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Hepatic gluconeogenesis is tightly balanced by opposing stimulatory (glucagon) and inhibitory (insulin) signaling pathways. Hepatocyte growth factor (HGF) is a pleiotropic growth factor that mediates diverse biological processes. In this study, we investigated the effect of HGF and its family member, macrophage-stimulating factor (MSP), on hepatic gluconeogenesis in primary hepatocytes. HGF and MSP significantly repressed expression of the key hepatic gluconeogenic enzyme genes, phosphoenolpyruvate carboxykinase (PEPCK), and glucose-6-phosphatase (Glc-6-Pase) and reduced glucose production. HGF and MSP activated small heterodimer partner (SHP) gene promoter and induced SHP mRNA and protein levels, and the effect of HGF and MSP on SHP gene expression was demonstrated to be mediated via activation of the AMP-activated protein kinase (AMPK) signaling pathway. We demonstrated that upstream stimulatory factor-1 (USF-1) specifically mediated HGF effect on SHP gene expression, and inhibition of USF-1 by dominant negative USF-1 significantly abrogated HGF-mediated activation of the SHP promoter. Elucidation of the mechanism showed that USF-1 bound to E-box-1 in the SHP promoter, and HGF increased USF-1 DNA binding on the SHP promoter via AMPK and DNA-dependent protein kinase-mediated pathways. Adenoviral overexpression of USF-1 significantly repressed PEPCK and Glc-6-Pase gene expression and reduced glucose production. Knockdown of endogenous SHP expression significantly reversed this effect. Finally, knockdown of SHP or inhibition of AMPK signaling reversed the ability of HGF to suppress hepatocyte nuclear factor 4alpha-mediated up-regulation of PEPCK and Glc-6-Pase gene expression along with the HGF- and MSP-mediated suppression of gluconeogenesis. Overall, our results suggest a novel signaling pathway through HGF/AMPK/USF-1/SHP to inhibit hepatic gluconeogenesis.

In this study, two quercetin-α- d -glucopyranosides were synthesized via the acceptor reaction of a glucansucrase obtained from Leuconostoc mesenteroides B-1299CB, with quercetin and sucrose. The two transfer products were purified via HPLC, and the structures of the products were identified as quercetin-4′-O-α- d -glucopyranoside (Q-G1) and quercetin-3′-O-α- d -glucopyranoside (Q-G1′), in accordance with the results of 1H, 13C, HSQC, H-H COSY, HMBC analyses. The primary product (Q-G1) evidenced slower effects on DPPH radical-scavenging activity (SC50 = 25.2 μM) than was seen with quercetin (SC50 = 6.5 μM). The water solubility of Q-G1 was 12.7 mM, whereas the quercetin was barely soluble in water. The Ki value of Q-G1 (674.5 μM) was almost identical to that of quercetin (673.3 μM) with regard to tyrosinase inhibition effects.

Three genera of plant viruses, Begomovirus (Geminiviridae), Crinivirus (Closteroviridae) and Ipomovirus (Potyviridae), contain members that infect sweet potato (Ipomoea batatas) and are transmitted by whiteflies. The begomoviruses, Sweet potato leaf curl virus (SPLCV) and Ipomoea leaf curl virus (ILCV), and the ipomovirus Sweet potato mild mottle virus are transmitted by Bemisia tabaci, the sweet potato whitefly. The crinivirus, Sweet potato chlorotic stunt virus (SPCSV), is transmitted by B. tabaci and Trialeurodes abutilonea, the bandedwinged whitefly. Transmission experiments were done with three of these viruses using laboratory-reared whiteflies and 2-day acquisition and transmission feeding periods. SPLCV and ILCV were transmitted from single and double infections by B. tabaci at rates of 5–10%. Transmission rates for SPLCV by B. tabaci were 15–20%. T. abutilonea transmitted SPCSV at a rate of ca. 3% but did not transmit ILCV or SPLCV.