'Suioh', a sweet potato (Ipomoea batatas L.) cultivar developed in Japan, has edible leaves and stems. The sweet potato leaves contain polyphenols such as caffeoylquinic acid (CQA) derivatives. It has multiple biological functions and may help to regulate the blood glucose concentration. In this study, we first examined whether sweet potato leaf extract powder (SP) attenuated hyperglycaemia in type 2 diabetic mice. Administration of dietary SP for 5 weeks significantly lowered glycaemia in type 2 diabetic mice. Second, we conducted in vitro experiments, and found that SP and CQA derivatives significantly enhanced glucagon-like peptide-1 (GLP-1) secretion. Third, pre-administration of SP significantly stimulated GLP-1 secretion and was accompanied by enhanced insulin secretion in rats, which resulted in a reduced glycaemic response after glucose injection. These results indicate that oral SP attenuates postprandial hyperglycaemia, possibly through enhancement of GLP-1 secretion.

Melanogenesis is the physiological process by which melanin is synthesized to protect the skin from UV damage. While paracrine interactions between keratinocytes and melanocytes are crucial for regulating epidermal pigmentation, the endothelin (EDN)-endothelin B-receptor (EDNRB) interaction is one of the key linkages. In this study, we found that a single exposure of normal human melanocytes (NHMs) with UVB stimulates the expression of EDNRB and its upstream transcription factor microphthalmia-associated transcription factor (MITF) at the transcriptional and translational levels. That stimulation can be abrogated by post-irradiation treatment with a French maritime pine bark extract (PBE). UVB stimulated the phosphorylation of p38 and c-jun N-terminal kinase (JNK), but not ERK, followed by the increased phosphorylation of MSK1 and CREB. The post-irradiation treatment with PBE did not affect the increased phosphorylation of p38 and JNK, but distinctly abrogated the phosphorylation of MSK1 and CREB. Post-irradiation treatment with the MSK1 inhibitor H89 significantly down-regulated the increased gene expression of MITF and EDNRB in UVB-exposed NHMs. Our findings indicate for the first time that the increased expression of MITF that leads to the up-regulation of melanocyte-specific proteins in UVB-exposed NHMs is mediated via activation of the p38/MSK1/CREB pathway but not the ERK/RSK/CREB pathway. The mode of action by PBE demonstrates that interrupting MSK1 activation is a new target for antioxidants including PBE which can serve as anti-pigmenting agents in a reactive oxygen species-depletion-independent manner.

Dietary proteins and trypsin inhibitors are known to stimulate the secretion of the satiety hormone cholecystokinin (CCK). A potato extract (Potein) contains 60% carbohydrate and 20% protein including trypsin inhibitory proteins. In this study, we examined whether Potein suppresses food intake in rats and whether it directly stimulates CCK secretion in enteroendocrine cells. In fasted rats, food consumption was measured up to 6 h after the oral administration of Potein or soybean trypsin inhibitor (SBTI). CCK-releasing activities of Potein and SBTI were examined in the murine CCK-producing cell line STC-1. Potein inhibited the trypsin activity in vitro with a potency 20-fold lower than that of SBTI. Oral administration of Potein dose-dependently suppressed food intake for 1-6 h. Potein, but not the SBTI, dose-dependently induced CCK secretion in STC-1 cells. These results suggest that Potein suppresses food intake through the CCK secretion induced by direct stimulation on enteroendocrine cells and through inhibition of luminal trypsin.

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Puerariae flower extract (PFE) is a crude extract of the Kudzu flower. Previous studies have shown that PFE supplementation exerts anti-obesity and anti-fatty liver effects in high-fat diet-fed mice. In this study, we aimed to identify the PFE components responsible for these effects and to determine their influence on energy expenditure and uncoupling protein 1 (UCP1) expression. Experiments were conducted on C57BL/6J male mice classified into 3 groups: (1) high-fat diet-fed (HFD), (2) high-fat diet-fed given PFE (HFD + PFE), and (3) high-fat diet-fed given the PFE isoflavone-rich fraction (HFD + ISOF). All groups were fed for 42 days. The HFD + PFE and HFD + ISOF groups showed significant resistance to increases in body weight, hepatic triglyceride level, and visceral fat compared to the HFD group. These groups also exhibited significant increases in oxygen consumption and UCP1-positive brown adipose tissue (BAT) area. Our results demonstrate that the active ingredients in PFE are present in the ISOF and that these compounds may increase energy expenditure by upregulation of BAT UCP1 expression. These findings provide valuable information regarding the anti-obesity effects of isoflavones.