Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Depressed somatic growth in the rat with streptozotocin diabetes is associated with greatly enhanced intestinal growth. In patients with diabetes mellitus, growth hormone is elevated. Therefore, we measured the association between gut growth and serum growth hormone in the streptozotocin-diabetic rat. At 10 days growth hormone did not differ in control, untreated diabetic and insulin-treated diabetic groups. At 20 days of diabetes, growth hormone was elevated in untreated diabetic groups, but depressed to control levels by insulin. Intestinal growth was markedly elevated in all diabetic groups by 10 days, prior to the increases in hormone levels. We conclude that the enhanced intestinal growth in diabetes is probably independent of growth hormone.
 ...
PMID:Increased intestinal growth in the streptozotocin-diabetic rat occurs prior to changes in hormone secretion. 306 58

To see what effect intraluminal amino acids would have on glicentin secretion, we put a mixture of 10 amino acids (1 g/kg) into the duodenum of five normal, conscious piglets. Their plasma nitrogen rose, as did insulin and glucagon measured with C-terminal-specific antiserum. Plasma total immunoreactive glucagon, determined with non-specific antiserum, rose from 2753 +/- 460 pg/ml to a peak of 4434 +/- 1352 pg/ml at 30 min. Plasma glicentin, determined with R 64 antiserum, rose from a fasting level of 297 +/- 70 pmol/l to a peak of 702 +/- 167 pmol/l at 45 min. We also gave oral arginine to 6 pancreatectomized dogs to investigate why the plasma glicentin rises after amino acid ingestion. Arginine raised the plasma total immunoreactive glucagon from 1120 +/- 214 pg/ml to a peak of 2266 +/- 512 pg/ml at 45 min. We conclude that intraluminally administered amino acids enhance glicentin secretion from the gut.
Diabetes Res Clin Pract 1988 Oct 14
PMID:Effect of intraluminal administration of amino acids upon plasma glicentin. 306 8

Glucagon-like peptide-1 (GLP-1) (1-37) and the fraction derived from it, GLP-1 (7-36 amide), are peptides encoded by the preproglucagon gene and possibly co-secreted with enteroglucagon. When added at a 25-nM concentration, GLP-1 (7-36 amide) decreased the release of glucagon from the perfused rat pancreas from 68.5 +/- 9.0 pg/ml to 41.5 +/- 11.5 pg/ml at 2 min in the presence of 11.2 mM glucose (P less than 0.01), and from 196.0 +/- 32.5 pg/ml to 87.0 +/- 23.5 pg/ml at 5 min in the presence of 2.8 mM glucose (P less than 0.05). Insulin levels increased from 12.6 +/- 3.0 microU/ml to 48.9 +/- 14.0 microU/ml at 10 min in the presence of 11.2 mM glucose (P less than 0.05) and from 2.0 +/- 0.4 microU/ml to 8.2 +/- 2.3 microU/ml at 2 min in the presence of 2.8 mM glucose (P less than 0.05). Glucagon and insulin release were not affected significantly by GLP-1 (1-37), irrespective of glucose concentration. We suggest that GLP-1 (7-36 amide) rather than enteroglucagon may be the true physiologic gut hormone and that it may act as 'incretin' in the enteroinsular axis. We suggest further that the glucagonostatic and insulinotropic activities of this peptide are unique and might be important in islet-cell function.
Diabetes Res Clin Pract 1988 Oct 14
PMID:Glucagon-like peptide-1 (7-36 amide): a potent glucagonostatic and insulinotropic hormone. 306 10

Due to the importance of diet in the management of noninsulin dependent diabetes, we are interested in constructing a model to study the glycemic response to different foods in normal and diabetic subjects. In this study, serum glucose and insulin values from individual normal subjects (Diab. 26, 1178) following the ingestion of different foods (corn, rice, bread, potato) high in complex carbohydrate were analyzed to determine glucose infusion rates (J) into the blood from the gut as a function of time following the ingestion of the food item. A Modular Modeling Program was designed to allow selection of data, curve fit, model, and tuning of parameters. The two models used were from Ackerman et al (Phys. Med. Biol. 9, 203) and the minimal model (VI) from Bergman and Cobelli (Fed. Proc. 39,110). The models were modified so that glucose and insulin values were used as input and J was the output. There was a good correspondence between the shape of the J curves predicted by the two models. While the J curves resembled serum glucose curves, they generally reached a peak earlier and declined more rapidly. Two peaks occurred in the J curves for bread, corn and rice. The second peaks may correspond to a delay in the release of glucose during digestion. The resulting infusion rate characterization of these foodstuffs maybe useful for modeling responses in diabetic patients with normal gut function but with impaired peripheral glucose utilization and in detecting abnormal gut function.
 ...
PMID:Glucose infusion rates from various complex carbohydrates estimated from two models. 307 7

Studies have indicated that verapamil inhibits insulin release from pancreatic beta cells in vitro. Studies in this clinic, however, showed that both oral pretreatment with verapamil for 1 week and intravenous infusion of the drug over a period of 3 hours improved oral glucose tolerance in patients with type II diabetes without affecting insulin release. In contrast, verapamil failed to increase further the hypoglycemic effect of oral glibenclamide therapy when administered intravenously in diabetic patients. This hypoglycemic effect of verapamil does not appear to be caused by reduced glucose absorption from the gut because intravenous infusion of verapamil left the portal vein glucose response to glucose ingestion unaffected in normoglycemic patients who underwent portal vein catheterization for diagnostic purposes. It is more likely that verapamil affects the liver, leading to decreased hepatic glucose output, which supports previous reports that have shown an inhibitory influence of verapamil on enzymes involved in the gluconeogenetic and glycogenolytic processes.
 ...
PMID:Influence of verapamil on human glucose tolerance. 308 74

Using the charcoal meal test, the effects of morphine (3, 5 and 7 mg/kg) on gastrointestinal transit was assessed in normoglycemic as well as in acute and chronic hyperglycemic mice. Acute hyperglycemia was induced by intraperitoneal injection of glucose (5.04 g/kg), while chronic hyperglycemia was induced by streptozotocin injection (200 mg/kg i.p., 7-8 days before). Acute hyperglycemia augmented the inhibitory effect of morphine on gut transit, however, chronic hyperglycemia failed to modify the effects of morphine. The results indicate that hyperglycemia per se may not be the primary mechanism for the altered sensitivity to morphine in experimental models of diabetes.
 ...
PMID:Effects of acute and chronic hyperglycemia on morphine-induced inhibition of gastrointestinal transit in mice. 323 59

It has been suggested that the gut hormone cholecystokinin (CCK), by modulating insulin output from pancreatic beta-cells, plays an important role in the enteroinsular axis. To investigate this hypothesis, eight rats were studied on two different occasions: after injection of L 364718, a specific antagonist of CCK binding to its membrane receptor, and after vehicle injection. In both studies a mixture of casein (11%) and glucose (9%) was infused through a chronic indwelling intraduodenal catheter to evoke CCK secretion. Plasma was analyzed for insulin, glucose, glucagon, and tyrosine many times during the procedure. Prior administration of the CCK antagonist significantly attenuated the increase in plasma insulin and glucagon after casein infusion. These results support the concept that cholecystokinin plays an important physiologic role in the in vivo regulation of postprandial plasma insulin and glucagon concentrations after protein ingestion.
Diabetes 1987 Oct
PMID:Physiological role of cholecystokinin in meal-induced insulin secretion in conscious rats. Studies with L 364718, a specific inhibitor of CCK-receptor binding. 330 89

Diarrhea is a common symptom in long-standing diabetes. The pathogenesis of this diarrhea remains obscure, although it appears to be related to the development of autonomic neuropathy, which may cause several abnormalities including altered gut motility. We studied fasting gastrointestinal motility for a mean of 210 min in a group of 12 type-II diabetics with diarrhea. All patients had peripheral neuropathy and symptoms of autonomic neuropathy. Their motor activity was compared with that of a group of six normal volunteers. In addition, gastrointestinal transit time was assessed by the hydrogen breath test. The presence of bacterial overgrowth was assessed by the hydrogen breath test and culture of jejunal secretions. The diabetics showed grossly disordered motor activity. There was a complete absence of phase-III activity in two patients. Most phase III's commenced in the distal duodenum or jejunum. The phase-III component was often of short duration at each recording site. There was increased velocity of propagation between sites. Continuous phase-II activity was noted in some patients. Antral activity was absent or reduced during phase II. Gastrointestinal transit time was significantly prolonged in the diabetics. Bacterial overgrowth was demonstrated in three diabetic subjects. These motility abnormalities are nonspecific and are unlikely to play a major role in the pathogenesis of diabetic diarrhea.
 ...
PMID:Abnormalities of the migrating motor complex in diabetics with autonomic neuropathy and diarrhea. 336 94

A monoclonal islet cell antibody, HISL-19, reactive with human, bovine, and porcine pancreatic islets has been used to identify and characterize a novel group of islet cell proteins (p120, p69, p67, and p56). Besides the islets, HISL-19-reactive antigenic determinants are also expressed on selected cell types, namely, gut endocrine cells, thyroid parafollicular cells (p120), anterior pituitary cells (p40 and p24), specific hypothalamic neuroendocrine cells, and a single layer of large pyramidal cells of the cerebral cortex, thus defining a new family of neuroendocrine molecules.
Diabetes 1986 Mar
PMID:Islet cell proteins defined by monoclonal islet cell antibody HISL-19. 351 40

There is general agreement as to the effects of diabetes on the concentrations of certain plasma lipoprotein lipids. Subdivision of diabetic subjects into several clearly defined subgroups has revealed that the detailed patterns of lipoprotein and lipid changes are dependent upon several factors, perhaps the most important of which is the degree of glycaemic control. Several aspects remain controversial, the most outstanding being whether or not plasma LDL cholesterol levels are elevated. It is possible that this is the case in certain clearly defined subgroups but not in others. In assembling the results of recent research for this review, two important aspects have emerged which require clarification. The first is the question of whether or not insulin directly stimulates hepatic VLDL secretion. The possibility that insulin might regulate production of lipogenic substrate by the gut may have an important bearing on this problem. The exact means by which insulin co-ordinates the metabolic activities of these organs in such a way as to ensure plasma lipid balance is not yet known and further research in this area may help to resolve some outstanding problems associated with diabetic hyperlipidaemia. Second, changes in the relative lipid composition of certain lipoprotein fractions in diabetic subjects has provided indirect evidence that increased lipoprotein 'remnant' concentrations may contribute to the abnormalities observed in some groups of diabetic subjects. This interesting possibility has been supported by metabolic studies, mainly in experimental animals. If this proves to be correct, then it remains to be determined whether the remnants involved are of hepatic or intestinal origin and whether the metabolic defect is related to abnormal production, clearance, or both. Recent work on the effects of changes in the apoprotein and lipid content on the metabolism of other lipoproteins in diabetes may have a useful bearing on studies of this type. In this respect, the bulk of the evidence seems to suggest that these factors, rather than changes in lipoprotein receptor activity per se, are important in determining the clearance of atherogenic lipoproteins such as LDL in diabetes.
 ...
PMID:Hyperlipidaemia of diabetes. 353 93


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>