Contrary to the conclusions of 3 recent systematic reviews, we found no evidence to support the use of antibiotic treatment for bacterial vaginosis or Trichomonas vaginalis in pregnancy to reduce the risk of preterm birth or its associated morbidities in low- or high-risk women.

The ileal proglucagon-derived peptides (PGDPs) play important roles in the regulation of gastric function and insulin secretion. We have previously demonstrated the existence of a proximal-distal enteroendocrine loop mediated by glucose-dependent insulinotropic peptide (GIP), through which intestinal PGDP secretion is stimulated after placement of nutrients in the duodenum. To study the possible involvement of neuropeptides in this loop, we infused gastrin-releasing peptide (GRP) into anesthetized rats at 47, 235, or 470 ng/h. GRP stimulated secretion of the intestinal PGDPs only at the highest dose, from 250 +/- 18 to 321 +/- 9 pg/ml (P < 0.05). Gastrin secretion was also increased by GRP infusion (from 20 +/- 7 to 75 +/- 19 pg/ml; P < 0.05); however, GIP release was not altered from basal levels. Placement of fat into the duodenum stimulated the secretion of both the intestinal PGDPs and GIP (to 618 +/- 221 and 417 +/- 154 pg/ml above basal, respectively; P < 0.05). However, infusion of the GRP antagonist, BW10 (3 ng/h), completely abrogated the PGDP response to duodenal fat (P < 0.05). In contrast, the GIP response was reduced by 56 +/- 15% (P < 0.05) with BW10 administration, but remained elevated compared to the basal level (P < 0.05). Removal of the entire intestine distal to the fat-infused duodenal segment prevented the rise in intestinal PGDPs, but not that of GIP, demonstrating the distal and proximal origins of these peptides, respectively. Thus, placement of fat into the duodenum stimulated the release of the PGDPs from the distal intestine through a GRP-dependent mechanism. Although GIP plays a role in regulating intestinal PGDP secretion in the rat, GRP appears to exert its effects independent of changes in GIP.

Of the two known forms of intestinal somatostatin, somatostatin-28 (S28) and S14, S28 predominates in the distal mucosa, whereas S14 is localized in the foregut. Although S14 release has been well studied, little is known about the factors regulating secretion of S28 from the intestine. Therefore, fetal rat intestinal cultures, which have been previously demonstrated to synthesize and secrete predominantly S28, were treated with potential nutrient, neuromodulator/ transmitter, and peptide secretagogues (n ϭ 4 -6/experiment). Oleic acid dose dependently stimulated the release of somatostatin-like immunoreactivity (SLI) to 272 Ϯ 81% of the control value at 1.5 ϫ 10 Ϫ4 M (P Ͻ 0.01). Gel permeation analysis (n ϭ 3) demonstrated that this increment was accounted for not only by an increase in the release of S28, but also by an increase in that of S14, such that the secretion of both peptides was increased in parallel. Of the neuromodulators tested, only the enteric peptide gastrin-releasing peptide stimulated intestinal SLI secretion, to 386 Ϯ 60% of the control value at 10 Ϫ6 M (P Ͻ 0.001); similar to oleic acid, the effects on S28 and S14 were equivalent. Galanin, vasoactive intestinal peptide, bethanechol, and epinephrine did not affect SLI release. The duodenal hormone secretin also stimulated SLI release to 310 Ϯ 78% of the control value at 10 Ϫ6 M (P Ͻ 0.001); however, secretin caused a preferential release of S14 over that of S28 (S14, 7.8 Ϯ 2.8-fold; S28, 1.5 Ϯ 0.1-fold). In contrast, gastrin, cholecystokinin, glucose-dependent insulinotropic peptide, neurotensin, peptide YY, epidermal growth factor, and transforming growth factor-␣ had no effect on intestinal SLI release. Thus, luminal nutrients and neuro/endocrine peptides exert differential effects on S28 release from the rat intestine compared with those on S14. These findings implicate S28 as a distinct regulatory peptide in the physiological setting. (Endocrinology 139: 148 -155, 1998) A LTHOUGH widely distributed in the brain, pancreas, and peripheral autonomic nervous system, the gastrointestinal tract provides the largest source of somatostatin in the periphery (1-3). Within the gastrointestinal tract, differential posttranslational processing of prosomatostatin generates two major biologically active peptides, somatostatin-14 (S14) and S28, the distribution of which forms a gradient along the aboral axis. In the mucosa of the stomach and duodenum, S14 is the major product of processing, whereas S28 predominates in the D cells of the distal jejunum and ileum (1-4). S14 is also distributed throughout the length of the small intestine within the myenteric plexi. Both peptides have potent inhibitory effects on digestive functions, including gastric and pancreatic exocrine secretion, neuro/endocrine peptide release, and intestinal growth (5). Of particular note are studies suggesting that S28, rather than S14, may be the physiological regulator of postprandial insulin secretion in humans (6, 7). Although regulation of S14 secretion from the st...

No abstract