The gastric inhibitory polypeptide (GIP) is the main hormone of the incretin type acting on the entero-insular axis. It is released after fat, glucose or meal ingestion. The variations of this secretion are described in obesity and in some pancreatic and gastrointestinal diseases: it is increased in maturity onset diabetes mellitus, obesity or duodenal ulcer, variable according to the food taken and the severity of the pancreatic lesion in chronic pancreatitis and cystic fibrosis, normal in insulinoma and decreased in celiac disease. The impaired absorption of the food-stuffs and the defective feed-back regulation of GIP secretion by insulin are the major causes of these variations. To a lesser degree, gastric acid secretion, gastric emptying and vagal control may also influence GIP secretion.

Body Water↗

PubMedDate not supplied

Nightly amended IRI/BG ratio in fasting test during sleeping periods in subjects with insulinoma and in normal, diabetic and obese subjects.

In order to obtain a dynamic picture of the way abnormal insulinemia, as a function of blood glucose, occurs in the morning in subjects with insulinoma, we have measured amended plasma insulin (IRI)/blood glucose (BG) ratio during the fasting period of 4 sleeping subjects with insulinoma. Healthy subjects and subjects suffering from other diseases were used as reference in order to determine variations of this ratio during the night. BG and IRI were assayed at intervals of 15 or 30 min. Subjects with insulinoma differed from the other subjects by a very elevated ratio dispersion around the mean value with highly significant peaks (greater than 100). Mean value always remained outside the range (7-82) which covers the total range of values measured in healthy and pathological subjects.

Adenoma, Islet Cell↗

PubMedDate not supplied

Portal, hepatic and peripheral insulin immunoreactive substances before and after removal of an insulinoma.

Plasma insulin immunoreactivity (IRI) results from high molecular weight substances with insulin immunoreactivity (HWIRI), proinsulin (PI) and insulin (I). Their respective concentrations and percentages of IRI were determined preoperatively in the hepatic and peripheral circulations and after surgery in the latter two and in the portal circulation in a patient with a pancreatic adenoma. Removal of the insulinoma resulted in a highly significant reduction of PI concentration in the hepatic (from 16.2 +/- 1.9 microU/ml to 7.3 +/- 0.8 microU/ml) and in the peripheral (from 24.0 +/- 2.0 microU/ml to 9.2 +/- 1.2 micro U/ml) venous systems. Similarly, I concentration decreased in the hepatic (from 36.9 +/- 3.4 microU/ml to 28.0 +/- 1.0 microU/ml) and peripheral (from 33.8 +/- 3.4 microU/ml to 19.8 +/- 2.0 microU/ml) venous systems. HWIRI concentration decreased in the hepatic venous system (from 6.9 +/- 0.8 microU/ml, to 4.8 +/- 0.6 microU/ml), but the decrease in the peripheral venous system (from 9.7 +/- 1.4 microU/ml to 8.2 +/- 1.2 microU/ml) was not significant. It was found that the concentration of I virtually was the same in hepatic and peripheral blood prior to operation in contrast to a decrease seen after the operation. This indicates that the hyperinsulinemia caused primarily by the autonomous hypersecretion of the insulinoma was amplified by a decreased degradation of insulin by the liver and kidney. Our results also indicate that HWIRI was found with the highest concentration in the peripheral blood independently of the adenoma.

Adenoma, Islet Cell↗

PubMedDate not supplied

Influence of caloric intake on gastric inhibitory polypeptide, VIP and gastrin release in man.

Blood glucose, gastric inhibitory polypeptide (GIP), vasoactive intestinal polypeptide (VIP) and gastrin secretions were measured over a three-hour period following the ingestion by normal subjects of a mixed meal with two different caloric levels (1055 Kcal and 1192 Kcal). No VIP secretion was observed after either meal. Gastrin release was not modified by the increase of caloric intake (mainly carbohydrates and lipids), whereas GIP secretion was significantly more important after the meal with the highest caloric value (peak at 30 mm: 499.5 +/- 250.4 vs. 273.4 +/- 128.7 pg/ml and integrated response 53.3 +/- 20.5 vs. 28.2 +/- 9.9 ng X ml-1 X 180 min-1-p less than 0.05). This difference could not be attributed to glucose since the blood glucose levels were not significantly different. It is more probably related to the total amount of ingested food. This suggests the existence of rapid mechanisms of adaptation to the incoming load of the GIP-producing cells.

Adult↗

PubMedDate not supplied

A quantum mechanical/neural net model for boiling points with error estimation.

We present QSPR models for normal boiling points employing a neural network approach and descriptors calculated using semiempirical MO theory (AM1 and PM3). These models are based on a data set of 6000 compounds with widely varying functionality and should therefore be applicable to a diverse range of systems. We include cross-validation by simultaneously training 10 different networks, each with different training and test sets. The predicted boiling point is given by the mean of the 10 results, and the individual error of each compound is related to the standard deviation of these predictions. For our best model we find that the standard deviation of the training error is 16.5 K for 6000 compounds and the correlation coefficient (R2) between our prediction and experiment is 0.96. We also examine the effect of different conformations and tautomerism on our calculated results. Large deviations between our predictions and experiment can generally be explained by experimental errors or problems with the semiempirical methods.

Journal Article↗