Neochlorogenic acid (3-CQA) and cryptochlorogenic acid (4-CQA), isolated from prune (Prunus domestica L.), were identified by NMR and MS analyses. In addition, the quantity of chlorogenic acid isomers in prune were measured by HPLC. These isomers, 3-CQA, 4-CQA, and chlorogenic acid (5-CQA), were contained in the ratio 78.7:18. 4:3.9, respectively. 4-CQA was identified and quantified in prune for the first time, and relatively high amounts of this isomer were characteristic. Antioxidative activities of the chlorogenic acid isomers, such as scavenging activity on superoxide anion radicals and inhibitory effect against oxidation of methyl linoleate, were also evaluated. Each isomer showed antioxidative activities which were almost the same.

Late-onset hypogonadism (i.e. androgen deficiency) raises the risk for abdominal obesity in men. The mechanism for this obesity is unclear. Here, we demonstrated that hypogonadism after castration caused abdominal obesity in high-fat diet (HFD)-fed, but not in standard diet (SD)-fed, C57BL/6J mice. Furthermore, the phenotype was not induced in mice treated with antibiotics that disrupt the intestinal microflora. In HFD-fed mice, castration increased feed efficiency and decreased fecal weight per food intake. Castration also induced in an increase of visceral fat mass only in the absence of antibiotics in HFD-fed mice, whereas subcutaneous fat mass was increased by castration irrespective of antibiotics. Castration reduced the expression in the mesenteric fat of both adipose triglyceride lipase and hormonesensitive lipase in HFD-fed mice, which was not observed in the presence of antibiotics. Castration decreased thigh muscle (i.e. quadriceps and hamstrings) mass, elevated fasting blood glucose levels, and increased liver triglyceride levels in a HFD-dependent manner, whereas these changes were not observed in castrated mice treated with antibiotics. The Firmicutes/Bacteroidetes ratio and Lactobacillus species increased in the feces of HFD-fed castrated mice. These results show that androgen (e.g. testosterone) deficiency can alter the intestinal microbiome and induce abdominal obesity in a dietdependent manner.Obesity is a global epidemic problem due to its strong association with an increased risk of cardiovascular diseases 1,2 . The excess accumulation of abdominal visceral fat, a diagnostic criterion of the metabolic syndrome 2 , increases the disorder in lipid metabolism, including an elevation of hepatic triglyceride levels 3 . In contrast, subcutaneous fat reduces the incidence of cardiovascular diseases, indicating the importance of body fat distribution 1,2 . Recent results show that the changes in intestinal microbiota are related to the development of obesity and to the increase of visceral fat mass [4][5][6][7] . Testosterone is a male sexual hormone (viz. androgen) that exerts a broad range of male physiological functions, such as the development of reproductive organs and the emergence of sexual behaviors 8,9 . Hypogonadism (i.e. low testosterone level) increases in men the risk of obesity, cardiovascular diseases, and even mortality [10][11][12][13] through the increase of body fat, in particular visceral fat 14,15 ; and testosterone treatment reduces the amount of visceral fat 16 . Androgen deprivation therapies, such as either castration or an leteinizing hormone-releasing hormone analog for prostate cancer patients, also promote the development of obesity [17][18][19] . Because the blood bioactive testosterone level steadily drops approximately 2% per year after around the age of 20 to 30 in men 20 , the age-dependent decline of testosterone is a risk factor for the age-related prevalence of abdominal obesity and its related diseases in men 14,20 . Despite increasing evidence in both clinical an...

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