides discharged into the environments, there is an increasing need to find a way to remediate sulfonamide-contaminated environments. Two bacterial strains capable of degrading sulfonamides, HS21 and HS51, were isolated from marine environments. HS21 and HS51 were identified as members of Escherichia sp. and Acinetobacter sp., respectively, based on 16S rRNA gene sequencing. Degradation of each sulfonamide by Escherichia sp. HS21 and Acinetobacter sp. HS51 was characterized using capillary electrophoresis. About 66 or 72% of sulfapyridine and 45 or 67% of sulfathiazole contained in the media was degraded by Escherichia sp. HS21 or Acinetobacter sp. HS51, respectively, after incubation for 2 days. The supernatant from culture of Escherichia sp. HS21 or Acinetobacter sp. HS51 grown in sulfapyridine or sulfathiazole contained media had much attenuated cytotoxicity against HeLa cells. These results suggest that Escherichia sp. HS21 and Acinetobacter sp. HS51 are new bacterial resources for biodegrading sulfonamides and indicate the potential of isolated strains for the bioremediation of sulfonamide-polluted environments.