Predicted body fat percentage, fat mass and lean body mass in relation to risk of prostate cancer: Results from the NHANES 1999 to 2010.

The purpose of this study is to examine the relationship between fat mass (FM), body fat percentage (BF%), lean body mass (LM), and prostate cancer (PCa), and evaluate their potential impact on the risk of PCa. Data from the National Health and Nutrition Examination Survey (NHANES) of the United States were utilized. Adult male participants from 6 survey cycles between 1999 and 2010 were selected as the study sample. Multivariable logistic regression analysis was conducted to explore the association between BF%, LM, and PCa, while controlling for potential confounding variables. Among the 8440 participants, 359 cases of PCa were diagnosed. The relationship between BF%, LM, and PCa was nonlinear. In the multivariable logistic regression analysis, there was an independent association between BF% and PCa risk (OR: 1.04, 95% CI: 1.02-1.06), suggesting that higher BF% levels are associated with an increased risk of PCa. Conversely, higher LM levels were associated with a decreased risk of PCa (OR: 0.96, 95% CI: 0.95-0.98). The findings of this study demonstrate a correlation between BF% and LM with PCa, but do not provide direct evidence of a causal relationship. Higher BF% levels are associated with an increased risk of PCa, while higher LM levels are associated with a decreased risk. These results provide valuable insights for understanding and potentially preventing PCa, although further research is needed to fully comprehend the underlying mechanisms.

Adiponectin inhibits KISS1 gene transcription through AMPK and specificity protein-1 in the hypothalamic GT1-7 neurons.

Adiponectin secreted from adipose tissues plays a role in the regulation of energy homeostasis, food intake, and reproduction in the hypothalamus. We have previously demonstrated that adiponectin significantly inhibited GNRH secretion from GT1-7 hypothalamic GNRH neuron cells. In this study, we further investigated the effect of adiponectin on hypothalamic KISS1 gene transcription, which is the upstream signal of GNRH. We found that globular adiponectin (gAd) or AICAR, an artificial AMPK activator, decreased KISS1 mRNA transcription and promoter activity. Conversely, inhibition of AMPK by Compound C or AMPKα1-SiRNA augmented KISS1 mRNA transcription and promoter activity. Additionally, gAd and AICAR decreased the translocation of specificity protein-1 (SP1) from cytoplasm to nucleus; however, Compound C and AMPKα1-siRNA played an inverse role. Our experiments in vivo demonstrated that the expression of Kiss1 mRNA was stimulated twofold in the Compound C-treated rats and decreased about 60-70% in gAd- or AICAR-treated rats compared with control group. The numbers of kisspeptin immunopositive neurons in the arcuate nucleus region of Sprague Dawley rats mimicked the same trend seen in Kiss1 mRNA levels in animal groups with different treatments. In conclusion, our results provide the first evidence that adiponectin reduces Kiss1 gene transcription in GT1-7 cells through activation of AMPK and subsequently decreased translocation of SP1.