-This study examined gastrointestinal hormone and peptide responses when glucose was ingested after prolonged exercise. Six endurance-trained male athletes ran on a treadmill for 2 h at 60% V O2 max. Immediately after the run, the athletes consumed 75 g of glucose in 250 ml of water (ExGLU) or flavored water as a placebo control (ExPL). On a separate visit, the athletes rested for 2 h and then consumed glucose (Con-GLU). During the first 60 min of recovery from exercise alone (ExPL), plasma vasoactive intestinal peptide (VIP), gastrin, and glucagon-like peptide-1 (GLP-1) all increased significantly, whereas glucose, insulin, and gastric inhibitory polypeptide (GIP) were unchanged from the immediate postexercise value. When glucose was ingested after exercise (ExGLU), glucose, insulin, VIP, gastrin, GLP-1, and GIP were all increased (P Ͻ 0.01). However, when glucose was ingested after resting for 2 h (ConGLU), VIP levels were unaffected, although glucose, insulin, gastrin, GLP-1, and GIP levels increased (P Ͻ 0.05). The plasma glucose response was greater (P Ͻ 0.03) and the plasma insulin response lower (P Ͻ 0.004) during ExGLU compared with ConGLU. There was a significantly higher (P Ͻ 0.01) VIP response during the initial period of recovery in ExGLU than there was with both ExPL and ConGLU. Plasma VIP showed a modest negative correlation with circulating glucose (r ϭ Ϫ0.35, P Ͻ 0.03) and insulin (r ϭ Ϫ0.37, P Ͻ 0.03) during the ExGLU recovery period. In summary, when glucose is ingested after prolonged exercise, there is mild insulin resistance and a corresponding rapid transitory increase in plasma VIP. These data suggest that VIP may play an important glucoregulatory role when glucose is ingested during the immediate postexercise recovery period. insulin resistance; gut peptides; exercise performance; carbohydrate THE IMMEDIATE POSTEXERCISE PERIOD appears to be associated with mild reversible insulin resistance, which is characterized by an attenuated insulin response and an increased glucose response to oral glucose (10,21,25,27,33,37,39,43). The physiological basis for the increased glucose response has been shown to be partly a function of greater release of glucose from the splanchnic tissues (20,30,39). Gut peptides and hormones of the enteroinsular axis may also play an important functional role in fuel homeostasis and contribute to maintaining a balance between energy utilization and mobilization. The metabolic role of peptides from the enteroinsular axis, including vasoactive intestinal peptide (VIP), gastric inhibitory polypeptide (GIP; also called glucose-dependent insulinotropic polypeptide), and glucagon-like peptide-1 (GLP-1), are known. However, the response of these peptides during recovery from exercise and the role they may play after glucose ingestion in the immediate postexercise period is less clear.VIP is secreted by the central (CNS) and peripheral (including enteric) nervous systems in response to duodenal acidification, gastric distention, and meal consumption (6, 40). Its actions incl...

Helicobacter pylon infection increases the serum concentration of gastrin, and this may be one of the mechanisms by which it predisposes to duodenal ulceration. Different forms of circulating gastrin were studied both basally and postprandially in 13 duodenal ulcer patients before and one month after eradication of H pylon. Three antisera that are specific for particular regions of the gastrin molecules were used. Gel chromatography indicated that >90% of the circulating gastrin consisted ofgastrin (G) 17 and G34 both before and after eradicating the infection. The basal median total immunoreactive gastrin concentration fell from 26 pmol/l (range 11-43) to 19 pmolIl (8-39) (p<0-05), entirely because of a fail in G17 from 6 pmol/l (<2.4-25) to <2-4 pmoil/ (<2.4-23) (p<0.001). The median (range) basal G34 values were similar before (15 pmol (2-36)) and after (10 pmol (2-30)) eradication. The median total immunoreactive gastrin concentration determined 20 minutes postprandially fell from 59 pmolll (38-114) to 33 pmol/ (19-88) (p<0 005), and again this was entirely the result of a fall in G17 from 43 pmol/l (9-95) to 17 pmolfl (<2-4-52) (p<0-001).The median postprandial G34 values were similar before (13 pmol/l, range 6-42) and after (15 pmolll, range 6-30) eradication. Eating stimulated a noticeable rise in G17 but little change in G34, both in the presence and absence of H pylori. The finding that H pylon infection selectively increases G17 explains why the infection causes mainly postprandial hypergastrinaemia. G17 is increased selectively because H pylon predominantly affects the antral mucosa which is the main source of G17 whereas G34 is mainly duodenal in origin. This study also indicates that the increased concentration ofgastrin in Hpylon infection is the result of an increase in one of the main biologically active forms of the hormone. (Gut 1993; 34: 757-761)

This is the first reported study of GLP-2 in coeliac disease. After a GFD there is recovery of the intestine and a reduction in the GLP-2 trophic response. Our findings support the theory that GLP-2 may be part of the mucosal healing and maintenance mechanisms in coeliac disease.

To assess the effect of increasing age on circulating gastrin, we surveyed serum gastrin, Helicobactor pylori seroantibody status and gastric autoimmunity in 366 hospitalized patients aged 15-90 years. Data were subjected to multivariate analysis, using logarithmic transformation to normalize the distribution of gastrin concentrations (presented as geometric means and 95% CIs). The frequency of H. pylori-positive antibody status increased with age from 28% in the second decade to > 70% beyond the fourth decade. Fasting gastrin concentrations rose significantly from 44 ng/l (41-48) in the second decade to 95 ng/l (67-131) by the eighth decade (p = 0.001) in the total group. Twenty-seven patients (6.8% of the total) tested positive for gastric auto-antibodies: 2% of patients in the second decade, rising to 15.9% in the eighth decade. These patients formed a distinct group with respect to circulating gastrin concentrations. Excluding these 27, fasting gastrin concentrations still rose significantly, from 44 ng/l (41-48) in the second decade, to 67 ng/l (50-89) in the eighth decade (p = 0.003) in the remaining 341 patients. Fasting gastrin concentrations were significantly higher in patients who were H. pylori-seropositive (59 ng/l, 54-64 vs. sero-negative 41 ng/l, 37-46) (p = 0.002), and there was no increase in circulating gastrin concentrations with increasing age in either the H. pylori-positive or the H. pylori-negative group. The increase in circulating fasting gastrin observed with increasing age is due to an increased incidence of gastric antibodies associated with auto-immune atrophic gastritis, and an increased incidence of H. pylori infection.

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