Sugar Consumption Is Negatively Associated with Semen Quality.

Recently, in parallel to decrease in semen quality, the consumption of sugar has risen sharply. This provided the rationale to study the association between whole dietary sugar consumption and semen quality. Our aim was to investigate the association between sugar consumption and semen quality. The final cross-sectional study population (n = 280 of initial n = 593, after applying inclusion and exclusion criteria) attending routine semen analysis at sperm bank laboratory was subject to semen quality analysis according to WHO criteria (volume, sperm concentration, total sperm count, percentage total motility, and percentage normal morphology) and filled food frequency questionnaire (FFQ) and lifestyle questionnaire. Associations between consumed sugars and semen quality were analyzed using multivariate regression adjusted to relevant cofounders for 2 food components containing sugar including soft drinks (SoftD) and total added sugar to food products (SugProd). We found negative association between higher consumption of dietary sugar in all 2 dietary sub-categories and sperm concentration. Significant sperm concentration decrements of 18% and 23% were associated with SoftD median consumption of 0.2 drinks/day (IQR; 0.1-0.5 drinks/day). Significant sperm concentration decrements of 15% and 17% were associated with median SugProd consumption of 25 teaspoons of added sugar/day (IQR; 19-31 teaspoons of added sugar/day). In conclusion, our study findings demonstrate that sugar consumption is negatively associated with sperm concentration.

Dietary patterns are positively associated with semen quality.

OBJECTIVE: To study association of semen quality with a priori whole dietary pattern indexes, which reflect real-world dietary practices and the numerous combinations by which foods are consumed: Healthy Eating Index (HEI), Dietary Approaches to Stop Hypertension (DASH), alternate Mediterranean Diet score (aMED), and Alternative Healthy Eating Index (AHEI). DESIGN: A cross-sectional single-center study. SETTING: Hospital fertility center and university. PATIENT(S): A total of 280 men attending fertility center from 2012 to 2015. INTERVENTION(S): Food frequency questionnaire (FFQ) and semen and sperm analysis. MAIN OUTCOME MEASURE(S): Food consumption with the use of FFQ and HEI, AHEI, aMED, DASH nutritional individual scoring indexes. Semen parameters, including semen volume, sperm concentration, motility, total count, and morphology. RESULT(S): Comparing the highest and lowest quartiles of the nutritional indexes, men in the highest quartiles of HEI, AHEI, aMed, and DASH indexes had significantly higher adjusted means of sperm concentration (by 10%, 45%, and 24% for HEI, AHEI, and DASH, respectively), normal sperm morphology (by 21% and 8% for AHEI and DASH, respectively), total sperm count (by 29% for AHEI), and sperm motility (by 6% and 11% for aMed and HEI, respectively). CONCLUSION(S): Adherence to any of the four dietary indexes is associated with better overall sperm quality, with AHEI best associated. Following our novel findings, we recommend using AHEI as a clinical and practical tool for public whole nutritional recommendation for semen quality.

Neurospora crassa protein arginine methyl transferases are involved in growth and development and interact with the NDR kinase COT1.

The protein arginine methyltransferaseas (PRMTs) family is conserved from yeast to human, and regulates stability, localization and activity of proteins. We have characterized deletion strains corresponding to genes encoding for PRMT1/3/5 (designated amt-1, amt-3 and skb-1, respectively) in Neurospora crassa. Deletion of PRMT-encoding genes conferred altered Arg-methylated protein profiles, as determined immunologically. Δamt-1 exhibited reduced hyphal elongation rates (70% of wild type) and increased susceptibility to the ergosterol biosynthesis inhibitor voriconazole. In ▵amt-3, distances between branches were significantly longer than the wild type, suggesting this gene is required for proper regulation of hyphal branching. Deletion of skb-1 resulted in hyper conidiation (2-fold of the wild type) and increased tolerance to the chitin synthase inhibitor polyoxin D. Inactivation of two Type I PRMTs (amt-1 and amt-3) conferred changes in both asymmetric as well as symmetric protein methylation profiles, suggesting either common substrates and/or cross-regulation of different PRMTs. The PRMTs in N. crassa apparently share cellular pathways which were previously reported to be regulated by the NDR (Nuclear DBF2-related) kinase COT1. Using co-immunprecipitation experiments (with MYC-tagged proteins), we have shown that SKB1 and COT1 physically interacted and the abundance of the 75 kDa MYC::COT1 isoform was increased in a Δskb-1 background. On the basis of immunological detection, we propose the possible involvement of PRMTs in Arg-methylation of COT1.

From fat cell biology to public health preventive strategies - pinpointing the critical period for obesity prevention.

The prevalence of childhood and adolescence obesity is increasing to alarming proportions worldwide and poses a major public health problem by significantly elevating the risks of chronic diseases. There is strong evidence that childhood overweight and obesity are risk factors for severe obesity over the whole life course. In fact, longitudinal studies have found that most overweight/obese children would become overweight and obese adults. There is a lack of coupling in the scientific literature between adipose tissue development and biology to obesity prevention and treatment strategies. This is of utmost importance, especially regarding childhood and adolescence, as the major scientific paradigm in studies of adiposity is that the major number of adipocytes is set for life at this early age. This review discusses the current adipose cell biology paradigms to pinpoint the critical factors and periods in childhood overweight and obesity and, consecutively, to develop relevant prevention strategies.

Paraoxonase 1 interactions with HDL, antioxidants and macrophages regulate atherogenesis - a protective role for HDL phospholipids.

Macrophage cholesterol accumulation and foam cell formation is the hallmark of early atherogenesis. In addition to macrophages, at least three more major players regulate atherosclerosis development; paraoxonase 1 (PON1), antioxidants, and HDL. PON1 is an HDL-associated lactonase which posses antioxidant and anti-atherogenic properties. PON1 protects against macrophage-mediated LDL oxidation, and increases HDL binding to macrophages which, in turn, stimulates HDL's ability to promote cholesterol efflux. These two major anti-atherogenic properties of HDL (and of PON1) require, at least in part, macrophage binding sites for HDL-associated PON1. Indeed, PON1, as well as HDL-associated PON1, specifically binds to macrophages, leading to anti-atherogenic effects. Macrophage PON1 binding sites may thus be a target for future cardioprotection therapy. Studying the interactions among PON1, antioxidants, and macrophages can thus assist in achieving appropriate treatment and prevention of atherosclerosis.

Di-oleoyl phosphatidylcholine (PC-18:1) stimulates paraoxonase 1 (PON1) enzymatic and biological activities: in vitro and in vivo studies.

OBJECTIVE: Paraoxonase 1 (PON1) is a high-density lipoprotein (HDL)-associated enzyme which possess anti-atherogenic properties. Our aim was to analyze the effect of HDL phospholipids on HDL-associated paraoxonase (PON1) catalytic and biological activities. METHODS AND RESULTS: In HDL isolated from di-oleoyl-phosphatidylcholine (PC-18:1)-enriched serum, HDL-PC-18:1 levels, as well as PON1 lactonase, arylesterase and paraoxonase activities were increased by 23%, 35%, 47% and 63%, respectively, as compared to control HDL (p<0.01). Furthermore, PON1 contribution to HDL-mediated cholesterol efflux from J774A.1 macrophages was higher in PC-18:1-enriched HDL in comparison to control HDL. In vivo olive oil consumption by Balb C mice increased HDL phospholipids/protein (30%), and HDL-PON1 arylesterase (150%) and lactonase (94%) activities (p<0.01). Furthermore, in the olive oil-treated mice PON1 contribution to HDL-mediated macrophage cholesterol efflux was higher by 100%, in comparison to placebo mouse HDL (p<0.01). Similarly, olive oil consumption by healthy subjects increased HDL-PC-18:1 levels, HDL-PON1 arylesterase (88%), lactonase (52%), paraoxonase (140%) activities and PON1 stimulatory effect on HDL-mediated cholesterol efflux (53%) as compared to HDL before treatment (p<0.01). PC-18:1 stimulatory effect on recombinant PON1 mutant (lacks 20 amino acids at the N-terminal region) paraoxonase and lactonase activities was lower by 56% and 57%, respectively, in comparison to its effect on wild type PON1 (p<0.01). CONCLUSION: Intervention to increase PON1 activities by HDL enrichment with PC-18:1 could be proven as a beneficial anti-atherogenic therapy.

Macrophage paraoxonase 1 (PON1) binding sites.

Paraoxonase 1 (PON1), an HDL-associated esterase, is known to possess anti-oxidant and anti-atherogenic properties. PON1 was shown to protect macrophages from oxidative stress, to inhibit macrophage cholesterol biosynthesis, and to stimulate HDL-mediated cholesterol efflux from the cells. The aim of the present study was to characterize macrophage PON1 binding sites which could be responsible for the above anti-atherogenic activities. Incubation of FITC-labeled recombinant PON1 with J774 A.1 macrophage-like cell line at 37 degrees C, resulted in cellular binding and internalization of PON1, leading to PON1 localization in the cell's cytoplasm compartment. In order to determine whether PON1 uptake is mediated via a specific binding to the macrophage, FITC-labeled recombinant PON1 was incubated with macrophages at 4 degrees C, followed by cell membranes separation. Macrophage membrane fluorescence was shown to be directly and dose-dependently related to the labeled PON1 concentration. Furthermore, binding assays performed at 4 and at 37 degrees C, using labeled and non-labeled recombinant PON1 (for competitive inhibition), demonstrated a dose-dependent significant 30% decrement in labeled PON1 binding to the macrophages, by the non-labeled PON1. Similarly, binding assays, using labeled PON1 and non-labeled HDL (the natural carrier of PON1 in the circulation) indicated that HDL decreased the binding of labeled PON1 to macrophages by 25%. Unlike HDL, LDL had no effect on labeled PON1 binding to macrophages. Finally, HDL were pre incubated without or with PON1 or apolipoprotein AI (apoAI) antibodies, in order to block PON1 or apoAI ability to bind to the cells. HDL incubation with antibody to PON1 or to apoAI significantly decreased HDL ability to inhibit macrophages-mediated LDL oxidation (by 32% or by 25%, respectively). A similar trend was also observed for HDL-mediated cholesterol efflux from macrophages, with an inhibitory effect of 35% or 19%, respectively. These results suggest that blocking HDL binding to macrophages through its apo A-I, and more so, via its PON1, results in the attenuation of HDL-PON1 biological activities. In conclusion, PON1 specifically binds to macrophage binding sites, leading to anti-atherogenic effects. Macrophage PON1 binding sites may thus be a target for future cardio protection therapy.