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 Meta-Analyses. 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. Systematic Review Registration: PROSPERO 2013: CRD42013005953. Available at: http://www.crd.york.ac.uk/PROSPERO/display_record.asp?ID=CRD42013005953.

Objective: To determine if individualized education before Ramadan results in a safer fast for people with type 2 diabetes. Methods: Patients with type 2 diabetes who received care from participating clinics in Egypt, Iran, Jordan and Saudi Arabia and intended to fast during Ramadan 2014 were prospectively studied. Twelve clinics participated. Individualized education addressed meal planning, physical activity, blood glucose monitoring and acute metabolic complications and when deemed necessary, provided an individualized diabetes treatment plan. Results: 774 people met study criteria, 515 received individualized education and 259 received usual care. Those who received individualized education were more likely to modify their diabetes treatment plan during Ramadan (97% vs 88%, p<0.0001), to perform self-monitoring of blood glucose at least twice daily during Ramadan (70% vs 51%, p<0.0001), and to have improved knowledge about hypoglycemic signs and symptoms (p=0.0007). Those who received individualized education also reduced their body mass index (−1.1±2.4 kg/m² vs −0.2±1.7 kg/m², p<0.0001) and glycated haemoglobin (−0.7±1.1% vs −0.1±1.3%, p<0.0001) during Ramadan compared those who received usual care. There were more mild (77% vs 67%, p=0.0031) and moderate (38% vs 19%, p<0.0001) hypoglycemic events reported by participants who received individualized education than those who received usual care, but fewer reported severe hypoglycemic events during Ramadan (23% vs 34%, p=0.0017). Conclusions: This individualized education and diabetes treatment program helped patients with type 2 diabetes lose weight, improve glycemic control and achieve a safer fast during Ramadan.

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 ( PRR ^Adi/Y ) with almost no detectable white adipose tissues. As a consequence, the livers of PRR ^Adi/Y mice were enlarged and demonstrated a marked accumulation of lipids. Adipocyte-specific deficiency of PRR increased systolic blood pressure and the concentration of soluble PRR 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-fat– and low-fat–fed PRR ^Adi/Y mice had elevated insulin levels. Interestingly, adipocyte-PRR deficiency improved glucose tolerance in high-fat–fed PRR ^Adi/Y mice. In response to feeding either low-fat or high-fat diets, systolic blood pressure was greater in PRR ^Adi/Y mice than in control mice. High-fat feeding elevated soluble PRR concentration in control and PRR ^Adi/Y mice. In vitro knockdown of PRR by siRNA significantly decreased mRNA abundance of PPARγ (peroxisome proliferator-activated receptor gamma), 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 systolic blood pressure regulation.

Adipose tissue macrophages have been proposed as a link between obesity and insulin resistance. However, the mechanisms underlying these processes are not completely defined. Calpains are calcium-dependent neutral cysteine proteases that modulate cellular function and have been implicated in various inflammatory diseases. To define whether activated calpains influence diet-induced obesity and adipose tissue macrophage accumulation, mice that were either wild type (WT) or overexpressing calpastatin (CAST Tg), the endogenous inhibitor of calpains were fed with high (60% kcal) fat diet for 16 weeks. CAST overexpression did not influence high fat diet-induced body weight and fat mass gain throughout the study. Calpain inhibition showed a transient improvement in glucose tolerance at 5 weeks of HFD whereas it lost this effect on glucose and insulin tolerance at 16 weeks HFD in obese mice. However, CAST overexpression significantly reduced adipocyte apoptosis, adipose tissue collagen and macrophage accumulation as detected by TUNEL, Picro Sirius and F4/80 immunostaining, respectively. CAST overexpression significantly attenuated obesity-induced inflammatory responses in adipose tissue. Furthermore, calpain inhibition suppressed macrophage migration to adipose tissue in vitro. The present study demonstrates a pivotal role for calpains in mediating HFD-induced adipose tissue remodeling by influencing multiple functions including apoptosis, fibrosis and inflammation.