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Background Recent data suggest a role for the intestinal microbiota in the pathogenesis of functional bowel disorders (FBD). Probiotic studies in FBD generated inconsistent results suggesting a strain and product specific effect. Aim To investigate the clinical efficacy of Lactobacillus acidophilus NCFM (L-NCFM) and Bifidobacterium lactis Bi-07 (B-LBi07) in non-constipation FBD. Methods A double-blind, placebo-control clinical trial of the probiotic bacteria L-NCFM and B-LBi07 bid (2×1011cfu/day) vs. placebo over 8-weeks. Primary endpoints: global relief of GI symptoms and satisfaction with treatment. Secondary endpoints: Change in symptoms severity, well being, and quality of life. Microbiology effect was assessed by qPCR on fecal samples. Results Sixty subjects (probiotic n=31; placebo n=29), 72% females, 84% whites, mean age 37 years. Abdominal bloating improved in the probiotics compared to the placebo group at 4 weeks (4.10 vs. 6.17, p=0.009; change in bloating severity p=0.02) and 8 weeks (4.26 vs. 5.84, p=0.06; change in bloating severity p<0.01). Analyses on the IBS subgroup (n=33) showed similar results. Conclusions L-NCFM and B-LBi07 BID improve symptoms of bloating in patients with FBD. This data supports the role of intestinal bacteria in the pathophysiology of FBD and the role for probiotic bacteria in the management of these disorders.

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In mammalian oocytes, the maintenance of meiotic prophase I arrest prior to the surge of LH that stimulates meiotic maturation depends on a high level of cAMP within the oocyte. In mouse and rat, the cAMP is generated in the oocyte, and this requires the activity of a constitutively active, Gs-linked receptor, GPR3 or GPR12, respectively. To examine if human oocyte meiotic arrest depends on a similar pathway, we used RT-PCR and Western blotting to look at whether human oocytes express the same components for maintaining arrest as rodent oocytes. RNA encoding GPR3, but not GPR12, was expressed. RNA encoding adenylate cyclase type 3, which is the major adenylate cyclase required for maintaining meiotic arrest in the mouse oocyte, was also expressed, as was Galphas protein. To determine if this pathway is functional in the human oocyte, we examined the effect of injecting a function-blocking antibody against Galphas on meiotic resumption. This antibody stimulated meiotic resumption of human oocytes that were maintained at the prophase I stage using a phosphodiesterase inhibitor. These results demonstrate that human oocytes maintain meiotic arrest prior to the LH surge using a signaling pathway similar to that of rodent oocytes.

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