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Disturbances of the entero-insular axis.
The entero-insular axis comprises direct substrate stimulation of the islet cells by the absorbed nutrients and signal transmission by endocrine factors and nerves. The extent of neural influences has not yet been evaluated. GIP is the main incretin candidate. GIP release is dependent on nutrient absorption. Therefore, GIP abnormalities occur in a large number of gastrointestinal and metabolic diseases. These secondary changes are rarely of clinical significance. GIP hypersecretion may, however, contribute to the increased lipogenesis in obesity and the hypoglycemia in the late dumping syndrome. In type II diabetes hyper- and hyposecretion of GIP has been found but no correlation between GIP and insulin response. GIP abnormalities are not identical with disturbances of the entero-insular axis. These can only be evaluated by estimating the incretin effect (comparing the insulin response to oral glucose with the insulin response to an isoglycaemic iv glucose infusion). A decreased incretin effect has been observed in patients with jejuno-ileal bypass and in type II diabetes. In neither condition was a correlation found between incretin effect and GIP response. It is concluded that disturbances of the entero-insular axis are rarely explained by GIP abnormalities. Therefore, other humoral gut factors must exist. Also the neural part of the entero-insular axis requires exploration in health and disease.
Alterations of gastrin secretion in obese rats with ventromedial hypothalamic lesions.
Basal plasma gastrin levels were significantly higher in obese rats induced by ventromedial hypothalamic lesions (VMH rats) than in sham-operated controls. Gastrin secretion in response to insulin hypoglycemia and a liquid diet load was higher in VMH rats than in controls. The antral gastrin concentration was also elevated in VMH rats. Pair-fed rats with VMH lesions showed increased gastrin secretion as did the non-pair-fed group. These results show that gastrointestinal hormone secretions as well as pancreatic endocrine function are abnormal in obese rats with VMH lesions. Increased gastrin secretion is probably induced by factors other then hyperphagia, such as disturbance of the autonomic nervous system due to the VMH lesions.
[Influence of anatomical variations of the pancreatic artery on the surgical technic of segmental pancreas transplantation in dogs].
The surgical technique in clinical pancreas transplantation is still not standardized. Animal experimentation should allow a reproducible and reliable model by choosing the cervical region in dogs as the site of segmental grafting. A goal of the experiments was to determine the influence of preservation, operation technique, duct occlusion, immunosuppression, and gastrointestinal hormones (Somatostatin, Cyclosporin A). 50 grafts have been transplanted. It could be clearly demonstrated that in 54% the vascularization of the left lobe of the canine pancreas differs extremely from man. Successful results are to expect being aware of the anatomical variations. The varieties of the arterial blood supply indicate which technique has to be performed to avoid ischemic grafts due to inadequate preservation.
Potential pharmacological approaches to management of gut motility disorders.
Recent advances in gut neuropathology, electrophysiology, manometry, and quantification of luminal transit rates have improved our understanding of gut motility disorders and facilitated their early diagnosis. However, therapeutic progress has generally lagged behind, despite some very significant pharmacological developments. The main categories of gut motility disorders and their postulated pathogenetic mechanisms are described, and potential pharmacological approaches to their management are reviewed.
[Chronic idiopathic intestinal pseudo-obstruction].
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[Motilin - spectrum and analysis of effects].
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[The stimulating effect of gastrin on the proliferation of gastric fundus mucosa].
Many gastrointestinal hormones have a stimulating action on the proliferation and growth of stomach and intestinal mucosa and on pancreas. This so-called trophic action was investigated most intensive on gastrin. We reproduced this effect autoradiographically by 3H-thymidine incorporation on the stomach corpus mucosa of rats. The animals had increased serum gastrin levels by partial stomach corpus resection that increased the endogenous serum gastrin level. The proliferation stimulating action of gastrin is also detectable at chronic oral application of N-Methyl-N'-nitroso-N-nitroguanidine for induction of stomach and intestinal tumors simultaneously to pentagastrin administration or partial stomach resection in the intact, tumor free oxyntic mucosa of stomach.
[Experimental study on the role of vagus nerve in the release of motilin].
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[Intestinal motility and the serum motilin levels after abdominal surgery].
Correlation of intestinal motility and serum motilin after abdominal surgery was investigated experimentally and clinically. The results were summarized as follows: The recovery of intestinal motility was faster in the dogs simply laparotomized than gastrectomized. The recovery of the small intestinal motility was followed by that of the large intestinal motility in the dogs. The intravenous infusion of the synthetic motilin markedly stimulated the intestinal motor activity in early postoperative period. Serum motilin levels significantly dropped one after abdominal surgery and rose again both in the dogs and the patients. The rate of increase of serum motilin levels at the postoperative period closely correlated with the recovery of the intestinal motility both in the dogs and the patients, that is, the higher the rate of increase was, the faster the recovery was.
[Effects of truncal vagotomy on serum motilin levels, gastric motility patterns and gastric emptying: an experimental study].
Using adult mongrel dogs, gastroduodenal motility, gastric emptying and pertinent serum motilin levels were measured under conscious states before and after transthoracic truncal vagotomy. Gastroduodenal motility was recorded by chronically planted strain gage transducers along the gastrointestinal tract. Gastric emptying was measured by X-ray examinations after barium-meat-meal ingestions or by gastric contents sampling method through the total pouch cannula after normal dog food ingestions. Results were as follows; Gastric motility patterns recorded by strain gage transducers were classified into two patterns that were a digestive pattern (D.P.) and an interdigestive pattern (I.P.). Serum motilin levels were elevated during high-amplitude contractions and lowered during resting phase of interdigestive periods. After vagotomy, strengths (heights) of antral contractions and phasic changes were decreased with the lack of I.P. These postvagotomy changes were thought to be related with the delayed gastric emptying after vagotomy. Gastric lavage through the cannula or pyloroplasty produced no effect on recovery of I.P. This fact suggested that the lack of I.P. was the direct effect of vagotomy and not due to delayed gastric contents emptying. On the assumption that motilin had the major role on the regulation of I.P., vagotomy seemed to produce an effect to prevent phasic motilin release.
Inhibition of interdigestive contractile activity in the stomach by peptide YY in Heidenhain pouch dogs.
The inhibitory effect of peptide YY on contractile activity in the innervated main stomach and the vagally denervated fundic pouch in conscious Heidenhain pouch dogs was investigated. Peptide YY was given in i.v. bolus injections of doses between 12.5 and 100 pmol/kg body wt. During the digestive state, 2-3 h after feeding, peptide YY was found to have no effect on contractile activity in either the innervated or the vagally denervated stomach. In the interdigestive state, it was found that peptide YY inhibited the interdigestive migrating contractions in the innervated main stomach dose-dependently for 1.2 +/- 0.1 to 5.8 +/- 0.3 min, but did not affect pouch contractions at all. This peptide, however, did not influence the cycle of the interdigestive migrating contractions. Pentagastrin, on the other hand, suppressed the interdigestive migrating contractions in the innervated main stomach when the bolus doses were greater than 300 pmol/kg body wt, but did not inhibit pouch contractions completely with this dose. Atropine (0.05 mg/kg body wt) suppressed contractions in both the main stomach and the vagally denervated pouch. Peptide YY inhibits the interdigestive migrating contractions in the stomach through the extrinsic nerves.
Effect of infusion of nutrient solutions into the ileum on gastrointestinal transit and plasma levels of neurotensin and enteroglucagon.
The small bowel transit time of 100 ml of lactulose solution infused at the ligament of Treitz was measured by breath hydrogen excretion in paired studies carried out in 43 healthy volunteers during infusion (1.2 ml/min) of equal volumes (100 ml) of isotonic solutions of either fat emulsion (Intralipid, Prosparol, or Calogen), protein hydrolysate, glucose, or saline into either the jejunum (90 cm from the teeth), ileum (205 cm from the teeth), or colon (350 or 400 cm from the teeth). Ileal infusion of Intralipid or protein hydrolysate resulted in significant delays in small bowel transit time (125 +/- 21 min and 71 +/- 11 min, respectively) compared with infusion of saline (50 +/- 3 min; p less than 0.02 and p less than 0.05). These delays were not associated with any significant alteration in plasma levels of neurotensin or enteroglucagon. Small bowel transit time was unaffected by infusion of nutrients into the colon or jejunum, although jejunal infusion of Intralipid increased the plasma levels of enteroglucagon and neurotensin (p less than 0.01 and p less than 0.02, respectively) after the start of lactulose infusion. In a separate series of paired experiments, infusion of Intralipid into the ileum in 5 volunteers significantly delayed the transit of a solid test meal labeled with 25 microCi of 99mTc-sulfur colloid through both the stomach and small intestine. These data support the existence of a mechanism whereby the presence of unabsorbed food in the ileum may enhance absorption by delaying the passage of food through the small intestine.
Variations in concentrating function of the gallbladder in the conscious monkey.
Hepatic bile is concentrated in the gallbladder by absorption of water and electrolytes. The rate of water absorption can be influenced in vitro and in vivo by gastrointestinal hormones and neurogenic transmitters. Recent studies have demonstrated that besides its absorbing activity, the gallbladder has the ability to secrete fluid into its lumen. In the present experiments, we studied the rate of net water absorption in the gallbladders of pig-tailed monkeys sitting in restraining chairs. Bile from the common bile duct and the gallbladder was led out through cannulas to a stream splitter, samples were obtained, and bile was returned to the duodenum. By measuring outflow from the gallbladder and the concentration of bile acids in hepatic bile and bile that had passed through the gallbladder, net water absorption from the gallbladder bile could be calculated. The results demonstrate that during daytime fasting there was a net absorption corresponding to 30% of the fasting gallbladder volume per hour, and after feeding there was a net secretion of fluid into the gallbladder lumen. Compared with the awake fasting state, net water absorption from the gallbladder decreased at night while the animal was fasting and asleep. Physiologically, secretion of fluid after a meal could help to empty the gallbladder, and changes in net water absorption by the gallbladder could influence the kinetics of the enterohepatic circulation of bile acids.
Relationship between porcine motilin-induced migrating motor complex-like activity, vagal integrity, and endogenous motilin release in dogs.
Both the vagus nerve and motilin have been implicated in the initiation of phase III of the fasting migrating motor complex. To investigate the contribution of each, the effects of intravenous porcine motilin, vagosympathetic nerve blockade, and atropine were assessed. Intralumenal pressures of the lower esophageal sphincter, stomach, and upper small intestine, and plasma motilin levels were monitored. Porcine and canine motilin in plasma were distinguished by radioimmunoassay using two different antibodies. Injection of porcine motilin (75-370 pmol), initiated dose-dependent phase III-like motor activity in the lower esophageal sphincter, stomach, and small bowel if the vagi were intact; if the vagi were blocked, activity was initiated in the small bowel only. Moreover , a significant (p less than 0.001), dose-dependent peak in canine plasma motilin was observed after the onset of the induced motor activity when the vagi were intact or blocked, with plasma motilin peaks comparable to those occurring spontaneously. In both intact and vagally blocked dogs, atropine abolished both the spontaneous motor activity and associated rise in motilin level, and also abolished porcine motilin-induced activity. However, a diminished, but significant (p less than 0.01) peak in porcine motilin-induced canine motilin persisted in the presence of atropine. These results in dogs indicate that while spontaneous phase II motility in the upper gastrointestinal tract and phase III activity in the lower esophageal sphincter and stomach are dependent on vagally mediated excitatory pathways, spontaneous and induced phase III motor activity in the small intestine are dependent on nonvagal cholinergic innervation. Canine motilin release induced by porcine motilin is mediated primarily by a nonvagal cholinergic (muscarinic) pathway, with minor contributions from vagal noncholinergic, and nonvagal noncholinergic mechanisms. Because spontaneous or induced motilin release peaks well after the onset of phase III motor activity, it is unlikely that motilin is the primary factor responsible for initiation of the migrating motor complex in the dog. Motilin may, however, modulate motility produced by preexisting neural excitation.
Effect of 13-norleucin motilin on water and ion transport in the human jejunum.
Passage of the interdigestive migrating myoelectric complex through the proximal small bowel is associated with elevated plasma motilin levels and an increase in transmucosal potential difference suggesting altered ion transport. The aim of the present study was to investigate whether motilin may have an effect on intestinal water and ion transport. Steady state jejunal perfusion studies were carried out in healthy volunteers while either saline (control) or synthetic motilin (256 pmol/kg X h) was infused via peripheral vein. Plasma motilin levels rose from a mean of 31 to a plateau of 832 pmol/L. Motilin infusion significantly reduced absorption of water, sodium, potassium, and chloride when a plasmalike electrolyte solution was perfused. During perfusion with a bicarbonate-free salt solution, motilin significantly enhanced secretion of water, potassium, and chloride. Chloride secretion was active inasmuch as it occurred against both an electrical and chemical gradient. Motilin infusion had no effect on transit time during perfusion of the 30-cm jejunal test segments. We conclude that motilin can act as an intestinal secretagogue in the human jejunum.
The interdigestive migrating complex and its significance in man.
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