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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Amylase inhibition has gastrointestinal and metabolic effects that may aid in the treatment of diabetes and obesity. We tested whether 4 g of a commercially available wheat amylase inhibitor (WAI) affected postprandial carbohydrate (CHO) absorption and plasma glucose or hormones. Twelve persons (four lean and four obese nondiabetics and four obese type II diabetics) were studied on 2 separate days. After eating a weight maintenance diet (55% CHO, 20% protein, and 25% fat, as percentage of calories) for 3 days, subjects ate a breakfast containing 650 kcal, the same proportion of nutrients as calories, and in random order, either WAI or no WAI. Breath H2 and plasma glucose and hormones were measured every 15 and 30 min, respectively, for 7 h. WAI decreased the delta peak postprandial plasma glucose concentrations in 10 of 12 subjects (p < 0.05) and increased the breath H2 levels in 11 (p = 0.02); the increases in breath H2 were small, generally <20 ppm. No subject experienced a change in stools, diarrhea, or bloating. In response to WAI, gastric inhibitory peptide decreased (p < 0.05), peptide YY increased (p < 0.05), and there was a trend toward increased human pancreatic polypeptide (p = 0.07). Although WAI delays CHO absorption and reduces peak postprandial plasma glucose concentrations, overall CHO malabsorption is minimal (as reflected by breath hydrogen and hormones) and without symptoms. It, therefore, may be useful in treating type II diabetes mellitus.
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PMID:Acute postprandial gastrointestinal and metabolic effects of wheat amylase inhibitor (WAI) in normal, obese, and diabetic humans. 970 Sep 50

Patients with long-standing diabetes commonly suffer from gastric neuromuscular dysfunction (gastropathy) causing symptoms ranging from postprandial bloating to recurrent vomiting. Autonomic neuropathy is generally believed to be responsible for diabetic gastropathy and the underlying impairments in gastric emptying (gastroparesis) and receptive relaxation, but the specific mechanisms have not been elucidated. Recently, it has been recognized that interstitial cells of Cajal generate electrical pacemaker activity and mediate motor neurotransmission in the stomach. Loss or defects in interstitial cells could contribute to the development of diabetic gastroparesis. Gastric motility was characterized in spontaneously diabetic NOD/LtJ mice by measuring gastric emptying and by monitoring spontaneous and induced electrical activity in circular smooth muscle cells. Interstitial cells of Cajal were studied by Kit immunofluorescence and transmission electron microscopy. Diabetic mice developed delayed gastric emptying, impaired electrical pacemaking, and reduced motor neurotransmission. Interstitial cells of Cajal were greatly reduced in the distal stomach, and the normally close associations between these cells and enteric nerve terminals were infrequent. Our observations suggest that damage to interstitial cells of Cajal may play a key role in the pathogenesis of diabetic gastropathy.
Diabetes 2000 Oct
PMID:Remodeling of networks of interstitial cells of Cajal in a murine model of diabetic gastroparesis. 1101 58

Our understanding of gastric motility disorder--diabetic gastroparesis has advanced in the last ten to fifteen years, but the published data regarding pathogenesis are confusing and show conflicting results. The pathogenesis is sometimes linked with hyperglycemia, autonomic neuropathy, gastrointestinal hormone or myogenic mechanism. Antral hypomotility is often associated with hyperglycemia which is often accompanied by reduction in duodenal waves. Varying level of motilin, a gastrokinetic hormone has been reported. However none of the mechanism could explain the exact pathogenesis. The relationship of this mortality disorder with clinical symptoms is not always established, however nausea and vomiting lasting for days or weeks are the prominent symptoms. Other symptoms are post-prandial fullness, early satiety, bloating, belching, and vague abdominal discomfort. In a few cases, it may be the cause of poor nutrition, uncontrolled diabetes and recurrent ketoacidosis. Last one or two decades have seen some advancement in the investigational procedures like scintigraphy, radio-opaque markers, breath test, electrogastrography and MRI. Which can lead to a proper diagnosis. Such objective assessment is all the more important as nearly half of the patients do not have any symptom. Symptomatic improvement of gastroparetic patients should be the aim and in asymptomatic patients, treatment is often not recommended. Some dietary advice and prokinetic agents like metoclopramide, cisapride etc. are often prescribed but much needs to be further known as management is not always uniformly rewarding.
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PMID:Diabetic gastroparesis. 1122 21

As available data on Helicobacter pylori infection in patients with diabetes are scattered and discordant, we evaluated the prevalence of H. pylori and its relationship to dyspeptic symptoms in adult patients with diabetes and subjects with dyspepsia. H. pylori infection (evaluated using the 13C urea breath test) and dyspeptic symptoms (nausea, bloating, and epigastric distress) were investigated in 71 consecutive diabetic outpatients; the presence of gross lesions, histologic gastritis, and Helicobacter was verified in the patients with a positive urea test who agreed to undergo upper gastrointestinal tract endoscopy. Seventy-one age- and gender-matched subjects with dyspepsia were used as controls. Helicobacter pylori infection was detected in 49 (69%) patients with diabetes and in 33 (46%) subject with dyspepsia (p = 0.007). Helicobacter pylori was present in 27 (77%) of 35 patients with diabetes with dyspeptic symptoms and in 22 (61%) of 36 patients without dyspeptic symptoms. Endoscopy revealed peptic ulcers in 13 of 23 patients; H. pylori infection was histologically confirmed in the gastric antrum of all patients with diabetes, and in the body of the stomach in 74%. The significantly higher prevalence of H. pylori infection in the patients with diabetes may partially explain their dyspeptic symptoms. The high prevalence of H. pylori infection, esophagitis, and peptic ulcers found in our patients with diabetes (with or without dyspepsia) suggests that this population should be considered "at risk" for H. pylori infection and suitable candidates for treatment.
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PMID:Helicobacter pylori prevalence in patients with diabetes and its relationship to dyspeptic symptoms. 1124 46

Electrogastrography is the recording and measurement of gastric myoelectrical activity from electrodes placed on the surface of the epigastrium. Normal electrogastrograms (EGGs) reflect 3 cycles per min (cpm) gastric myoelectrical activity produced by specialized pacemaker cells, the interstitial cells of Cajal, located in the muscular wall of the gastric corpus and antrum. Gastric dysrhythmias (tachygastrias and bradygastrias) are disturbances of the normal gastric pacesetter potentials and are associated with symptoms of nausea, epigastric fullness, and bloating and with hyperglycemia and delayed gastric emptying. In diabetic gastropathy, the normal 3-cpm electrical rhythm is replaced with bradygastrias, tachygastrias, and mixed or nonspecific dysrhythmias. Diagnosis of gastric dysrhythmias identifies an objective neuromuscular abnormality in diabetic patients with upper gastrointestinal (GI) symptoms. Correction of gastric dysrhythmias decreases upper GI symptoms and may improve gastric emptying all of which may enhance glucose control. The EGG diagnosis of gastric dysrhythmias provides new insights into gastric neuromuscular abnormalities and guides therapies to improve upper GI symptoms in patients with diabetes mellitus.
Diabetes Technol Ther 2001
PMID:Electrogastrography: physiological basis and clinical application in diabetic gastropathy. 1146 8

Gastroparesis may be related to a variety of underlying disorders, but diabetes mellitus is by far the most common cause. Symptoms of gastroparesis include early satiety, postprandial bloating, nausea and vomiting. Gastric scintigraphy with 99-technetium-labeled low-fat meal is the gold standard method of diagnosing delayed gastric emptying. Dietary measures and prokinetic drugs bring symptomatic relief in most patients. Some patients with severe nausea and vomiting will require antiemetic medications. Few patients will fail medical therapy and will continue to have debilitating symptoms of gastroparesis; such patients may benefit from a venting gastrostomy or a jejunostomy placed surgically, endoscopically, or fluoroscopically. Gastric electrical stimulation is an exiting new approach in the management of gastroparesis. As the treatment of gastroparesis is far from ideal, nonconventional approaches and nonstandard medications are presented.
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PMID:Gastroparesis and its management. 1209 72

Diabetic gastroparesis is a common and debilitating condition affecting millions of patients with diabetes mellitus worldwide. Although gastroparesis in diabetes has been known clinically for more than 50 years, treatment options remain very limited. Until recently, the scientific literature has offered few clues regarding the precise aetiology of gastric dysfunction in diabetes.Up to 50% of patients with diabetes may experience postprandial abdominal pain, nausea, vomiting and bloating secondary to gastric dysfunction. There is no clear association between length of disease and the onset of delayed gastric emptying. Gastroparesis affects both type 1 (insulin dependent) and type 2 (non- insulin dependent) forms of diabetes. Diagnosis requires identifying the proper symptom complex, while excluding other entities (peptic ulcer disease, rheumatological diseases, medication effects). The diagnosis of gastroparesis may be confirmed by demonstrating gastric emptying delay during a 4-hour scintigraphic study. Treatment options are limited and rely on dietary modifications, judicious use of available pharmacological agents, and occasionally surgical or endoscopic placement of gastrostomies or jejunostomies. Gastric pacing offers promise for patients with medically refractory gastroparesis but awaits further investigation. Current pharmacological agents for treating gastroparesis include metoclopramide, erythromycin, cisapride (only available via a company-sponsored programme) and domperidone (not US FDA approved). All of these drugs act as promotility agents that increase the number or the intensity of gastric contractions. These medications are not uniformly effective and all have adverse effects that limit their use. Cisapride has been removed from the open market as a result of over 200 reported cases of cardiac toxicity attributed to its use. Unfortunately, there is a paucity of clinical studies that clearly define the efficacy of these agents in diabetic gastroparesis and there are no studies that compare these drugs to each other. The molecular pathophysiology of diabetic gastroparesis is unknown, limiting the development of rational therapies. New studies, primarily in animals, point to a defect in the enteric nervous system as a major molecular cause of abnormal gastric motility in diabetes. This defect is characterised by a loss of nitric oxide signals from nerves to muscles in the gut resulting in delayed gastric emptying. Novel therapies designed to augment nitric oxide signalling are being studied.
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PMID:Current concepts in diabetic gastroparesis. 1282 60

Microscopic colitis (MC) encompasses the two morphologically distinct entities of collagenous colitis (CC) and lymphocytic colitis (LC). MC was first described less than 30 years ago but is presently recognized as a relatively common cause of chronic diarrhea in the adult population. Remarkably, up to 10% of adults who have a colonoscopy for the investigation of chronic diarrhea, and have endoscopically normal appearing mucosa, may have MC. Patients with MC generally present with chronic diarrhea, which can be associated with cramping and bloating. Endoscopic and radiological examinations are usually normal. Histological assessment reveals inflammation consisting predominantly of lymphocytic infiltration, and a thickened subepithelial collagen band is diagnostic of CC. Both LC and CC can be associated with autoimmune diseases such as celiac disease, diabetes, arthritis and thyroiditis, yet the mechanisms involved in the pathogenesis remain unclear. Emerging studies suggest that a stepwise approach be taken in the medical management of MC. This approach includes antidiarrheal agents and stopping of any offending agents; budesonide or bismuth subsalicylate; and cholestyramine or 5-acetylsalicylic acid agents. In resistant cases, oral corticosteroids and other immune modulatory therapy have been used.
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PMID:Lymphocytic and collagenous colitis: the emerging entity of microscopic colitis. An update on pathophysiology, diagnosis and management. 1291 15

Gastroparesis is a condition of abnormal gastric motility characterised by delayed gastric emptying in the absence of mechanical outlet obstruction. It is seen commonly in people with diabetes but is idiopathic in a third of patients. Symptoms include nausea and vomiting, post-prandial fullness and early satiety, and abdominal bloating and discomfort. Investigations fall into three categories: gastric emptying studies, intraluminal pressure measurements and recording of gastric myoelectrical activity. Nuclear scintigraphy is considered the gold standard for diagnosing and quantifying delayed gastric emptying. Treatment options include diet and behavioural changes, prokinetic drugs and surgical interventions. New advances in drug therapy and gastric electrical stimulation techniques hold considerable promise.
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PMID:Current perspectives on the management of gastroparesis. 1579 44

Diabetic gastroparesis is a long term complication of diabetes mellitus which could basically be defined as dysregulated gastric emptying leading to various pathological, biochemical and clinical changes in absence of any structural changes. Symptoms include nausea, vomiting, bloating, epigastric pain, anorexia, weight loss and so on. For symptomatic gastroparesis prokinetic drugs like metoclopramide, domperidone, cisapride, erythromycin and itcopride are used. Itopride is currently emerging as a prokinetic drug of choice. There is also scope of surgery.
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PMID:Management of diabetic gastroparesis. 1617 96


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