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

In order to elucidate the mechanisms of the action of gel-forming fibre in diabetes, we measured insulin, C-peptide and GIP responses to meals during treatment with guar gum and placebo in normal and non-insulin-dependent diabetic (NIDD) subjects. Dietary supplementation with guar gum caused a sustained reduction of the GIP response in normal and diabetic subjects (p less than 0.05), but did not influence insulin responses. On the other hand, guar gum increased the C-peptide response to meals in normal subjects (p less than 0.05) resulting in a 40% decrease of the insulin/C-peptide ratio (p less than 0.01). Assuming that the insulin/C-peptide ratio reflects the hepatic extraction of insulin, this would be compatible with increased hepatic removal of insulin. The change in insulin/C-peptide ratio was positively correlated with the change in GIP response after guar gum (r = 0.75; p less than 0.001) and this correlation was strengthened in normal subjects (r = 0.91; p less than 0.001). Our data thus suggest that guar gum stimulates rather than suppresses insulin secretion. The apparent insulinotropic action of GIP may partly be explained by a reduced hepatic extraction of insulin.
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PMID:Relationship between changes in GIP concentrations and changes in insulin and C-peptide concentrations after guar gum therapy. 353

The changes in plasma concentrations of immunoreactive gastric inhibitory polypeptide (IR-GIP) in response to a standard meal were examined in 21 normal subjects and 15 Type 1 (insulin dependent) diabetic patients 7 days, 14 days, and 3, 6, 9, 12, and 18 months after time of diagnosis. During the first 4 tests significantly lower plasma IR-GIP concentrations were found in the diabetic patients after the standard meal. At 9 months and during the remaining tests there was no difference in IR-GIP concentrations between the diabetic and the normal subjects. The IR-GIP response was normalized faster if the diabetic patients were treated with initial short term intensive insulin therapy than if they were treated conventionally with 1 or 2 daily injections of insulin. beta-Cell function, evaluated by the C-peptide response to the meal, increased significantly during the first 3 months. After 3 months maximal beta-cell function was found while the corresponding IR-GIP responses were significantly lower than those of the normal subjects. Thereafter beta-cell function declined gradually and significantly, coinciding with the normalization of the IR-GIP response. No individual covariation between IR-GIP and beta-cell function during the 18 months was found in any patient. The IR-GIP response to a meal was diminished at the onset of Type 1 (insulin dependent) diabetes mellitus. After the start of insulin therapy the response improved, perhaps as a function of the quality of metabolic control, and within a year it was comparable to that of normal subjects. Lack of endogenous GIP therefore does not explain the diminished beta-cell function in Type 1 diabetes a few months after onset of the disease. No causal relationship between the changes in beta-cell function and IR-GIP during the first 18 months after the onset of the disease seems to exist.
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PMID:Immunoreactive gastric inhibitory polypeptide response to a meal during the first eighteen months after diagnosis of type 1 (insulin dependent) diabetes mellitus. 388 May 59

Food can affect the production and secretion of hormones by direct actions on the gut, by nervous reflexes, through changes in the concentration of various metabolites in the blood, or secondary to changes in circulating gut hormone levels. Not only is the composition of the diet important but also its texture, quantity and duration. GIP and insulin are used as examples of hormones whose production and secretion are diet-dependent. Their possible involvement in the pathogenesis of obesity and non-insulin-dependent (type II) diabetes is discussed.
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PMID:How our food affects our hormones. 388 42

Experimental and clinical work over the last 6 years has confirmed and broadened, but also challenged, the incretin concept. The nervous component of the entero-insular axis is still poorly defined, especially the peptidergic nerves, of which several contain insulinotropic regulatory peptides. The incretin effect is preserved after complete denervation of the porcine pancreas. Type 2 (non insulin-dependent) diabetic patients have a significantly decreased incretin effect. GIP (gastric inhibitory polypeptide; glucose dependent insulin releasing peptide) remains the strongest incretin factor. Its secretion depends on the absorption of nutrients. However, the correlation between the GIP response and disturbances of the entero-insular axis in some gastrointestinal diseases and, in particular, Type 2 diabetes, is poor. Furthermore, physiological concentrations of exogenous GIP do not produce fully the incretin effect and injection of GIP antibodies does not abolish the incretin effect. This suggests the existence of additional humoral incretin factors. On the other hand, GIP seems to have direct metabolic effects independent of its insulinotropic activity. The incretin effect of oral glucose is smaller if plasma levels of C-peptide rather than insulin are measured. However, decreased hepatic extraction of insulin after glucose ingestion only accounts partially for the incretin effect. GIP is unlikely to be the gut factor which regulates hepatic insulin extraction.
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PMID:New developments in the incretin concept. 390 45

In a single-blind randomized placebo-controlled cross-over study in hypertensive patients we have examined the effects of treatment with the non-selective beta-adrenoceptor antagonist nadolol on the responses of glucose, intermediary metabolites and the hormones of the enteroinsular axis to the ingestion of a mixed meal. During treatment with nadolol the plasma insulin concentration 30 min after ingesting the meal was significantly lower than on placebo and the plasma glucose rose more slowly. Plasma concentrations of GIP tended to be higher during nadolol than placebo treatment. No significant effects of treatment with nadolol were noted on pancreatic glucagon or intermediary metabolites.
Diabetes Res 1985 May
PMID:The effect of chronic treatment with a non-selective beta-adrenoceptor antagonist on the enteroinsular axis and intermediary metabolites. 390 82

The available data show that GIP is at present the strongest candidate for the insulin-secreting factor of the gut named incretin. Its release is triggered by the absorption of ingested nutrients. GIP acts on the B-cells of the pancreas by potentiating glucose-induced insulin secretion. The role of GIP as an enterogastrone is less well established. The release of GIP from the gut cells seems to be regulated by the composition and the amount of the ingested food, by the rate of absorption of nutrients by neural factors (vagal), and by feedback control mediated by insulin. In addition, the adaptation of the intestine to individual eating habits influences the response of the GIP cells. It is suggested that an overactive enteroinsular axis, i.e. enhanced GIP secretion, participates in the development of the hyperinsulinaemia of obesity and maturity onset diabetes mellitus. In gastrointestinal diseases accompanied by malabsorption the GIP response is diminished. In gastrointestinal disorders with rapid gastric emptying (duodenal ulcer) or with accelerated passage of the nutrients through the intestine, hypersecretion of GIP and insulin occurs. This may be significant for the reactive hypoglycaemia of these conditions.
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PMID:Gastric inhibitory polypeptide. 610 91

The role of GIP in the pathogenesis of spontaneous syndromes of obesity-diabetes was examined in ob/ob mice of the Aston stock and db/db mice of the C57BL/KsJ background. Compared with lean controls, fed adult ob/ob and db/db mice, respectively, exhibited 1.8-fold and 2.1-fold increases in body weight, 1.8-fold and 2.8-fold elevations of plasma glucose, and 15.4-fold and 5.6-fold elevations of plasma insulin. As indicated by the relative magnitude of the hyperglycemia and hyperinsulinemia, db/db mice displayed a particularly severe form of diabetes. Plasma GIP concentrations of ob/ob and db/db mice were elevated 15.1-fold and 6.2-fold, respectively; the increments closely corresponded with the degrees of hyperinsulinemia. Small intestinal weight was increased 1.4-fold and 1.8-fold in ob/ob and db/db mice, respectively, but the intestinal GIP content expressed as microgram/g intestine or microgram/intestine was raised only in ob/ob mice (1.9-fold and 2.8-fold, respectively). Since glucose stimulation of insulin release is defective in both mutant strains, the results strongly implicate pathologically raised GIP concentrations in the hyperinsulinemia and related metabolic abnormalities of the obesity-diabetes syndromes. It is suggested that hypersecretion of GIP results in part from loss of normal feedback inhibition by endogenous insulin.
Diabetes 1983 May
PMID:Abnormalities of GIP in spontaneous syndromes of obesity and diabetes in mice. 634 Nov 26

The release of immunoreactive gastric inhibitory polypeptide (IR-GIP) in response to a standard meal was examined in 10 normal subjects and 15 type I (insulin-dependent) diabetics 7 days (test I), 14 days (test II), and 3 months (test III) after time of diagnosis. During all three tests, the diabetics had significantly lower plasma IR-GIP concentrations than the controls from 15-90 min after the standard meal. The IR-GIP response in the diabetics measured as the integrated area under the response curve corresponded to 70% of that of normal subjects. beta-cell function evaluated from the C-peptide response to the meal increased significantly from test I to test III whereas the IR-GIP response was similar during all three tests. As GIP is known to potentiate glucose-induced insulin secretion and possibly the biosynthesis of insulin, the low IR-GIP responses in subjects with type I diabetes may significantly influence insulin levels and hyperglycemia.
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PMID:Diminished immunoreactive gastric inhibitory polypeptide response to a meal in newly diagnosed type I (insulin-dependent) diabetics. 634 93

To study the role of enteroinsular hormones in fetal macrosomia and neonatal hypoglycemia in infants of diabetic mothers, we measured plasma concentrations of free and total immunoreactive insulin, C-peptide, pancreatic glucagon, enteroglucagon, and gastric inhibitory polypeptide at birth in 35 IDMs and 35 infants of normal mothers. Twenty fasting adults of normal weight were also studied. Sixteen IDMs were macrosomic at birth; 17 developed neonatal hypoglycemia over the first postnatal hours. The IDMs had ten times higher concentrations of free IRI than the normal infants in cord blood. Free IRI concentrations were related to the severity of maternal diabetes, with the infants of white class D to F mothers having the highest levels. The IDMs with macrosomia had a twofold increase in the concentrations of free IRI when compared with IDMs of normal weight. There was a significant correlation between the birth weight ratio and the concentrations of free IRI. The IDMs who developed neonatal hypoglycemia had considerably higher concentrations of free IRI than did normoglycemic IDMs. The decrease of blood glucose over the first postnatal hours correlated strongly with the free IRI concentrations in the cord blood. The IDMs had a threefold increase of the C-peptide concentrations over those in normal infants. Six IDMs had a molar ratio of C-peptide to free IRI of less than 1. Both the IDMs and normal infants had substantially higher concentrations of enteroglucagon and lower concentrations of GIP than did the fasting adults. Our data provide direct evidence that IDMs are markedly hyperinsulinemic at birth and that ambient hyperinsulinemia plays a crucial role in the development of fetal macrosomia and neonatal hypoglycemia. Moreover, the observed discrepancy in the relative increase of free IRI and C-peptide, combined with the low molar ratio of C-peptide to IRI, suggests a decreased metabolic clearance of insulin or transplacental passage of insulin from the maternal circulation in infants of mothers with insulin-treated diabetes.
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PMID:Relation of enteroinsular hormones at birth to macrosomia and neonatal hypoglycemia in infants of diabetic mothers. 635 86

The entero-insular axis comprises direct substrate stimulation of the islet cells by the absorbed nutrients and signal transmission by endocrine factors and nerves. The extent of neural influences has not yet been evaluated. GIP is the main incretin candidate. GIP release is dependent on nutrient absorption. Therefore, GIP abnormalities occur in a large number of gastrointestinal and metabolic diseases. These secondary changes are rarely of clinical significance. GIP hypersecretion may, however, contribute to the increased lipogenesis in obesity and the hypoglycemia in the late dumping syndrome. In type II diabetes hyper- and hyposecretion of GIP has been found but no correlation between GIP and insulin response. GIP abnormalities are not identical with disturbances of the entero-insular axis. These can only be evaluated by estimating the incretin effect (comparing the insulin response to oral glucose with the insulin response to an isoglycaemic iv glucose infusion). A decreased incretin effect has been observed in patients with jejuno-ileal bypass and in type II diabetes. In neither condition was a correlation found between incretin effect and GIP response. It is concluded that disturbances of the entero-insular axis are rarely explained by GIP abnormalities. Therefore, other humoral gut factors must exist. Also the neural part of the entero-insular axis requires exploration in health and disease.
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PMID:Disturbances of the entero-insular axis. 635 14


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