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Biomedical subjects

V L Go

Publications and source records attributed to V L Go.

At least 217 records · Page 12Linked to original sources
PubMed1980

Gastric, pancreatic, and biliary responses to meals in hyperthyroidism.

Upper gastrointestinal function in response to a mixed nutrient meal was evaluated in hyperthyroid patients, both before and after therapy, and in healthy controls. Gastric secretion, gastric emptying, and pancreatic secretion were all normal and normally integrated postprandially in the hyperthyroid patients. Bile acid output was reduced (P less than 0.05) in this group of patients relative to healthy controls. Duodenal bile acid concentrations, however, were above the critical micellar concentration in most of the hyperthyroid patients, and the bile acid output and concentration remained unchanged in all patients three months after treatment. After radioactive iodine therapy, when gastrointestinal symptoms were returning toward normal, a small but statistically significant increase in gastric secretion was observed. However, gastric emptying and pancreatic secretion, like biliary secretion, remained unchanged. Abnormalities responsible for the diarrhoea and steatorrhoea in hyperthyroidism appear to reside primarily distal to the duodenum. However, reduced bile acid output may be a contributory factor in some patients.

Adult↗
PubMed1980

Interaction of fat-stimulated gastric inhibitory polypeptide on pancreatic alpha and beta cell function.

Gastric inhibitory polypeptide (GIP) is considered to be the principal mediator of the enteroinsular axis. A glucose-insulin clamp technique was used to study the effects of differing blood glucose levels on the insulinotropic and glucagonotropic actions of fat-stimulated GIP in seven healthy subjects, as well as the effect of physiologic hyperinsulinemia on GIP secretion. Blood glucose levels were clamped for 4 h at 43+/-2 mg/dl (hypoglycemic clamp), 88+/-1 mg/dl (euglycemic clamp), and 141+/-2 mg/dl (hyperglycemic clamp) in the presence of a constant insulin infusion (100 m U/kg per h). Under hypoglycemic clamp conditions there was no increase in C-peptide nor glucagon after Lipomul ingestion, despite an increase of GIP of 51.7+/-8.7 ng/ml per 120 min. Under euglycemic clamp conditions, small and inconsistent increases in C-peptide and glucagon were observed after fat ingestion and a concomitant increase of GIP of 35.2+/-9.4 ng/ml per 120 min. Under hyperglycemic clamp conditions after fat ingestion and a GIP increase of 24.0+/-5.7 ng/ml per 120 min, C-peptide increased from 6.4+/-5 ng/ml to 11.0+/-1.1 ng/ml (P < 0.01) but glucagon did not change. These findings confirm that in healthy man GIP exerts its insulinotropic properties only under hyperglycemic conditions and indicate that GIP is not glucagonotropic. Under euglycemic clamp conditions (plasma glucose, 89+/-1 mg/dl) and physiologic hyperinsulinemia (serum immunoreactive insulin, 137+/-3 muU/ml) GIP responses to fat ingestion (39.7+/-9.8 ng/ml per 120 min) were not different from the GIP responses to fat ingestion in the absence of hyperinsulinemia (39.7+/-11.1 ng/ml per 120 min). Therefore, insulin under normoglycemic conditions does not exert an inhibitory effect on fat-stimulated GIP secretion. The higher GIP response to oral fat in the hypoglycemic clamp, and the lower GIP response in the hyperglycemic clamp compared to the response in the euglycemic clamp suggests an effect of glycemia itself on GIP secretion in the presence of hyperinsulinemia.

Adult↗
PubMed1980

Interrelationships among insulin, glucagon, and gastric inhibitory polypeptide in insulinoma.

The interrelationships of serum insulin, glucagon, and gastric inhibitory polypeptide were examined in 13 patients with insulinoma during fed and fasted states. Compared with normal subjects, patients with insulinoma had significantly lower glucose and higher insulin levels during both the fed and the fasted states. Although glucagon concentration was higher at the completion of the fast in patients with insulinoma compared with normals, no significant differences were apparent during the fed state. No difference was noted in gastric inhibitory polypeptide either during the fed state or at the termination of the fast. Under the conditions of the study, no direct suppressive effect of insulin on glucagon or gastric inhibitory polypeptide secretion was apparent. In addition, as opposed to that in normals, the insulinotropic effect of glucagon did not appear to be blunted by hypoglycemia in most of the patients. After glucagon injection, all symptomatically hypoglycemic patients experienced an amelioration of symptoms and restoration of the plasma glucose into the normal range.

Adenoma, Islet Cell↗
PubMed1980

Gastric motor abnormalities in diabetic and postvagotomy gastroparesis: effect of metoclopramide and bethanechol.

Gastroparesis is a relatively uncommon but clinically troublesome disorder that develops in some patients with diabetes mellitus or after gastric operations. Its pathogenesis remains obscure. We used a manometric technique to record pressure changes in fasting patients in the gastric fundus, distal stomach, and adjacent small bowel of patients with severe gastroparesis, asymptomatic diabetic patients, asymptomatic postsurgical patients, and healthy controls. Patients with gastroparesis had normal interdigestive motor cycles (phase III) in the intestine but not in the stomach. Sporadic motor activity in the stomach (phase II) also was markedly reduced. Metoclopramide and bethanecol significantly increased gastric motor activity in these patients, often triggering an intense burst of motor activity in the stomach, similar to phase III. These observations suggest that gastroparesis is a potentially reversible disorder and should encourage further attmpts for pharmacologic control of the syndrome.

Adult↗
PubMed1980

In the absence of nutrients, pancreatic-biliary secretions in the jejunum do not exert feedback control of human pancreatic or gastric function.

Feedback inhibition of basal pancreatic enzyme secretion by luminal pancreatic enzymes appears to be an important regulator of pancreatic secretion in some laboratory animals. To determine whether pancreatic enzymes in the jejunum influence pancreatic or gastric functions in healthy man, we intubated six subjects with a gastric sump tube and a four-lumen duodenal tube which provided (1) a duodenal perfusion site, (2) a duodenal aspiration site, (3) an inflatable balloon immediately distal to the aspiration site, and (4) a jejunal perfusion site immediately beyond the balloon. In this way, the gastroduodenal segment could be functionally separated from the remainder of the intestine. The jejunum was exposed to normal saline, active pancreatic-biliary secretions, or pancreatic-biliary secretions in which the enzymes had been inactivated by heat. Ten minutes after initiation of each jejunal perfusion, normal saline was instilled into the stomach. No differences in trypsin secretion, gastric acid secretion, or gastric emptying occurred with the different jejunal perfusates. We therefore conclude that normal man, in the absence of intraluminal nutrients, does not exhibit a jejunal pancreatic enzyme-dependent feedback control mechanism for pancreatic enzyme or gastric secretion. However, our study does not exclude the possibility of a duodenal feedback regulatory mechanism.

Adult↗
PubMed1980

Can endogenous gastrin inhibit canine interdigestive gastric motility?

Our aim was to determine whether endogenously released gastrin inhibits cyclic interdigestive motility in the proximal stomach. In 4 dogs with chronic duodenal electrodes and isolated innervated antral pouches, we constructed proximal gastric pouches, the external neural connections of which were completely severed by autotransplanting the pouches to the left pelvis. After recovery, the antral pouch was irrigated with 0.2% acetylcholine for 3.7 hr at 90 ml/hr, while intraluminal pressure was monitored in the proximal gastric pouch and myoelectric activity was recorded from the duodenum. Blood was collected concurrently for radioimmunoassay of gastrin. The antral irrigations increased serum gastrin from a mean +/- SEM of 85 +/- 14 pg/ml before irrigation to a mean +/- SEM of 350 +/- 54 pg/ml after 30 min of irrigation (P less than 0.001), and the increased levels continued throughout the remaining 3.2 hr of irrigation. The irrigations also suppressed the cycles of interdigestive motor activity in the proximal gastric pouch and the cycles of interdigestive myoelectric activity in the duodenum. The cycles had a mean duration +/- SEM of 105 +/- 5 min before irrigation in both the proximal gastric pouch and duodenum, but were abolished in every test during irrigation. Irrigation inhibited the cycles even when cimetidine was given intravenously at 200 mg/hr to block gastrin-stimulated secretion of HCl, duodenal acidification, and subsequent release of duodenal hormones. However, cimetidine alone had no effect on the interdigestive cycles. We concluded that antral irrigation with acetylcholine inhibited interdigestive cyclic motility in the proximal stomach via a hormonal mechanism and that gastrin was likely the hormone involved.

Acetylcholine↗
PubMed1980

Comparison of the effects of cholecystokinin and cholecystokinin octapeptide on pancreatic secretion, gallbladder contraction, and plasma pancreatic polypeptide in man.

To assess the possible clinical utility of the C-terminal CCK-OP as a stimulus to exocrine and endocrine pancreatic secretin and gallbladder contraction in man, we administered increasing doses of CCK (0.066, 0.125, 0.25, and 0.5 CHR U/kg/hr) and CCK-OP (20, 40, 80, and 160 ng/kg/hr) in random order by constant intravenous infusion to six healthy volunteers. Standard intestinal perfusion methods were used, and duodenal outputs of lipase, trypsin, bicarbonate, and total bile acids and plasma levels of HPP were measured. CCK-OP, in a dose of 40 ng/kg/hr given simultaneously with intravenously administered secretin, produced maximal pancreatic enzyme secretion and gallbladder contraction, comparable to that induced by CCK. CCK-OP plus secretin produced only small increases in plasma HPP levels, whereas values after all doses of CCK were significantly higher (p < 0.05) and were similar to values caused by a meal. We concluded that the combination of intravenous CCK-OP (40 ng/kg/hr) plus secretin (0.25 U/kg/hr) should be an accurate and relatively inexpensive test of exocrine pancreatic function and gallbladder contraction in man. Further, an undefined component of 20% CCK is a potent stimulus for HPP release.

Adult↗
PubMed1980

Reflux of duodenal contents into the pancreatic duct of dogs.

Previously we demonstrated that postprandial duodenal pressure transiently exceeds pancreatic duct pressure in the dog. To determine whether this presure gradient causes reflux from the duodenum into the pancreatic duct, we provided each of five dogs with a permanent pancreatodochal catheter and three indwelling duodenal cutaneous catheters. 14C-PEG was infused through the proximal duodenal catheter; intraluminal pressures were monitored through the middle catheter at the level of the pancreatic duct orifice; and 15 cm abroad, duodenal contents were recovered from the third catheter. Fifteen-minute pooled samples were collected 1 hr preprandially and 2 hr postprandially from the pancreatic duct and duodenum and were analyzed for volume, lipase activity, and marker concentration. Reflux of duodenal contents occurred only in 10.8% of fasting periods but was observed in 38% of postprandial periods (p < 0.05). The total volume of duodenal content refluxed per 15 min approximated 0.1 ml and represented between 0.5% and 1% of total pancreatic volume flow and between 0.05% and 0.07% of total duodenal volume flow. Thus we have provided evidence that small amounts of duodenal contents may reflux into the pancreatic duct of dogs in our experimental model. This finding may be relevant to the pathogenesis of pancreatitis and pancreatic cancer.

Animals↗
PubMed1980

Enterohepatic physiology of 1,25-dihydroxyvitamin D3 metabolites in normal man.

Within 6 hr of the intravenous administration of radiolabeled 1,25(OH)2D3 to five normal vitamin D-replete human subjects, 15.6% of the injected dose appeared in bile as polar metabolites of 1,25(OH)2D3. Of the injected dose, 27% and 7.5% appeared in the feces and urine, respectively, at 24 hr. In another two subjects, biliary radioactivity was sampled at two jejunal sites separated by a distance of 40 cm; a 24.8% decrease in radioactivity over this segment of bowel was noted. These data demonstrate that products of 1,25(OH)2D3 are excreted in normal human bile. Furthermore, these products are reabsorbed as such or as free 1,25(OH)2D3 in the intestine and re-excreted as polar products in bile. Our data suggest that there is an enterohepatic circulation of the products of 1,25(OH)2D3 in normal man.

Adult↗
PubMed1979

Different gastric, pancreatic, and biliary responses to solid-liquid or homogenized meals.

We have compared responses to an ordinary solid-liquid (S) meal and to a homogenized (H) meal of identical composition (sirloin steak, bread, butter, ice cream with chocolate syrup, and water) by measuring simultaneously postprandial gastric, pancreatic, and biliary functions by marker-perfusion techniques. Responses to each (S or H) meals differed strikingly both in magnitude and pattern. S meals elicited a stronger early gastric secretory response (acid, pepsin, and volume) which compensated for faster initial emptying and resulted in higher gastric acidity and volume than after H meals. Further, nutrients ingested with S meals were emptied at a slower rate than H (as evidenced by a more gradual decline in intragastric buffer and osmolality, as well as time required for complete emptying of the meal). This, in turn, prolonged pancreatic and biliary responses since stimulation of these organs continued for as long as meal was delivered into the duodenum. However, early biliary outputs (gallbladder response) were less after S than H, probably because nutrients entered the duodenum more slowly and were initially diluted by rapidly emptying water. The physical characteristics of each meal (encompassing appearance, taste, and form of ingestion) probably accounted for early differences in digestive responses. Later, interactions between gastric (motor and secretory), pancreatic, and biliary functions played a major role. Our findings suggest that gastric, pancreatic, and biliary responses to liquid test meals introduced into the stomach may differ substantially from the presumably more physiological response to ordinary solid-liquid meals.

Adult↗
PubMed1979

Control of human postprandial pancreatic exocrine secretion: a function of the gastroduodenal region.

Regulation of the exocrine pancreatic secretion elicited by a meal in man is incompletely understood. In this study, we attempted to localize in the gastrointestinal tract areas that control postprandial trypsin secretion and to determine the effects of individual components of jejunal chyme on the meal-stimulated trypsin secretion. Trypsin outputs elicited by ingesting a mixed-nutrient meal and diverting it at the ligament of Treitz proximal to an occlusive balloon were compared with those occurring when the same meal was ingested, diverted at the ligament of Treitz, and immediately reinfused distal to the balloon, a procedure that exposed the entire gastrointestinal tract to chyme. Two different meals, one of semielemental and one of complex nutrients, were used with similar results. Trypsin outputs were similar whether or not jejunal chyme was diverted. In addition, no component--exogenous nutrients or endogenous secretions--of chyme reaching the jejunum after a meal further modified the trypsin secretion elicited by the gastroduodenal segment. This finding suggests that the gastroduodenal segment is sufficient to elicit the entire postprandial trypsin output and is the physiologic determinant of meal-stimulated trypsin secretion.

Adult↗
PubMed1979

Does motilin regulate canine interdigestive gastric motility?

Our objective was to determine whether motilin increases the frequency of cyclic interdigestive motor activity in the canine proximal stomach. In 4 conscious dogs with autotransplanted proximal gastric pouches and gastrointestinal electrodes, intravenous infusions of motilin (0.6 microgram/kg body wt/hr) increased the frequency of the interdigestive cycles by 30% both in the pouch and in the main gastrointestinal tract. However, the 3-min interval between the end of a cycle in the pouch and the end of a cycle in the duodenum was unchanged by motilin. In control experiments, without motilin infusion, the concentration of endogenous motilin in the plasma during the intense contractile phase of the cycles (overall mean 385 pg/ml) was greater in each dog (P less than 0.01) than the concentration during the quiescent phase (overall mean, 256 pg/ml). The concentration of plasma motilin was also greater in the contractile phase (mean, 717 pg/ml) than in the quiescent phase (mean, 587 pg/ml) during exogenous infusions of motilin in two of three dogs (P less than 0.01). We concluded that motilin increased the frequency of cyclic interdigestive motor activity in the canine proximal stomach and that the increase was not dependent on intact proximal gastric extrinsic innervation.

Action Potentials↗
PubMed1979

Effect of proximal gastric vagotomy and truncal vagotomy and pyloroplasty on gastric functions and growth in puppies after massive small bowel resection.

The effects of truncal vagotomy and pyloroplasty and proximal gastric vagotomy on gastric acid hypersecretion, hypergastrinemia, and growth after massive bowel resection were studied in beagle puppies. In puppies with 80% enterectomy, neither type of vagotomy alters significantly the postprandial hypersecretion of acid from the Heidenhain pouch or the concentration of serum gastrin. Proximal gastric vagotomy tended to decrease the hypersecretion more than did truncal vagotomy. In beagle puppies undergoing 70% small bowel resection, growth was significantly decreased but survival was not impaired. Neither proximal gastric vagotomy nor truncal vagotomy and pyloroplasty reversed completely the impaired growth produced by massive resection. Proximal gastric vagotomy caused a small improvements in growth, while truncal vagotomy and pyloroplasty resulted in a slight decrease in growth. It remains possible that proximal gastric vagotomy could be of value in the management of growing infants with hypersecretion of acid due to short bowel syndrome.

Animals↗