Summary Capsaicinoids are responsible for the spicy flavor of pungent peppers (Capsicum). The cultivar CH‐19 Sweet is a non‐pungent pepper mutant derived from a pungent pepper strain, Capsicum annuum CH‐19. CH‐19 Sweet biosynthesizes capsaicinoid analogs, capsinoids. We determined the genetic and metabolic mechanisms of capsinoid biosynthesis in this cultivar. We analyzed the putative aminotransferase (pAMT) that is thought to catalyze the formation of vanillylamine from vanillin in the capsaicinoid biosynthetic pathway. Enzyme assays revealed that pAMT activity catalyzing vanillylamine formation was completely lost in CH‐19 Sweet placenta tissue. RT‐PCR analysis showed normal mRNA transcription of the pAMT gene; however, SNP analysis of the cDNA sequence showed a T nucleotide insertion at 1291 bp in the pAMT gene of CH‐19 Sweet. This insertion formed a new stop codon, TGA, that prevented normal translation of the gene, and the pAMT protein did not accumulate in CH‐19 Sweet as determined using Western blot analysis. We developed a dCAPS marker based on the T insertion in the pAMT gene of CH‐19 Sweet, and showed that the pAMT genotype co‐segregated with the capsinoid or capsaicinoid fruit phenotype in the F2 population. The T insertion was not found in other pungent and non‐pungent Capsicum lines, suggesting that it is specific to CH‐19 Sweet. CH‐19 Sweet’s pAMT gene mutation is an example of a nonsense mutation in a single gene that alters a secondary metabolite biosynthetic pathway, resulting in the biosynthesis of analogs. The dCAPS marker will be useful in selecting lines with capsinoid‐containing fruits in pepper‐breeding programs.

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Background: Grape seed extracts (GSE) are known to present health benefits such as antioxidative and anti-obesity effects in animal models. The purpose of this research is to determine whether the specially manufactured GSE, catechin-rich GSE (CGSE), can protect against obesity induced by a high-fat diet (HFD) and to address the mechanism underlying this effect. Methods: The componential analysis of CGSE was performed using liquid chromatography/mass spectrometry. Oxygen consumption and the respiratory quotient were determined using 500 mg/kg CGSE administered orally for 3 days in 14- to 15-week-old male C57BL/6J mice. Nine-week-old male C57BL/6J mice were supplemented with 0.5 or 1% CGSE in a HFD for 12 weeks, and their body weight and food intake were monitored. Blood and tissue samples were collected and analyzed. Results: The main polyphenol components of CGSE were catechin and epicatechin. CGSE supplementation in the HFD-induced obesity model chronically suppressed the increase in body weight and the weight of fat pads. Furthermore, CGSE improved metabolic parameter abnormalities and upregulated the fatty acid oxidation-related genes in the liver. Conclusions: These findings suggest that CGSE contains monomeric catechins in high concentrations and ameliorates HFD-induced obesity in C57BL/6J mice.

The crude aqueous ethanol extract of the cones of Alnus glutinosa (L.) Gaertn. (Betulaceae; black alder, European alder) was obtained and further partitioned between water and various organic phases. The active water and butanol phases were subjected to assay-guided (DPPH) fractionation using repetitive RP HPLC until individual compounds were isolated. Their antioxidative activities, measured as SC₅₀ values, were evaluated. The chemical structures of the isolated compounds were elucidated with the help of mass spectroscopy, (1)H NMR technique, UV spectroscopy, and chemical approaches. One novel ellagitannin, glutinoin (2), along with two known compounds, pedunculagin (1) and praecoxin D (3), were isolated and found to contribute to antioxidative activity of the A. glutinosa cones extract. The activities (SC₅₀) of 1-3 were evaluated as 0.95 (1), 1.00 (2) and 1.01 µg mL⁻¹ (3). The scavenging effects of glutinoin (2) and praecoxin D (3) were reported for the first time.