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Query: UMLS:C0011849 (diabetes)
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This review briefly outlines the gastrointestinal manifestations of diabetes mellitus. Usually, gastrointestinal abnormalities are asymptomatic. Severe gastrointestinal dysfunction may be quite debilitating, however. Gastrointestinal symptoms that are a consequence of diabetes may be confused with other primary gastrointestinal disorders. We attempt to provide a clinical approach to differentiating the basis of symptoms and outline the therapeutic plan that we generally employ. Much additional research is necessary to clarify our understanding of the pathophysiology of the gastrointestinal complications of diabetes and to develop improved therapeutic strategies.
Diabetes Care
PMID:Gastrointestinal manifestations of diabetes mellitus. 38 88

Gastroparesis causes gastric emptying disorders in patients with chronic diabetes mellitus and it results from reduced smooth muscle contractility secondary to autonomic dysfunction. Today there has been little objective evidence of improvement in gastric emptying following correction of both uremia and diabetes by combined kidney-pancreas transplantation. We used gastrointestinal symptom scores, solid gastric emptying tests and electrogastrography to evaluate the effect of combined kidney-pancreas transplantation on gastric emptying in 8 uremic diabetic patients. The mean age of the patients was 40 years (range: 30-51 years) and the mean duration of diabetes was 24 years (range: 16-30 years). The patients had been on dialysis up to 24 months. The pretransplant A1 mean was 6.5 before improving to 4.3 after transplantation. All patients were receiving exogenous insulin. Our study data indicate that uremic diabetics have a high prevalence of symptomatic gastrointestinal dysfunction including abnormalities of gastric emptying and gastric electrical activity. Following transplantation, the gastrointestinal symptomatology improved significantly. Significant improvement in the rate of gastric emptying also correlated with improvement in the symptom complex. Gastric electrical activity also improved during the follow-up period.
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PMID:Changes in gastric emptying in recipients of successful combined pancreas-kidney transplants. 180 83

Forty-eight patients with acute renal failure (ARF) who were referred to the Department of Renal Medicine, Singapore General Hospital for acute dialysis between August 1985 and August 1989 were studied retrospectively to identify risk factors associated with ARF that serve as prognostic indicators. There was no difference in the mean age of survivors and non-survivors (49.5 +/- 17.5 years vs 53.5 +/- 18 years, p greater than 0.05). The overall mortality rate was 52%. ARF as a result of surgical complication had a higher mortality rate in comparison to ARF from medical complications (66% vs 50%, p greater than 0.05). Septicaemia was the most common cause of ARF requiring dialysis. Hepatobiliary sepsis was the most frequent cause of septicaemia. Pre-dialysis serum urea and creatinine levels, and the number of dialysis treatments did not affect the outcome. Poor prognostic indicators included oliguria or anuria, fluid overload and coma. Patients tended to have a worse outcome if they had more than three risk factors taken from the following list:-decreased renal perfusion, assisted ventilation, coma, gastrointestinal dysfunction, recent surgery, sepsis, congestive heart failure, hepatobiliary dysfunction, malignancy, diabetes mellitus, chronic renal insufficiency and poor nutritional status. Early referral of patients with septicaemia due in particular to hepatobiliary infection may improve the prognosis.
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PMID:Acute renal failure prognostic indices in hospital inpatients referred for haemodialysis. 192 73

Reactive hypoglycemia is a relatively uncommon meal-induced hypoglycemic disorder. Most patients with adrenergic-mediated symptoms have a diagnosis other than reactive hypoglycemia. In many patients with this self-diagnosis, other disorders can be attributed as a cause for symptoms, especially neuropsychiatric disease. The continued use of the terminology "functional hypoglycemia" only contributes vagueness to our correct understanding of this metabolic condition. There are a number of conditions associated with postprandial hypoglycemia. One category is the reactive hypoglycemias, which occur in patients with diabetes mellitus (diabetes reactive hypoglycemia), gastrointestinal dysfunction (alimentary reactive hypoglycemia), hormonal deficiency states (hormonal reactive hypoglycemia), and a large patient group characterized as having idiopathic reactive hypoglycemia. Of these causes the alimentary, hormonal, and diabetic patients are less disputed, whereas the idiopathic reactive hypoglycemic group has been referred to as a "nondisease" group. Characteristic alterations in insulin secretion accompany each of these conditions. In bona fide patients, dysinsulinism or hyperinsulinism usually accounts for the hypoglycemia. Some patients may have increased insulin sensitivity, but this association is doubtful or very rare. Patients with this meal-related eating disorder are characterized as ingesting excessive quantities of refined carbohydrate. In the research setting, the disorder can easily be elicited with the oral glucose tolerance test. However, to establish clinical relevance, the hypoglycemia needs documentation in the home setting with measurements of blood glucose during a postpradial symptomatic episode. The reactive hypoglycemic patients are frequently confused with patients with underlying psychiatric illness. Both syndromes are similar, with adrenergic-mediated symptoms and a common characteristic personality as noted on Minnesota Multiphasic Personality Inventory (MMPI) testing. Patients with bona fide meal-related reactive hypoglycemia should be treated primarily with dietary restriction of refined carbohydrates; other patients may require medications.
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PMID:Reactive hypoglycemia. 264 26

Current evidence suggests that high-fiber diets, especially of the soluble variety, and soluble fiber supplements may offer some improvement in carbohydrate metabolism, lower total cholesterol and low-density lipoprotein (LDL) cholesterol, and have other beneficial effects in patients with non-insulin-dependent diabetes mellitus (NIDDM). Diets enriched with wheat bran and guar gum induce 10-20% reductions in serum cholesterol and LDL in both normo- and hypercholesterolemic subjects and have the ability to blunt the hypertriglyceridemic effects of diets high in carbohydrate and low in fiber. In insulin-dependent diabetes mellitus (IDDM) the situation is less clear, but a decrement of the circadian glucose profile has been shown. Americans, in general, consume too little fiber. With the need to restrict fat and reduce protein, an increase in carbohydrates is mandatory. A practical goal would be to establish the present level of fiber intake (15-30 g/day) and to gradually increase it. An intake of up to 40 g of fiber per day or 25 g/1000 kcal of food intake appears beneficial; in many individuals on weight-reducing diets higher levels may be unacceptable because of gastrointestinal side effects. The level of maximum benefit has not been determined. Fiber supplementation appears beneficial only if given with a diet comprising approximately half of the calories as carbohydrate. Foods should be selected with moderate to high amounts of dietary fiber from a wide variety of choices to include both soluble and insoluble types of fiber. Insufficient data are available on the long-term safety of high-fiber supplements. People at risk for deficiencies, such as postmenopausal women, the elderly, or growing children, may require supplements of calcium and trace minerals. People with upper gastrointestinal dysfunction are at risk of bezoar formation and cautioned against a diet high in fiber of the leafy vegetable type. Careful attention must be paid to insulin dose because hypoglycemia can result if there is a radical change in fiber intake and insulin dose is not reduced appropriately. Care must be exercised in the use of "novel" fibers, including the wood celluloses, because little is known of their safety and efficacy.
Diabetes Care 1988 Feb
PMID:Dietary fiber in management of diabetes. 283 32

Complications of the gastrointestinal tract in patients with diabetes mellitus can cause marked discomfort and may modify the ability of the patient to maintain normal glucostasis. In an attempt to elucidate some of the factors causing gastrointestinal dysfunction in experimental diabetes we examined the responses of jejunal smooth muscle in streptozotocin-induced diabetes in rats to some of the neurotransmitters and autocoids found in the enteric nervous system. Jejunal tissues from 4- to 5-week diabetic rats were examined for their responses to neurokinin (NK) A, NKB, substance P (SP), bradykinin, neurotensin, bethanechol, isoproterenol and phenylephrine. The affinities for all these agonists, except for SP which increased slightly with diabetes, were the same in both control and diabetic tissues. NKA was the most potent neurokinin and elicited the largest contractile responses from jejunal tissues of both control and diabetic animals. The contractile response to NKA, but not that to NKB or SP, was increased in the jejunum from diabetic animals. Part of this increased responsiveness was antagonized by atropine. The contractile effects of the cholinergic agonist, bethanechol, were not altered by the diabetic state. Decreased relaxation responses in the jejunum from diabetic animals were observed for bradykinin, neurotensin and isoproterenol, but not for phenylephrine. These results suggest that the myogenic actions of several agonists are modified in experimental diabetes.
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PMID:Modified smooth muscle responses of jejunum in streptozotocin-diabetic rats. 290 44

Gastrointestinal (GI) dysfunction in diabetes mellitus has never been evaluated systematically in all parts of the digestive system in a group of diabetics. Therefore, we have evaluated the frequency, extent, and clinical significance of GI complications in 75 consecutive, male, insulin-requiring diabetics (46 with neuropathy). Nineteen percent of the 75 patients and 30% of those with neuropathy had one or more GI symptoms. Esophageal, gastric, gallbladder, and small intestinal functions were studied in 30 patients using radionuclide esophageal and gastric emptying, postprandial gallbladder emptying, and intestinal transit of lactulose. We divided them into three groups: (1) 10 without neuropathy, (2) 10 with peripheral neuropathy, and (3) 10 with autonomic and peripheral neuropathy. Twenty-five patients (83%) had abnormalities of at least one GI organ, and 57% had abnormalities of two. Nineteen of the 25 patients (76%) with GI involvement and 8 of 9 (89%) symptomatic diabetics had delayed esophageal emptying. Symptomatic diabetics had more diabetic retinopathy, neuropathy, and autonomic dysfunction than asymptomatic diabetics and also had more widespread and more severe gastrointestinal involvement than asymptomatic diabetics. Therefore, our results indicate that in diabetics, (1) gastrointestinal motor abnormalities are common even though they are usually asymptomatic and (2) gastrointestinal dysfunction, especially in symptomatic diabetics, is often widespread and usually includes the esophagus.
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PMID:Gastrointestinal involvement in insulin-requiring diabetes mellitus. 344 33

Enteric nerves in the ileum of rats 8 weeks after streptozotocin-induction of diabetes were examined under the electron microscope before and after immunolabeling for vasoactive intestinal polypeptide (VIP). These studies have provided evidence of degenerative changes in the myenteric nerve fibres of diabetic rats, many of which were shown to contain VIP. It is suggested that VIP-ergic nerves in the gut may play a role in the development of gastrointestinal dysfunction in diabetes.
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PMID:Enteric nerves in diabetic rats: electron microscopic evidence for neuropathy of vasoactive intestinal polypeptide-containing fibres. 373 23

Adrenergic, cholinergic, and serotoninergic nerves were studied in the myenteric plexus of ileum and colon from streptozotocin-treated rats, an animal model of juvenile-onset diabetes. In view of clinical reports implicating diabetic autonomic neuropathy as the cause of gastrointestinal dysfunction in diabetes mellitus, neurochemical and histochemical techniques were used to study changes in the innervation of the gut. In the myenteric plexus of the ileum from diabetic animals, adrenergic nerves displayed signs of degeneration and the brightness of fluorescence in serotoninlike immunoreactive nerves was lower. Cholinergic nerves, however, did not display any signs of reduction in the ileum, and both choline acetyltransferase and acetylcholinesterase activities per centimeter were increased. In contrast, in the proximal colon 8 wk after induction of diabetes, neurochemical assays revealed significant increases in noradrenaline and serotonin levels as well as choline acetyltransferase activity, although no obvious changes in the pattern of innervation could be detected histochemically. The results indicate that changes do occur in the innervation of the gut of the streptozotocin-diabetic model shortly after the induction of diabetes, although they differ significantly in the ileum and colon; these may be of relevance to the types of gastrointestinal dysfunction displayed in human diabetes.
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PMID:Myenteric plexus in streptozotocin-treated rats. Neurochemical and histochemical evidence for diabetic neuropathy in the gut. 669 66

Some diabetic patients--particularly those with nausea and vomiting--frequently have evidence of delayed gastric emptying while other diabetic patients may in fact exhibit accelerated gastric emptying. Whether the presence or absence of symptoms of upper gastrointestinal dysfunction correlated with objective measures of gastric emptying in insulin dependent diabetic subjects was investigated. Twenty one insulin dependent diabetic patients underwent a solid phase gastric emptying scintiscan using in vivo labelled chicken liver. Thirteen patients had symptoms suggestive of gastrointestinal dysfunction (nausea, vomiting, early satiety, or constipation), while eight patients had no gastrointestinal symptoms. Eleven patients had orthostatic hypotension. All patients had been diabetic since childhood or adolescence. As a group, the diabetic patients showed a half time (T50) of gastric emptying (mean (SD) 150.0 min (163.7) that was not significantly different from that of 12 healthy control subjects (148.1 min (62.4)). Those diabetic patients without gastrointestinal symptoms and without orthostatic hypotension, however, showed a gastric emptying half time (70.1 min (41.6)) that was significantly faster than that of the control subjects. Conversely, those diabetic patients with nausea, vomiting, and early satiety (or early satiety alone) showed T50 values that were significantly greater than those of the diabetic patients without these symptoms. No correlation was found between the T50 value and the duration of diabetes, the fasting blood glucose at the time of study, or the respiratory variation in heart rate (E:I ratio). These observations indicate that highly variable rates of gastric emptying occur in insulin dependent diabetic patients, and that accelerated gastric emptying may occur in diabetic patients who have no symptoms of gastrointestinal dysfunction.
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PMID:Highly variable gastric emptying in patients with insulin dependent diabetes mellitus. 856 52


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