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

Some neurochemical changes in the gut of rats after five weeks of alloxan-induced diabetes were investigated. It was found that at this stage of diabetes the changes were restricted mainly to the small intestine with a special selectivity for the duodenum. No changes were found in the most part of the large intestine and rectum. The methionine-enkephalin content was markedly reduced throughout the small intestine, while vasoactive intestinal polypeptide was increased in duodenum, ileum and caecum. Substance P content was unaffected, while at later stages of the disease it was significantly reduced in the entire small intestine. Sympathetic noradrenaline and intrinsic serotonin contents were significantly increased in the duodenum and unchanged throughout the rest of the intestine. These data suggest that the small intestine and caecum might be the early target of diabetic autonomic neuropathy, that might involve progressively the rest of the large intestine at later stages as recent results have suggested. It is likely that the gastrointestinal dysfunctions, often present in diabetic patients, might also be due to the combined pre-synaptic alterations, and to the functional imbalance between Gs and Gi/Go transduction proteins recently reported. Insulin therapy, begun seven days after alloxan treatment, reduced drastically the hyperglycaemia, restored normal body growth and prevented all the gut neurochemical changes associated with alloxan-induced diabetes.
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PMID:Early neurochemical changes in the autonomic neuropathy of the gut in experimental diabetes. 128 97

Autonomic neuropathy and gastrointestinal problems are among the most common complications of diabetes. In this report it is shown that a possible correlation between the two disorders might exist, since diabetes causes a profound alteration of the peptidergic innervation of the gut. It is reported that 14 weeks after diabetes induction with alloxan the levels of substance P and methionine-enkephalin are markedly reduced throughout the intestine, while vasoactive intestinal polypeptide content is dramatically increased. Therefore the enteric innervation of diabetic animals is completely disorganized, with some systems undergoing atrophy and others undergoing hypertrophy. Treatment of diabetic animals with acetyl-L-carnitine prevents the onset of the marked peptide changes described above. The results suggest a potential for acetyl-L-carnitine in the treatment of autonomic neuropathies.
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PMID:Peptide alterations in autonomic diabetic neuropathy prevented by acetyl-L-carnitine. 128 98

The ester methyl [4-[2-[(2-hydroxy-3-phenoxypropyl)amino]ethoxy]phenoxy]acetate (1) (R1 = OMe) had previously been identified as the most interesting member of a series of selective beta 3-adrenergic agonists of brown adipose tissue and thermogenesis in the rat. In vivo it acts mainly via the related acid 1 (R1 = OH). Amides have been examined to determine whether they have advantages over the ester. In particular, in the rat and dog the half-lives of amides of appropriate potency were no longer than those of the ester. The amide (S)-4-[2-[(2-hydroxy-3-phenoxypropyl)amino]ethoxy]-N-(2- methoxyethyl)phenoxyacetamide [S-27, ICI D7114] was selected as having properties consistent with a sustained-release formulation should that prove necessary. Unlike the ester it is resistant to hydrolysis in the gut lumen. Further testing of ICI D7114 has shown that in the rat, cat, and dog it stimulates the beta 3-adrenergic receptor in brown adipose tissue at doses lower than those at which it affects beta 1- and beta 2-adrenergic receptors in other tissues. Slimming effects were observed in the dog. ICI D7114 may be a selective thermogenic agent in man and may be useful in the treatment of obesity and diabetes.
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PMID:Selective beta 3-adrenergic agonists of brown adipose tissue and thermogenesis. 2. [4-[2-[(2-Hydroxy-3-phenoxypropyl)amino]ethoxy]phenoxy]acetamides. 135 Mar 10

The paper describes three patients with small intestinal necrosis from different causes: One patient had diabetes, and severe ketoacidosis, which may cause microthrombosis in small intestinal vessels. This patient died in septic shock during laparotomy, removing the necrotic gut. The second patient was laparotomized because of free air in the abdomen originating from a clostridial intestinal infection. The third patient caught a salmonella infection during a holiday in the Canaries, thereafter peritonitis due to small intestinal necrosis. These three patients illustrate principal aspects of the surgical management of patients with intestinal necrosis. Firstly, necrotic intestinal segments must be removed as soon as possible. Delay represents a threat to the patient's life in all situations when intestinal segments are devascularized. Secondly, relaparotomy may be mandatory in clostridial intra-abdominal infections. We report these patients to illustrate that well known surgical principles may be life-saving if effectuated without delay. This applies also in the case of patients with uncommon diseases and complications.
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PMID:[Necrosis of the small intestine. A diagnostic and therapeutic challenge]. 141 9

Gut transit using radiopaque markers was assessed in 5 healthy subjects and 24 diabetic patients. In the diabetics, various parameters including duration of the disease and diabetic complications, such as neuropathy, retinopathy and nephropathy, were determined, and the relationships between gut transit times and these complications were evaluated. The effect of cisapride on gut transit was studied in 10 diabetic patients. Large intestinal, descending colon, distal colon, and whole gut transit times were delayed in diabetics with autonomic neuropathy compared to controls and to diabetics without autonomic neuropathy (P less than 0.01). There was no difference in proximal colon transit times among them. An inverse correlation was observed between CVRR and the transit times for descending colon, distal colon, large intestine and whole gut. Large intestinal and whole-gut transit times were delayed in diabetics with retinopathy or with nephropathy compared to diabetics without those complications (P less than 0.01). In the diabetics, oral administration of 7.5 mg/day of cisapride for 2 weeks significantly accelerated descending colon transit (P less than 0.05) and partially accelerated distal colon, large intestinal and whole-gut transit. It is concluded that diabetics with autonomic neuropathy have delayed transits for the whole gut and that this finding is apparent to some extent in the distal colon but not in the proximal colon. Chronic oral administration of cisapride, a gastrointestinal prokinetic drug, was effective to improve these gastrointestinal motility disorders in diabetics with autonomic neuropathy.
Diabetes Res Clin Pract 1992 Aug
PMID:Segmental gut transit in diabetes mellitus: effect of cisapride. 142 48

Twenty six patients with insulin dependent diabetes mellitus underwent a gastric emptying test, a gall bladder contraction test, an orocaecal transit study, and a colon transit test. Eleven patients had signs of cardiovascular autonomic neuropathy, 15 patients were without signs of cardiovascular autonomic neuropathy. Mean gastric clearance of radioopaque markers ingested with a meal averaged 29.5 (2.3) markers per six hours in subjects without cardiovascular autonomic neuropathy compared with 17.8 (2.3) markers per six hours in patients with cardiovascular autonomic neuropathy (p < 0.02). Gall bladder emptying in response to graded CCK8 stimulation was impaired in five of 11 patients with cardiovascular autonomic neuropathy, whereas it was normal in the patients without cardiovascular autonomic neuropathy (p < 0.01). Oral caecal transit times were not significantly different in the two patient groups, whereas colonic transit was slower in the patients with cardiovascular autonomic neuropathy compared with the group without cardiovascular autonomic neuropathy (p < 0.02). There was no correlation between disturbed gastric clearance, impaired gall bladder contraction, and prolonged colonic transit time in the patients with cardiovascular autonomic neuropathy nor was there a correlation between any disturbed motor function and age or duration of diabetes. It is concluded that autonomic neuropathy can affect motor functions throughout the gastro-intestinal tract. Any disturbed motor function in the gut could therefore be one of the numerous expressions of diabetic neuropathy affecting the cardiovascular, the endocrine or the gastrointestinal system.
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PMID:Non-invasive assessment of gastrointestinal motility disorders in diabetic patients with and without cardiovascular signs of autonomic neuropathy. 142 71

Percutaneous endoscopic gastrostomy (PEG) is used to provide nutrition for patients who are unable to eat but have a functionally intact gut. Clinical guidelines for PEG are uncertain and have been derived mainly from referral practices. We performed a population-based cohort study in 97 residents of Olmsted County, Minnesota, referred for PEG between January 1982 and December 1988 to determine complications, duration of tube feeding, and survival. Follow-up continued until death or February 1990. Inpatient and outpatient records were reviewed to determine indications, comorbid conditions, level of consciousness, and limitations in activities of daily living. Outcomes determined after referral for PEG included type and number of complications, tube removal, and survival. Statistical methods used included Kaplan-Meier and proportional hazards regression analyses. PEG placement was successful in 94% of patients. Although complications occurred in 70% of patients, they usually were minor (88%) and most occurred within 3 months. In 24 patients, tubes were removed because eating was resumed. The probability of surviving 30 days, 1.5 years, and 4 years after referral for PEG was 78%, 35%, and 27%, respectively. The major causes of death within and after 30 days were pneumonia, heart disease, and vascular disease of the central nervous system. An increased risk of death after referral for PEG placement was associated with older age, male gender, diabetes, and specific indications for PEG. If validated in other population-based studies, these predictors of survival after referral for PEG placement could be used to identify patients with a low probability of survival who may not benefit from PEG.
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PMID:Predictors of outcome after percutaneous endoscopic gastrostomy: a community-based study. 143 74

Mucormycosis is an opportunistic infection that has been mainly described in adults with preexisting disease affecting immune status, eg, diabetes, leukemia, lymphoma, and renal failure on peritoneal dialysis. Few cases have been described in neonates. The presentation of mucormycosis as a cause of neonatal necrotizing enterocolitis is an unusual phenomenon. Three fatal cases of mucormycosis of the gut in premature infants in the period 1990 to 1991 are described. It is not clear whether this should be considered a separate disease or a variant of necrotizing enterocolitis. All three patients died soon after laparotomy from septic shock and the histological diagnosis of mucormycosis was made too late for effective chemotherapy.
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PMID:Mucormycosis of the neonatal gut: a "new" disease or a variant of necrotizing enterocolitis? 150 Oct 34

To investigate the mechanism of oral carbohydrate-stimulated secretion of the two most potent incretin candidates, gastric inhibitory polypeptide (GIP) and truncated glucagon-like peptide-1 (tGLP-1), we studied the changes in the plasma levels of these peptides in five healthy men after sucrose ingestion with or without pretreatment with an alpha-D-glucosidase inhibitor (AO-128). After sucrose ingestion, plasma levels of GIP peaked at 15 min and remained high up to 120 min. Plasma levels of GLP-1 NT measured with antiserum R1043 (N-terminal specific) tended to decrease gradually and those of GLP-1 CT measured with antiserum R2337 (C-terminal specific) increased. Therefore, estimated plasma levels of tGLP-1 increased markedly within 30 min, then declined slightly over the next 60 min. After treatment with AO-128 (0.6 mg/day) for 1 week, increases in plasma glucose and insulin levels were attenuated and the increase in plasma GIP levels was diminished, while the increase in tGLP-1 levels was sustained much longer. It is concluded that GIP secretion is stimulated by glucose absorption and tGLP-1 secretion by the presence of sucrose in the gut.
Diabetes Res Clin Pract 1992 Mar
PMID:Differences in glucagon-like peptide-1 and GIP responses following sucrose ingestion. 157 19

Gastric inhibitory polypeptide (GIP), a hormone secreted from the proximal small gut, is recognized as a major component of the enteroinsular axis. However, circulating levels of GIP in diabetes have been reported to be exaggerated, normal or decreased following glucose ingestion, which may be due to the presence of variable crossreacting immunoreactive GIP forms in the circulation. We have raised an antibody (S705) which recognizes only 5 kDa GIP. Using this antiserum we have measured circulating GIP levels in 18 healthy volunteers, and 13 Type 2 diabetic and 9 Type 1 diabetic patients following ingestion of 75 g glucose. As expected, blood glucose levels and blood insulin levels are significantly abnormal in the diabetic groups. On the other hand, circulating GIP levels at all time-points and integrated incremental GIP over 120 min were not different from the control group. However, we cannot exclude the possibility that apparently normal immunoreactive GIP levels in diabetes might conceal subtle alterations in biological activity which could play a role in the pathogenesis of the disease.
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PMID:Gastric inhibitory polypeptide (GIP) response in diabetes using a highly specific antiserum. 164 2


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