The effects of sustained pectin ingestion on gastric emptying, glucose tolerance, and hormone responses were studied in 12 stable, non-insulin-dependent (type 2) diabetic patients. Patients were placed on a 2400 kcal, low-fiber (3 g) diet for 2 wk, followed by 4 wk of an isocaloric diet supplemented with 20 g apple pectin/d. Gastric-emptying half-time, plasma glucose, glucagon, and human pancreatic polypeptide levels were determined. Gastric-emptying half-time was prolonged 43% (p less than 0.025) by pectin supplementation and returned to normal 3 d after its discontinuation. Fiber supplementation decreased the incremental area under the glucose tolerance curve from 34.8 +/- 3.0 to 27.9 +/- 3.2 mmol/L (p less than 0.01) but did not affect hormonal responses to a meal. Sustained pectin ingestion slowed the gastric-emptying rate and improved glucose tolerance; however, a direct relationship could not be demonstrated between changes in gastric emptying and changes in the incremental area under the glucose curve (r = 0.22).
A new nonsteroidal, antiinflammatory drug, carprofen, was compared with indomethacin as to their effects on mucosal injury and prostanoid biosynthesis. A prospective, double-blind endoscopy study was performed in 40 healthy adults. After baseline normal endoscopy, 20 subjects were randomly assigned to either indomethacin (25 mg four times daily) or carprofen (150 mg twice daily) for eight days and re-endoscoped. Urinary and gastric mucosal prostaglandin generation, respectively, of PGE2 and PGF2 alpha, and PGE and 6-keto-PGF1 alpha was determined. Minor subjective symptoms occurred in six of 20 indomethacin (including four of eight with gastrointestinal injury) and in three of 20 carprofen subjects. Indomethacin and carprofen reduced gastric and urinary prostaglandin synthesis to a similar degree. Gastrointestinal injury was present in eight of 20 indomethacin and in none of 20 carprofen subjects. This study fails to establish a relationship between duodenal mucosal lesions and gastric prostanoid generation and confirms the lack of correlation between indomethacin-induced duodenal injury and subjective symptomatology. Carprofen appears to produce less objective damage in the upper gastrointestinal tract than indomethacin at comparable clinical doses.
The role of calcium in gastric acid secretion is still uncertain. The effect of verapamil on basal and pentagastrin-stimulated gastric acid secretion was evaluated in eight normal men. Submaximal pentagastrin tests (2 micrograms/kg/hr) were performed after pretreatment with intravenous verapamil at a concentration of 0.1 mg/kg and followed 1 hr later with a second bolus injection of 0.15 mg/kg. On a separate day, subjects received a placebo injection of saline solution at the same designated times as the verapamil. Verapamil did not alter basal or stimulated gastric acid secretion. All subjects showed ECG evidence of significant calcium-channel blocking (i.e., prolongation of PR interval). Data indicate that therapeutic doses of a calcium slow-channel antagonist do not alter gastric acid secretion in normal subjects. Results support the concept that in vivo, secretory function of the human parietal cell is not affected by alteration in cellular calcium flux.
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