Effect of bariatric surgery on in vitro fertilization in infertile men with obesity.

BACKGROUND: Obesity has previously been related to reduced female fertility, with prolonged waiting time to pregnancy among women with a body mass index (BMI) >35 kg/m2 but there are few studies investigating the relationship between high BMI, bariatric surgery, and male fertility. OBJECTIVES: The primary objective of this article was to investigate the effect of bariatric surgery on in vitro fertilization (IVF) outcomes in a cohort of men with morbid obesity who underwent sleeve gastrectomy (SG). SETTING: University hospital, bariatric surgery unit. METHODS: Pre- and postsurgery data on patient age, body mass index (BMI), and variables related to male fertility (semen volume, concentration, progressively motile sperm count, and sperm morphology) were collected; assisted reproductive technology outcomes before and after bariatric surgery were measured by the number of metaphase II oocytes; the number of top-quality oocytes and embryos; the number of fertilized oocytes; the number of transferred embryo; the implantation rate; the pregnancy rate; the live birth rate and the miscarriage rate. RESULTS: Thirty-five men with obesity and idiopathic infertility were included in this study. We found a significant increase, after bariatric surgery, in semen volume, total sperm concentration, progressively motile sperm count, and sperm morphology. Considering IVF outcomes, mean number of top-quality oocytes, mean number of fertilized oocytes, mean number of embryos obtained, and top-quality embryos were significantly increased after bariatric procedure. CONCLUSION: Bariatric surgery is confirmed to be safe and effective in increasing the outcomes of assisted reproductive technology treatment also in case of infertile men with obesity, both in terms of pregnancy and live birth rate.

Impaired Duodenal Palmitoylethanolamide Release Underlies Acid-Induced Mast Cell Activation in Functional Dyspepsia.

BACKGROUND & AIMS: Acid hypersensitivity is claimed to be a symptomatic trigger in functional dyspepsia (FD); however, the neuroimmune pathway(s) and the mediators involved in this process have not been investigated systematically. Palmitoylethanolamide (PEA) is an endogenous compound, able to modulate nociception and inflammation, but its role in FD has not been assessed. METHODS: Duodenal biopsy specimens from FD and control subjects, and peroxisome proliferator-activated receptor-α (PPARα) null mice were cultured at a pH of 3.0 and 7.4. Mast cell (MC) number, the release of their mediators, and the expression of transient receptor potential vanilloid receptor (TRPV)1 and TRPV4, were evaluated. All measurements also were performed in the presence of a selective blocker of neuronal action potential (tetradotoxin). FD and control biopsy specimens in acidified medium also were incubated in the presence of different PEA concentrations, alone or combined with a selective PPARα or PPAR-γ antagonist. RESULTS: An acid-induced increase in MC density and the release of their mediators were observed in both dyspeptic patients and controls; however, this response was amplified significantly in FD. This effect was mediated by submucosal nerve fibers and up-regulation of TRPV1 and TRPV4 receptors because pretreatment with tetradotoxin significantly reduced MC infiltration. The acid-induced endogenous release of PEA was impaired in FD and its exogenous administration counteracts MC activation and TRPV up-regulation. CONCLUSIONS: Duodenal acid exposure initiates a cascade of neuronal-mediated events culminating in MC activation and TRPV overexpression. These phenomena are consequences of an impaired release of endogenous PEA. PEA might be regarded as an attractive therapeutic strategy for the treatment of FD.