Gastrointestinal Hormone Levels Research Articles

Gastric emptying and plasma levels of gastrointestinal hormones in patients with peptic ulcer.

To study the plasma level of gastrointestinal hormones and the time of gastric emptying in patients with peptic ulcer. Thirty patients with gastric ulcer (GU), 29 patients with duodenal ulcer (DU), and 12 healthy controls were studied. Plasma levels of somatostatin (SS), vasoactive intestinal peptide (VIP) and substance P (SP) were measured by radioimmunoassay. Gastric emptying half-time (GET1/2) was measured by the TC-99(m) resin/solid meal method. GET1/2 was significantly longer in the GU patients than that in the healthy controls (65.9 ± 14.8 min vs 53.3 ± 4.3 min, P < 0.01) and plasma VIP levels were significantly higher (37.5 ± 10.7 ng/L vs 18.4 ± 5.9 ng/L, P < 0.05).There was a significant positive correlation between GET1/2 and plasma VIP levels (r = 0.55, P < 0.01). No significant differences were found in SS and SP levels when GU patients were compared with healthy controls (P > 0.05). GET1/2 was markedly shorter in the DU patients than in the healthy controls (41.7 ± 10.2 min vs 53.3 ± 4.3 min, P < 0.01) and plasma SS levels were significantly lower (6.4 ± 2.5 ng/L vs 11.9 ± 3.4 ng/L, P < 0.01). There was a significant positive correlation between GET1/2 and SS levels (r = 0.56, P < 0.01). Plasma SP levels in the DU patients were significantly higher than those in the healthy controls (54.4 ± 12.7 ng/L vs 41.6 ± 5.8 ng/L, P < 0.01). There was a significant negative correlation between GET1/2 and SP levels (r = -0.68, P < 0.01). No significant differences were found in the plasma VIP levels when DU patient were compared to healthy controls (P > 0.05). Elevation in VIP may contribute to occurrence of GU and its associated delay in GET1/2. Increased SP and reduced SS may play important roles in GET1/2 acceleration and in the pathogensis of DU.

The oxytocin receptor antagonist 1-deamino-2- d-Tyr-(OEt)-4-Thr-8-Orn-oxytocin inhibits effects of the 5-HT 1A receptor agonist 8-OH-DPAT on plasma levels of insulin, cholecystokinin and somatostatin

The aim of the present study was to investigate whether the 5-HT 1A receptor agonist 8-OH-DPAT, which previously has been shown to release oxytocin, also influences plasma levels of gastrointestinal and pancreatic hormones, and if so, whether such an effect is mediated by an oxytocinergic mechanism. For this purpose 8-OH-DPAT (0.5 mg/kg s.c.) was injected to male rats pretreated with the oxytocin receptor antagonist 1-deamino-2- d-Tyr-(OEt)-4-Thr-8-Orn-oxytocin (1 mg/kg s.c.), or vehicle. Thirty min after injection of 8-OH-DPAT, plasma levels of oxytocin were significantly increased. 8-OH-DPAT also increased insulin and decreased CCK and somatostain levels, effects that were blocked by pretreatment with the oxytocin antagonist. Taken together, these data suggest that the effect of 8-OH-DPAT on plasma levels of insulin, somatostatin and CCK may be mediated by oxytocin. In previous experiments, we have shown that following i.c.v. application of oxytocin, plasma levels of insulin are increased through a cholinergic mechanism. In this study, 2 ng of oxytocin decreased plasma levels of CCK, gastrin and somatostatin, effects that were blocked by pretreatment with atropine. Since oxytocinergic fibers which originate in the PVN project to the DMX, we suggest that the effect on the release of insulin, CCK and somatostatin induced by the 5 HT 1A receptor agonist 8-OH-DPAT may be mediated by an oxytocinergic activation of a vagal mechanism.

Octreotide in malignant intestinal obstruction.

Octreotide has proved an effective agent in the palliation of refractory malignant intestinal obstruction. This may be achieved through a pro-absorptive effect on the small bowel mucosa, an effect on improving gastrointestinal motility, by a reduction in gastrointestinal hormone levels and by a direct anti-neoplastic effect on the obstructing tumour. The simple route of administration of octreotide and the paucity of side effects reported in two recent studies should make the physician consider its use in this particularly distressing complication of advanced cancer.

Octreotide eliminates the increases in gastrointestinal hormone levels and gallbladder contraction evoked by jejunal feeding in patients with pancreatic pseudocysts: [formula omitted], F. Hajnal, J. Németh, L. Czakó, J. Lonovicz and ∗Á Pap. First Department of Medicine, Albert Szent-Györgyi Medical University, Szeged, and ∗Szent Imre Hospital, Budapest, Hungary

Octreotide eliminates the increases in gastrointestinal hormone levels and gallbladder contraction evoked by jejunal feeding in patients with pancreatic pseudocysts: [formula omitted], F. Hajnal, J. Németh, L. Czakó, J. Lonovicz and ∗Á Pap. First Department of Medicine, Albert Szent-Györgyi Medical University, Szeged, and ∗Szent Imre Hospital, Budapest, Hungary

The relationship between fasting and postprandial levels of gastrointestinal hormones and characteristics of gastric emptying after food ingestion in different phases of the migrating motor complex

The relationship between fasting and postprandial levels of gastrointestinal hormones and characteristics of gastric emptying after food ingestion in different phases of the migrating motor complex

Sepsis increases production of total secreted proteins, vasoactive intestinal peptide, and peptide YY in isolated rat enterocytes

The effect of sepsis on the synthesis of endogenous and secretory proteins, including vasoactive intestinal peptide (VIP) and peptide YY (PYY), was determined in enterocytes from jejunum of rats. Sepsis was induced by cecal ligation and puncture (CLP). Control rats were sham-operated. Total endogenous and secreted protein synthesis was assessed in incubated jejunal enterocytes by measuring incorporation of 3H-phenylalanine into protein. Release of VIP and PYY into the medium of incubated enterocytes and cellular levels of the gut peptides were measured by radioimmunoassay. Sixteen hours after CLP, synthesis rates of both endogenous and secreted proteins were increased, and this effect of sepsis was most pronounced in cells from the lower parts of the villi and crypts. Enterocytes from septic rats released more VIP and PYY into the incubation medium, and approximately half of the peptides they released were newly synthesized VIP and PYY. Intracellular levels of VIP and PYY were increased as early as 4 hours after induction of sepsis. Our results suggest that sepsis stimulates the synthesis of endogenous and secretory proteins, including certain gut peptides, in small intestine mucosa. This is consistent with previous observations of increased circulating levels of VIP, PYY and other gastrointestinal hormones during sepsis. The biological significance of increased synthesis of gut peptides and other intestinal proteins during sepsis remains to be determined.

Effects of dietary menhaden oil on mucosal adaptation after small bowel resection in rats

Adaptive hyperplasia of the small intestine is important in the outcome of short bowel syndrome. Previous studies have shown that long-chain fats stimulate this process. In the present study, the trophic effects of dietary menhaden oil, a highly unsaturated fat source, on mucosal adaptation following small bowel resection in rats was evaluated. Thirty weanling Sprague-Dawley rats and their controls were fed diets containing fats provided primarily as menhaden oil, safflower oil, or beef tallow. After 4 weeks, animals underwent a 70% jejunoileal resection. Mucosal mass, DNA, protein, and sucrase levels were assessed 14 days after a 70% jejunoileal resection or control feeding. Serum fatty acid composition and several gastrointestinal hormone levels were measured. Resected animals fed menhaden oil showed a marked increase in mucosal weight, DNA, and protein levels compared with rats fed the other fat sources. Enteroglucagon level was increased in all resected groups, but least increased in the menhaden-fed animals. In contrast, peptide YY concentrations were most increased in animals fed menhaden oil. Menhaden oil appears more effective in inducing intestinal adaptation than less highly unsaturated fats. Analysis of gastrointestinal hormones revealed no clear-cut explanation for this finding, other than a modest but associated increase in peptide YY levels.

Role of efferent and afferent vagal nerve activity during reproduction: Integrating function of oxytocin on metabolism and behaviour

The vagal nerves convey information between the brain and the gastrointestinal tract in both afferent and efferent direction. The efferent vagal nerves regulate gastrointestinal secretory and motor function and also the activity in the endocrine system of the gut. Gastrointestinal function and anabolic metabolism is optimized during gestation and lactation as a means of saving energy for this calorie-demanding process. This enhanced activity seems to involve central oxytocinergic transmission which increases efferent vagal nerve activity as reflected by altered levels of gastrointestinal hormones in plasma. In parallel a behaviour pattern characterized by sedation is induced. In addition, vagal afferents transfer information from the gut to the brain, e.g. as to the presence or absence of calories in the gastrointestinal tract. It is well known that satiety and sedation following a meal is in part caused by an activation of vagal afferents in response to food intake. Cholecystokinin released from the intestine is one of the factors that triggers the afferent vagal nerve activity. Also reproductive “interactive behaviours” such as milk ejection and maternal behaviour can be induced by CCK via afferent activation of vagal nerves. In contrast, when no food reaches the gut, milk production and ejection is blocked. Parts of these effects are vagally mediated, since they can be observed in vagotomized rats receiving full amounts of calories.

Pathophysiology of infection with Ostertagia ostertagi in cattle

Infection with the abomasal nematode, Ostertagia ostertagi, is an important cause of impaired productivity in young cattle in temperate parts of the world. Such losses have been associated with marked changes in feed intake, gastrointestinal function, protein, energy and mineral metabolism, and in body composition. The reduction in feed intake is an important factor in the pathogenesis of infection and may account for a large part of the difference in weight gain between ad libitum fed control and infected calves. Despite the obvious importance of inappetance, only recently has an association been made between reduced intake, altered gut motility and elevated levels of certain gastrointestinal hormones, such as gastrin. It has been suggested that the elevated gastrin levels accompanying abomasal parasitism may impair reticulo-ruminal motility and slow down abomasal emptying, leading to a stasis of ingesta and a reduction in feed intake. The rise in blood gastrin levels may also be partly responsible for the marked hyperlasia of the fundic mucosa seen in abomosal infections. Pronounced changes in protein metabolism have been associated with Ostertagia infection. Radioisotopic studies have demonstrated increased losses of albumin into the gastrointestinal tract which are accompanied by an increased in the rate of synthesis in the liver. Dietary protein breakdown in the abomasum is also likely to be impaired, although there is evidence of a compensatory increase in protein digestion in the lower gut of parasitised calves. Increased losses of albumin are not always accomanied by increases in faecal nitrogen, suggesting that albumin is broken down and recycled as ammonia. Radioisotopic studies in animals with intestinal nematode infections have demonstrated a marked reduction in muscle protein synthesis and an increase in protein synthesis in gastrointestinal tissue. Such changes in the balance of protein synthesis are likely to be brought about by alteration in the balance of certain metabolic hormones. Marked changes in energy metabolism also accompany Ostertagia infection. Parasitised calves exhibit a marked increase in non-esterified fatty acid levels, resulting from the mobilisation of adipose tissue, and a reduction in digestive efficiency of energy, probably associated with the increase in cycling of protein through the gastrointestinal tract and the compensatory increases in protein synthesis. Mineral metabolism may also be affected although relatively little work has been conducted in cattle. Changes in body composition reflect a reduction in deposition of muscle protein and fat, and an increase in bone content and water retention.

Response of the antral mucosa of the rat stomach to 2,3,7,8-tetrachlorodibenzo- p-dioxin

2,3,7,8-Tetrachlorodibenzo- p-dioxin (TCDD) produces a striking hypergastrinemia in rats that is thought to mediate the antiatrophy effect of TCDD on the oxyntic gland mucosa of the stomach. However, effects of TCDD on the antral mucosa, which is the origin of most physiologically released gastrin and is not a target for the trophic action of gastrin, has yet to be thoroughly investigated. Also gastrin release from gastrin-containing cells (i.e., G-cells) in the antral mucosa is inhibited by the paracrine secretion of somatostatin from D-cells in the antrum. Our purpose was to determine if the antral mucosa is affected by the trophic influence of TCDD and if alterations in antral mucosa levels of gastrin or somatostatin cause the hyper-gastrinemia. TCDD (100 μg/kg, Day 14 post-treatment) had a trophic effect on the antral mucosa. This was demonstrated histologically and by significant increases in antral wet weight and antral mucosa height. In contrast, pair-fed control rats that lost the same amount of body weight developed antral mucosa atrophy. With respect to serum and antral levels of gastrointestinal hormones, TCDD produced a 7- to 10-fold increase in serum gastrin concentrations that was not detected until Day 14 post-treatment. In contrast, serum gastrin concentrations in pair-fed control rats were comparable to those of control rats. The number of G-cells in the antral mucosa was not affected by either TCDD treatment or paired-feed restriction. These findings demonstrate that hypergastrinemia in TCDD-treated rats is not caused by reduced feed intake or antral G-cell hyperplasia. A major finding was that antral mucosa levels of both gastrin and somatostatin were decreased significantly in TCDD-treated rats. However, the temporal development and dose-decreased of these TCDD effects on antral hormone levels were quite different than those for hypergastrinemia. TCDD-induced decreases in antral levels of gastrin and somatostatin were detected 1 week earlier than hypergastrinemia. Also, the ED50 of TCDD on Day 14 post-treatment for the decrease in antral mucosa content and concentration of gastrin (29 and 22 μg/kg, respectively) and somatostatin (24 and 19 μg/kg, respectively) was less than that for hypergastrinemia (46 μg/kg). These time- and dose-dependent differences demonstrate that hypergastrinemia in TCDD-treated rats is not a consequence of reduced antral levels of gastrin or somatostatin. We conclude that the antral mucosa, an epithelial tissue not responsive to the proliferative effect of gastrin, is nevertheless a target for the trophic influence and gastrointestinal hormone-altering effects of TCDD.

Enteroglucagon and peptide Y-Y response after construction of a pelvic reservoir in humans

The results of an investigation of plasma levels of gastrointestinal hormones in patients after the construction of a pelvic reservoir are reported. Enteroglucagon (EG) and peptide tyrosine-tyrosine (PYY), two hormones believed to play a relevant role in the adaptive response to bowel resection, were investigated using a specific radioimmunoassay in basal conditions and after a standard meal. Pouch patients showed a statistically significant increase in basal levels of both enteroglucagon and PYY compared with control subjects (P less than 0.02 and P less than 0.001, respectively). The response of enteroglucagon to food ingestion, evaluated by means of the total integrated response, was similar in patients and controls. Conversely, the response of PYY was significantly increased in pouch patients compared with control cases (P less than 0.02). Results of this investigation suggest that gut hormones may be involved in mediating the adaptive response of the intestine to pouch construction. Changes of gut peptides may explain, at least in part, the functional results observed after pouch construction.

Effects of multiple dose infections with Ascaris suum on blood gastrointestinal hormone levels in pigs

Ten consecutive daily doses of infective Ascaris suum eggs were administered to pigs in two experiments and the levels of gastrointestinal hormones in their blood were measured. The piglets in each experiment were divided into low-dose (LDI) and high-dose (HDI) infections and control groups. Infected pigs had lower feed consumption, lower weight gains, and lower feed efficiency than control pigs. Serum gastrin levels in infected pigs were significantly lower than the controls from Days 7 to 17 post first inoculation (PFI), and so were their serum glucagon levels from Days 12 to 24 PFI. Serum insulin levels in infected animals were sometimes lower than those in controls. These differences were usually more intense in the LDI pigs than in HDI pigs. The plasma cholecystokinin (CCK) levels in the LDI group were significantly higher than those in controls from Day 10 PFI to the end of the experiment, while the CCK levels in the HDI group did not differ significantly from the controls. Increased plasma CCK levels could be a satiety factor in A. suum infection since the time of occurence of high levels of CCK matched the period of reduced feed consumption.

Motility‐independent ultradian pattern of bile flow in fasted rats

Abstract The dynamics of bile secretion was studied on 53 cannulated male Wistar rats in normal conditions and during intravenous infusions of gastrointestinal hormones. Both secretin and CCK (Boots) induced the greatest choleretic response. Bile diversion caused a significant fall in bile flow rates as compared with rats receiving constant intraduodenal infusion of Na‐taurocholate. In all the groups clear 1.5–2 hr oscillations, lasting much longer than the interdigestive motility cycles in this species, were observed. The significance of these oscillations was confirmed by the Fisher's test and the normalized periodogram values computed for the frequency band 0.2–0.33 (1.5–2.5 hr) period were significant in all the experimental groups. However, the significance of the frequency band decreased along with the increasing stimulation potency of the hormones. Thus, neither changes in bile acid secretion nor alternations in main gastrointestinal hormone levels seem to be responsible for the occurrence of the ultradian rhythm of bile flow in the rat.

The effect of a 72-h fast on plasma levels of pituitary, adrenal, thyroid, pancreatic and gastrointestinal hormones in healthy men and women.

Seventeen human subjects fasted without electrolyte replacement for 3 days and hormone levels were measured before, during and after the fast. Immediate consequences of the fasting state in healthy human subjects include a marked increase in plasma cortisol. ACTH, beta-endorphin, beta-lipotrophic hormone, adrenaline, noradrenaline and dopamine. Levels of all these hormones were much greater on the first morning of the fast than in the post-prandial state, even though the plasma glucose level was no lower than that observed on the morning before the fast began. A clear fall in TSH and tri-iodothyronine (T3) levels was observed, but thyroxine levels did not change significantly. Insulin levels fell whereas proinsulin levels did not fall during the fast, though they did rise markedly upon re-feeding. An increase in GH levels was particularly apparent in male subjects, but was also seen in females when evening samples were compared. Pancreatic glucagon showed a modest rise during the fast, but fell again on refeeding; total glucagon also rose as the fast proceeded, but increased markedly upon re-feeding. Levels of gastrin and peptide YY remained low during the fast. Plasma electrolyte levels were unchanged. The following were closely correlated: cortisol with ACTH, T3 with log10 TSH, dopamine with noradrenaline, and (negatively, during the fast) pancreatic glucagon with glucose.

Effect of Ileal Perfusion of Carbohydrates and Amylase Inhibitor on Gastrointestinal Hormones and Emptying

To determine if carbohydrates perfused into the ileum affect gastric emptying and circulating levels of gastrointestinal hormones, 18 healthy subjects were intubated with an oroileal tube. A 400-cal (60% carbohydrate, 20% protein, 20% fat) homogenized meal labeled with 111In-DTPA was then infused into the stomach over 10 min. Simultaneously, a test solution of normal saline (n = 6) or 12.5 (n = 4), 25 (n = 4), 50 (n = 2), or 100 (n = 2) mg/min of carbohydrates (75% rice starch, 25% glucose) containing a nonabsorbable marker, polyethylene glycol, was continuously perfused into the terminal ileum at 3 ml/min for 7 h. In one-half of the subjects the perfusate contained an amylase inhibitor (3.3 mg/ml) that reduced starch digestion and carbohydrate absorption. Gastric emptying was measured by a dual-headed gamma-camera. Plasma concentrations of hormones and the amount of carbohydrates passing the ileum were measured every 10 min. The amylase inhibitor significantly reduced the absorption of complex carbohydrates from the terminal ileum (p less than 0.05). Gastric emptying was significantly slowed by ileal perfusion of carbohydrates (p less than 0.01). This effect was enhanced by the amylase inhibitor (p = 0.06). Plasma concentrations of C-peptide, glucagon, motilin, gastrin, and human pancreatic polypeptide were not related to gastric emptying or ileal perfusates, but decreased concentrations of gastric inhibitory polypeptide and neurotensin and increased concentrations of peptide YY were significantly associated (p less than 0.05) with slowing of gastric emptying. Perfusing carbohydrates into the ileum was associated with nausea, abdominal pain, and vomiting, but we could detect no direct relationship between the onset of these symptoms and gastric emptying. Slowing of gastric emptying of a homogenized mixed meal by the entry of complex carbohydrates into the ileum may be partly mediated by peptide YY or nonvagally mediated neural mechanisms.

An experimental study on the remnant gastric motilities and gastrointestinal hormones after various types of gastrectomies

Using adult mongrel dogs, remnant gastric motility in relation to the changes of gastrointestinal hormone (gastrin and motilin) levels were measured under conscious states before and after distal partial gastrectomy in the Billroth I (BI) or II (BII) reconstruction and proximal partial gastrectomy with or without pyloroplasty. Remnant gastric motility was studied during the digestive and interdigestive states by chronically implanted strain gage transducer (S.G.T.) along the gastrointestinal tract. Gastrointestinal hormone levels were determined by radioimmunoassay. Results were summarized as follows: 1. Remnant gastric motility after BI was different from BII, that is, digestive patterns after BII were more shorter than BI, as a result, gastric emptying times were shortened. 2. Gastrin release by the meal intake in the dogs with BI was greater than that in BII. On the other hand, motilin release in the dogs with BII was higher level than that in BI during the digestive and interdigestive states. Gastrointestinal hormone levels after BI were approximately as same responses as controls. These findings suggested that BI reconstruction for distal partial gastrectomy was more physiological surgical procedure than BII reconstruction. 3. Remnant gastric motility during the digestive state after proximal gastrectomy showed the excitatory pattern and gastric emptying time was remarkably shortened than in controls. 4. In gastrin and motilin levels stimulated by the meal in the dogs with proximal gastrectomy, the peak of gastrin and the depression of motilin were observed more early in relation to remnant gastric emptying time. These findings suggested that the pyloroplasty for the proximal gastrectomy was necessary to prevent an increased motility of the remnant stomach during the digestive states.

Plasma levels of gastrin, somatostatin, and cholecystokinin immunoreactivity during pregnancy and lactation in dogs

Plasma levels of gastrinlike, somatostatinlike, and cholecystokininlike immunoreactivity were determined by radioimmunoassay in peripheral blood from 11 beagles during pregnancy and in response to suckling during lactation. Cholecystokinin was determined in pooled and in individual plasma samples after separation of cholecystokinin and gastrin by high-performance liquid chromatography. Gastrin and somatostatin levels were significantly increased during the 8-wk-long dog pregnancy; peak values were recorded in week 7 and week 4, respectively. The cholecystokinin level rose and peaked at week 3, and remained elevated. In response to suckling, maternal gastrin levels rose significantly when tested in week 1 and 3 of lactation. Somatostatin levels did not respond significantly to suckling, but basal levels were elevated in week 1 compared to week 3 of lactation. Cholecystokinin rose in response to suckling both in week 1 and 3 of lactation. We suggest that the increased levels of gastrointestinal hormones during pregnancy and lactation may serve to increase digestive and anabolic capacity.

Pyloric motor activity and function with special reference to pyloroplasty after vagotomy

Using adult mongrel dogs, pyloric motor activity and gastric emptying observed by phototransducer (P.T.) under anesthesia and by strain gage transducer (S.G.T.) under consciousness. Pyloric motor activity and function were investigated in the dogs with distorted pylorus after instorations of Daclon tube, pyloric resection and pyloric stenosis. The pyloric sphincter responses to gastrin, pancreozymin, secretin, glucagon, atropine, morphine, naloxone and enkephalin administrated intravenously were observed. Gastroduodenal motor activity in relation to the changes of gastrointestinal hormone levels were measured before and after truncal vagotomy (TV) and selective proximal vagotomy (SPV) with or without pyloroplasty. Results are summarized as follows; 1. The pyloric motility recorded by P.T. was well correlated with the contractile activity recorded by S.G.T. under the anesthesia, although the pylorus was never completely closed and showed tonic movements. 2. The pyloric motor activity under the consciousness was different from gastric and duodenal motor activity. 3. After SPV, the gastrin responses to the test meals were significantly increased so that the pyloric motility was disturbed. The fact mentioned above, the pyloric functional disorder after the SPV was partly due to the hypergastrinemia. Pyloroplasty for the SPV inhibited the serum gastrin level. It was suggested that the pyloroplasty for the SPV was necessary to prevent possible hypergastrinemia after SPV.

Familial visceral neuropathy with autosomal dominant transmission

This report describes a family with a visceral neuropathy without extraintestinal manifestations transmitted over at least four generations in an autosomal dominant manner. Four of 7 living patients underwent extensive evaluation including histology, radiography, gastric emptying and secretory studies, esophageal and jejunal manometry, and measurements of plasma levels of gastrointestinal hormones. The only characteristic radiologic abnormality in 7 patients was dilatation of jejunum and ileum. Gastric emptying studies were normal in 2 patients, whereas 2 others showed accelerated emptying of liquids either alone or in combination with grossly delayed solid emptying. Manometry of the esophagus and proximal small intestine and gastric secretory studies were normal. Histologic studies showed hypertrophy of the smooth muscle, a markedly reduced number of argyrophilic neurons, and degenerative changes of argyrophilic neurons and nerve fibers but without Schwann cell proliferation, intranuclear inclusions, or inflammatory cells. This appears to be a familial visceral neuropathy characterized by (a) distinct involvement of the jejunum and ileum as defined radiographically, (b) histology different from that of two previously described forms of familial visceral neuropathy, (c) autosomal dominant transmission, and (d) no evidence for extraintestinal neurologic manifestations.

Guar in non‐insulin‐dependent diabetics

AbstractThis study examined the acceptability of a micro‐granulated guar preparation and assessed its effects on diabetic control and serum lipid and gastrointestinal hormone levels in 24 non‐insulin‐dependent diabetic patients. Eighteen patients completed the nine month trial, and 6 patients withdrew as a consequence of side‐effects of the guar or placebo. There was no significant effect on blood sugar control but, overall, a 12.1% reduction in serum cholesterol was observed, the greatest reduction being found in patients with hypercholesterolaemia. LDL cholesterol was significantly reduced, but HDL cholesterol was unchanged though the HDL3 fraction was reduced. There was no change in the HDL2 fraction (the fraction associated with atherosclerosis). Guar treatment did not influence the gastrointestinal hormone response to a standard test meal. We conclude that micro‐granulated guar is acceptable and has a clinically useful cholesterol‐lowering effect in non‐insulin‐dependent diabetic patients.