Context: Studies suggest that appropriate nutritional modifications can improve the natural conception rate of infertile couples. Objectives: The purpose of this study was to review the human trials that investigated the relation between nutrition and male infertility. Data Sources: A comprehensive systematic review of published human studies was carried out by searching scientific databases. Article selection was carried out in accordance with Preferred Reporting Items for Systematic Reviews and MetaAnalyses. The American Dietetic Association Research Design and Implementation Checklist was also used for quality assessment. Data Extraction: A total of 502 articles were identified, of which 23 studies met the inclusion criteria. Data Synthesis: Results indicated that a healthy diet improves at least one measure of semen quality, while diets high in lipophilic foods, soy isoflavones, and sweets lower semen quality. Conclusion: The role of daily nutrient exposure and dietary quality needs to be highlighted in male infertility. Mechanistic studies addressing the responsible underlying mechanisms of action of dietary modifications are highly warranted.

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Adipose tissue dysfunction related to obesity is overwhelmingly associated with increased risk of developing cardiovascular diseases. In the setting of obesity, (pro)renin receptor (PRR) is increased in adipose tissue of mice. We sought to determine the physiological consequences of adipocyte-PRR deficiency using Adiponectin-Cre mice. We report a unique model of adipocyte-PRR-deficient mice (PRRAdi/Y) with almost no detectable white adipose tissues. As a consequence, the livers of PRRAdi/Y mice were enlarged and demonstrated a marked accumulation of lipids. Adipocyte-specific deficiency of PRR increased systolic blood pressure (SBP) and the concentration of soluble PRR (sPRR) in plasma. To determine whether adipocyte PRR was involved in the development of obesity-induced hypertension, mice were fed a low-fat or a high-fat diet for 16 weeks. Adipocyte-PRR-deficient mice were resistant to diet-induced obesity. Both high- and low-fat-fed PRRAdi/Y mice had elevated insulin levels. Interestingly, adipocyte-PRR deficiency improved glucose tolerance in high-fat-fed PRRAdi/Y mice. In response to feeding either low-fat or high-fat diets, SBP was greater in PRRAdi/Y mice compared with control mice. High-fat feeding elevated sPRR concentration in control and PRRAdi/Y mice. In vitro knock down of PRR by siRNA significantly decreased mRNA abundance of PPARγ, suggesting an important role for PRR in adipogenesis. Our data indicate that adipocyte PRR is involved in lipid homeostasis and glucose and insulin homeostasis, and that soluble PRR may be a predictor of metabolic disturbances and play a role in SBP regulation.