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)

Intravenous infusion of porcine GIP in man induces insulin release when a degree of hyperglycemia is present. This glucose-dependent insulinotropic response occurs when a dose of GIP is administered to obtain circulating levels of approximately 1 ng/ml, a physiologic level that can be achieved by the ingestion of glucose or corn oil or a mixed meal. Serum GIP was measured by radioimmunoassay, and the single antiserum used in all the described studies measures 2 immunoreactive forms of GIP. In patients with chronic pancreatitis receiving an oral glucose load or mixed liquid test meal, GIP levels have been shown to be exaggerated. Similar elevated responses have been observed in obese patients and in maturity onset diabetes. A reduced GIP response has been seen in patients with celiac disease. A physiologic role for GIP in the enteroinsular axis has been established. However, involvement of the hormone in pathophysiologic situations is equivocal.
 ...
PMID:Clinical studies with gastric inhibitory polypeptide. 51 74

Responses of plasma immunoreactive gastric inhibitory polypeptide (IRGIP) to oral triglyceride or galactose were compared in normal and mildly diabetic (non-insulin-dependent) subjects. After triglyceride the responses of IRGIP were similar, but after galactose those of the diabetics were slightly exaggerated. Both stimuli evoked increments of plasma immunoreactive glucagon (IRG) in diabetics but not in normal subjects. Plasma immunoreactive insulin (IRI) did not change. In normal subjects given oral triglyceride or galactose followed by intravenous (I.V.) glucose the early-phase response of plasma IRI was enhanced and glucose tolerance improved. In the diabetics, oral triglyceride did not affect insulin release or glucose tolerance after I.V. glucose; oral galactose elicited a slight increase of insulin release without improving glucose tolerance. In the diabetics the rise of plasma IRG after ingestion of triglyceride or galactose was maintained after I.V. glucose. It is concluded that endogenous GIP is insulinotropic and that there is partial resistance to this action in diabetes. The results were compatible with feedback inhibition of GIP secretion by insulin and with the suggestion that the rise of plasma IRG associated with secretion of GIP in diabetics may be due to the glucagonotropic action of this peptide.
Diabetes 1978 Mar
PMID:Effects of ingestion of triglyceride or galactose on secretion of gastric inhibitory polypeptide and on responses to intravenous glucose in normal and diabetic subjects. 64 Feb 38

Serum GIP, insulin, and glucose concentrations were determined during a standard oral glucose tolerance test in 80 individuals, 45 of whom were normal and 35 of whom had adult-onset diabetes mellitus according to USPHS criteria. As a group, the diabetics had fasting hyperglycemia (219 +/- 17 mg./dl.) and, in response to glucose, displayed a peak serum glucose of 373 +/- 23 mg./dl. and sustained hyperglycemia (315 +/- 24 mg./dl.) at 180 minutes. There were no statistically significant differences in absolute serum insulin levels between the two groups. However, insulin secretion was delayed, IRI increments were smaller, and the IRI concentrations were inappropriately low for the simultaneous serum glucose concentrations in the diabetics at every time interval tested. Mean fasting serum GIP was 335 +/- 30 pg./ml. in the diabetics as against 262 +/- 15 pg./ml. in normal individuals (p less than 0.025). After the ingestion of glucose, diabetics had significantly higher (p less than 0.001) mean serum GIP levels between five and 120 minutes. By 180 minutes, serum GIP levels remained above fasting in both groups, but the diabetics had higher than normal serum concentrations (p less than 0.05). Peak serum GIP concentrations, which occurred at 30 minutes in both groups, were 1,376 +/- 106 and 806 +/- 75 pg./ml. in the diabetics and normals, respectively (p less than 0.001). Total integrated serum GIP was also greater in diabetics than normals (140,852 +/- 14,208 vs. 64,602 +/- 8,719 pg.-min./ml.-1, p less than 0.001). The higher serum GIP concentrations observed following glucose ingestion in diabetics could not be attributed to obesity or age. We conclude that both fasting and glucose-stimulated GIP concentrations are higher than normal in obese adult-onset diabetics. The significance of this observation is uncertain. However, since our current understanding suggests the GIP may be an important enteric signal for the release of insulin in man, and because GIP has been shown to stimulate the release of immunoreactive glucagon, GIP may play a role in the pathogenesis of diabetes mellitus.
Diabetes 1976 Oct
PMID:Gastric inhibitory polypeptide (GIP) in maturity-onset diabetes mellitus. 97 1

Studies were carried out in conscious dogs in which the immunoreactive gastric inhibitory polypeptide (IR-GIP) response to graded doses of oral fat (triglycerides) and glucose was investigated. The IR-GIP response to the doses of triglycerides used was greater and more prolonged than the response to the glucose loads employed. In addition, the relative insulinotropic potencies of exogenous porcine GIP and IR-GIP released by fat as against those released by oral glucose were assessed. When glucose was administered by the oral route, the immunoreactive insulin (IRI) response was magnified above the IRI response to a comparable intravenous glucose load. The serum IRI response to oral glucose was accompanied by a concomitant rise in serum IR-GIP levels, suggesting a causal relationship. IR-GIP released by oral fat was shown to augment the IRI response to an intravenous glucose load, resulting in an improvement of glucose tolerance. Fat-released IR-GIP augmented IRI levels to a lessor degree than either oral glucose or an infusion of porcine GIP.
Diabetes 1975 Dec
PMID:Gastric inhibitory polypeptide. Its physiologic release and insulinotropic action in the dog. 119 9

Pancreatic endocrine function was studied in 50 patients with cystic fibrosis (CF) and 15 healthy controls by measuring glucose, insulin, C-peptide, glucagon and gastro-inhibitory polypeptide responses to an oral glucose tolerance test (OGTT). Biochemical and clinical parameters were also measured, including glycosylated hemoglobin A1, serum immunoreactive trypsin, fasting urinalysis, pulmonary function, percentage body fat and 3-day dietary records. According to National Diabetes Data Group (NDDG) criteria, 6 CF patients had impaired glucose tolerance (ICF), with elevated serum glucose concentrations and reduced and delayed insulin secretion compared with control (CON) subjects, although none were overtly diabetic. Although the remaining 44 CF patients (NCF) did not meet NDDG criteria for impaired glucose tolerance, mean area under the concentration curve (AUC) for glucose was greater than control values and AUC for insulin diminished. HbA1 levels in the 2 CF groups were greater than that of controls subjects, but there was little difference between ICF and NCF groups. C-peptide levels paralleled those of insulin for the 3 groups throughout OGTT. There was little difference in GIP secretion between groups, and the enteroinsular axis was intact in the control and NCF groups and slightly increased in the ICF group. Basal glucagon concentrations and AUC for glucagon during OGTT were similar for the 3 groups, but glucose-induced glucagon suppressibility i.e., basal to nadir change in each subject, was reduced in the ICF group. Serum IRT concentration was significantly lower in the ICF and NCF groups compared to control subjects, and was lowest in the ICF group. A strong correlation was observed in the ICF group between FEF25-75 and AUC for insulin, as well as HbA1 level and AUC for glucose. The prevalence of impaired glucose tolerance in 50 CF patients was 12%. Despite extensive comparisons of biochemical and clinical parameters with endocrine function in this population, we were unable to define reliable criteria for predicting glucose intolerance.
Diabetes Res 1991 Oct
PMID:Postprandial hyperglycemia and pancreatic function in cystic fibrosis patients. 184 15

A disturbed intraduodenal milieu and pancreatic scarring in advanced chronic pancreatitis (CP) may lead to changes of gut and pancreatic hormones. In the present study, the gastroduodenal mucosal content of several regulatory peptides was determined in 8 patients with severe calcific CP and 8 healthy volunteers. In addition, hormone release into the bloodstream was estimated after intraduodenal acid/glucose stimulation in the control subjects and 8 CP patients each with or without secondary diabetes mellitus (DM), and in 8 patients with juvenile DM, so that disturbed gut hormone release could be attributed either to CP or DM. While VIP release into the circulation was similar in all participants, mucosal levels of VIP and substance P were significantly elevated in the duodenal bulb and descending duodenum of CP patients. The somatostatin content of gastroduodenal mucosa in CP was at least as high as in normals. Gastrin was significantly more abundant only in the duodenal bulb of CP patients, while plasma gastrin was normal. Duodenal CCK concentrations tended to be elevated in the duodenal bulb, but not significantly. The release of secretin seemed to be higher in type-1 diabetics than in CP patients. The mucosal pattern of GIP was nearly identical in CP patients and controls. Compatible with this finding, the GIP release did not show any peculiarities in CP with or without DM or in DM. Basal and stimulated plasma levels of motilin were abnormally high in CP. Pancreatic polypeptide plasma levels were normal in DM, but significantly reduced in CP, especially in CP with DM. Fasting PP and stimulated pancreatic enzyme outputs were linearly related.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Chronic pancreatitis and diabetes mellitus: plasma and gastroduodenal mucosal profiles of regulatory peptides (gastrin, motilin, secretin, cholecystokinin, gastric inhibitory polypeptide, somatostatin, VIP, substance P, pancreatic polypeptide, glucagon, enteroglucagon, neurotensin). 246 85

The study is of double-blind crossover design. In the first part of the study, rioprostil (300 micrograms and 600 micrograms) is given orally with a solid breakfast to 9 healthy male volunteers. Both doses of rioprostil delay and reduce the 3-h postprandial GIP release. They also reduce the maximal postprandial insulin concentration, but only rioprostil (600 micrograms) reduces the 3-h integrated release of insulin significantly (by approximately 20%). Neither dose modifies the postprandial glucose gastrin levels significantly. In another study two groups of 6 volunteers are studied in parallel; they are given either rioprostil (600 micrograms) or a placebo each evening for 14 days. On the mornings before and on days 13 and 14 of the study the volunteers take a solid breakfast and blood glucose is measured 1 h and 2 h postprandially. The results show that no differences in the basal and postprandial glucose levels are observed. In conclusion, rioprostil given with a meal can reduce the insulin release but it does not change the postprandial blood glucose levels when given as a single dose or repeatedly in an evening dose. This study shows that rioprostil can be given to patients with diabetes.
 ...
PMID:Effects of rioprostil on the postprandial glucose, GIP, insulin and gastrin levels in volunteers. 251 Feb 53

The authors wanted to test the long-term effectiveness of immunoisolation in the NOD mouse, an adequate model of Type I diabetes. Recipients were diabetic female NOD mice with sustained plasma glucose levels above 400 mg/100 ml. They were grafted intraperitoneally with permselective hollow fibers seeded with human insulinoma (n = 6), rodent insulinoma (n = 6), or human islets (n = 6). Controls were 15 nontreated diabetic females and 10 nondiabetic male NOD mice implanted with nonseeded macrocapsules. Electron microscopy (rectangular crystalline nucleoids characteristic of B-cells), in vitro release of insulin (during abrupt changes in glucose concentration from 40 to 400 mg/dl and return, M +/- SD insulin levels were 122 +/- 5 uu/ml and 315 +/- 17 at low and high glucose), evidence of binding hormone receptors (VIP and GIP, the binding sites being coupled with adenylyl cyclase stimulation) were used to assess the quality of the transplant. Survival was always prolonged in grafted animals. Taking complete and long-term (less than 3 months) correction of hyperglycemia as the criterion, the success rate was about 50% as observed in streptozotocin rats. Splenocytes isolated from cured and not cured recipients and injected into irradiated nondiabetic male NOD mice were always able to transfer the disease. Our bioartificial pancreas is efficient in preventing the recurrence of the disease in autoimmune diabetes.
 ...
PMID:Bioartificial pancreas in autoimmune nonobese diabetic mice. 284 60

Addition of purified fiber to carbohydrate test meals has been shown to flatten the glycemic response in both normal and diabetic volunteers, reduce the insulin requirement in patients on the artificial pancreas and in the longer term reduce urinary glucose loss and improve diabetes control. In the context of high fiber-high carbohydrate diets these findings have had a major impact in influencing recommendations for the dietary management of diabetes internationally. The mechanism of action appears in part to be due to the effect of fiber in slowing absorption rather than by increasing colonic losses of carbohydrate. Consequently postprandial GIP and insulin levels are reduced and the more viscous purified fibers (e.g., guar and pectin) appear most effective. In addition it has been suggested that colonic fermentation products of fiber may enhance glucose utilization. More recently it has become clear that many aspects of carbohydrate foods (food form, antinutrients, etc.) in addition to fiber may influence the rate of digestion and has led to a classification especially of starchy foods in terms of glycemic index to define the degree to which equicarbohydrate portions of different foods raise the blood glucose. Use of such data may maximize the effectiveness of high carbohydrate and high fiber diets in the management of diabetes and related disorders.
 ...
PMID:Dietary fiber and the glycemic response. 300 40

Measurements of various aspects of glucose, insulin and lipid metabolism were made before and after the administration of enprostil (a synthetic dehydroprostaglandin E2) for one week to ten patients with non-insulin-dependent diabetes mellitus (NIDDM). Both fasting (P less than 0.01) and postprandial (P less than 0.001) plasma glucose concentrations were significantly lower after one week of enprostil, and 24 hour urinary glucose excretion was reduced from (mean +/- SEM) 47 +/- 14 to 25 +/- 9 g/day. There was no change in either fasting or postprandial insulin concentration, but the postprandial GIP response was also significantly reduced (P less than 0.001). In addition, there were significant reductions in postprandial plasma free fatty acid (P less than 0.05) and triglyceride (P less than 0.001) concentrations, associated with a modest fall in fasting plasma triglyceride (P less than 0.05) and cholesterol (P less than 0.07) concentrations when measured after one week of treatment with enprostil. These results raise the possibility that enprostil may be of some benefit in the treatment of patients with non-insulin-dependent diabetes.
 ...
PMID:Effect of enprostil on plasma glucose, insulin and lipid metabolism in patients with non-insulin-dependent diabetes mellitus. 314 38


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