Obesity is an energy balance disorder associated with dyslipidemia, insulin resistance and diabetes type 2, also summarized with the term metabolic syndrome or syndrome X. Increasing evidence points to “adipocyte dysfunction”, rather than fat mass accretion per se, as the key pathophysiological factor for metabolic complications in obesity. The dysfunctional fat tissue in obesity characterizes a failure to safely store metabolic substrates into existing hypertrophied adipocytes and/or into new preadipocytes recruited for differentiation. In this review we briefly summarize the potential of redox imbalance in fat tissue as an instigator of adipocyte dysfunction in obesity. We reveal the challenge of the adipose redox changes, insights in the regulation of healthy expansion of adipose tissue and its reduction, leading to glucose and lipids overflow.

These data suggest that nitric oxide (NO) produced by iNOS could also contribute to overall NO-associated regulation of thermogenesis in IBAT. Namely, that iNOS, i.e. NO, in correlation with enhanced thermogenesis, additionally induced IBAT hyperplasia and UCP1 level compared to that induced by low temperature. Cooperative action of decreased apoptosis accompanied by increased tissue hyperplasia and UCP1 level, observed in IBAT of cold-acclimated rats, would be a way of meeting the metabolic requirements for increased thermogenesis.

Infertility is a global problem that is on the rise, especially during the last decade. Currently, infertility affects approximately 10-15% of the population worldwide. The frequency and origin of different forms of infertility varies. It has been shown that reactive oxygen and nitrogen species (ROS and RNS) are involved in the aetiology of infertility, especially male infertility. Various strategies have been designed to remove or decrease the production of ROS and RNS in spermatozoa, in particular during in vitro fertilization. However, in recent years it has been shown that spermatozoa naturally produce a variety of ROS/RNS, including superoxide anion radical (O2 ·− ), hydrogen peroxide and NO. These reactive species, in particular NO, are essential in regulating sperm capacitation and the acrosome reaction, two processes that need to be acquired by sperm in order to achieve fertilization potential. In addition, it has recently been shown that mitochondrial function is positively correlated with human sperm fertilization potential and quality and that NO and NO precursors increase sperm motility by increasing energy production in mitochondria. We will review the new link between sperm NO-driven redox regulation and infertility herein. A special emphasis will be placed on the potential implementation of new redox-active substances that modulate the content of NO in spermatozoa to increase fertility and promote conception. LINKED ARTICLESThis article is part of a themed section on Pharmacology of the Gasotransmitters. To view the other articles in this section visit http://dx.doi.org/10. 1111/bph.2015.172.issue-6 Abbreviations AR, acrosome reaction; EDRF, endothelial-derived relaxing factor; eNOS, endothelial NOS; ETC, electron transport chain; iNOS, inducible NOS; IVF, in vitro fertilization; L-NAME, N G -nitro-L-arginine methyl ester; MMP, mitochondrial membrane potential; mtNOS, mitochondrial NOS; NG, nitroglycerine; nNOS, neuronal NOS; O2 ·− , superoxide anion radical; RNS, reactive nitrogen species; ROS, reactive oxygen species; sGC, soluble GC; SNP, sodium nitroprusside; SOD, superoxide dismutase; ZP, zona pellucida IntroductionInfertility is one of the most serious medical problems worldwide. The prevalence of infertility is on the rise, especially during the last decade. Globally, one of six to seven couples worldwide currently has some difficulty with conception (Sharma et al., 2013). Infertility is usually defined as the inability to conceive after 1 year of regular unprotected intercourse, but in couples in which the female partner is >35 years of age, infertility is diagnosed after an inability to conceive for 6 months (Cooper et al., 2010). Although the frequency and origin of infertility varies, it has been established that nearly 40% of the issues involved with infertility are attributable to a male factor, another 40% due to a female factor, and 20% result from combined male and female factors (Sharlip et al., 2002). Over the past decade, significant advances have occurred in the diagnosis an...

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In an attempt to elucidate molecular mechanisms and factors involved in β cell regeneration, we evaluated a possible role of the L-arginine-nitric oxide (NO)-producing pathway in alloxan-induced diabetes mellitus. Diabetes was induced in male Mill Hill rats with a single alloxan dose (120 mg kg −1 ). Both non-diabetic and diabetic groups were additionally separated into three subgroups: (i) receiving L-arginine · HCl (2.25%), (ii) receiving L-NAME · HCl (0.01%) for 12 days as drinking liquids, and (iii) control. Treatment of diabetic animals started after diabetes induction (glucose level ≥ 12 mmol l −1 ). We found that disturbed glucose homeostasis, i.e. blood insulin and glucose levels in diabetic rats was restored after L-arginine treatment. Immunohistochemical findings revealed that L-arginine had a favourable effect on β cell neogenesis, i.e. it increased the area of insulin-immunopositive cells. Moreover, confocal microscopy showed colocalization of insulin and pancreas duodenum homeobox-1 (PDX-1) in both endocrine and exocrine pancreas. This increase in insulin-expressing cells was accompanied by increased cell proliferation (observed by proliferating cell nuclear antigen-PCNA immunopositivity) which occurred in a regulated manner since it was associated with increased apoptosis (detected by the TUNEL method). Furthermore, L-arginine enhanced both nuclear factor-kB (NF-kB) and neuronal nitric oxide synthase (nNOS) immunopositivities. The effect of L-arginine on antioxidative defence was observed especially in restoring to control level the diabetes-induced increase in glutathione peroxidase activity. In contrast to L-arginine, diabetic pancreas was not affected by L-NAME supplementation. In conclusion, the results suggest beneficial L-arginine effects on alloxan-induced diabetes resulting from the stimulation of β cell neogenesis, including complex mechanisms of transcriptional and redox regulation.