Chronic consumption of fructose dysregulates genes related to glucose and lipid metabolism in prostate tissue

Abstract

Fructose is commonly used as a taste enhancer in many processed foods. Excessive fructose consumption is highly associated with obesity and development of cancer particularly prostate cancer. This study aimed to investigate the biochemical and molecular changes in the prostate tissue of rats treated with 20% fructose for six months. A total of 18 rats weighted 200-250 g were divided into two groups, where each group consisted of 9 rats. Control group is given normal diet, while the treated group was given normal diet and 20% fructose in drinking water. After six months of treatment, both groups were sacrificed for further analysis. Body weight, blood pressure and glucose were measured. Lipid profiles were determined using quantitative colorimetric assay. Transcripts level of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), leptin (LEP), angiopoietin 1 (ANGPT1), microRNA (miR)-34a, miR-10b and miR-192 were determined using quantitative PCR, while the protein levels of 11β-HSD1 and leptin were determined using ELISA. The results showed that 20% fructose diet significantly increased blood glucose level as compared to the control (p<0.05). The transcript levels of LEP and miR-192 were significantly lower in the fructose-treated group as compared to the control (p<0.05). There was a significant linear relationship between prostate LEP and serum LDL/VLDL level as well as between the level of prostate LEP and serum total cholesterol level (p<0.05). Thus, our results showed that chronic consumption of fructose could down-regulate LEP and miR-192 expression in prostate tissue, and promote higher accumulation of fat in the tissue. Additionally, downregulation of miR-192 has been reported to be associated with the pathogenesis of prostate cancer. Thus, it can be concluded that long-term fructose diet leads to higher blood glucose level and down-regulation of LEP and miR-192 expression in prostate tissue.