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Biomedical subjects

C Kühl

Publications and source records attributed to C Kühl.

At least 91 records · Page 5Linked to original sources
PubMed1981

Gastro-entero-pancreatic hormones in normal pregnancy: response to a protein rich meal.

The plasma concentrations of gastrin, gastric inhibitory polypeptide (GIP), gut glucagon-like-immunoreactivity (gut GLI), insulin, glucagon, and pancreatic polypeptide (PP) were studied following the ingestion of a protein rich meal in late pregnancy and postpartum in 11 normal women. In pregnancy, the fasting plasma concentrations of glucose (mean +/- SEM in pregnancy: 4.1 +/- 0.1 mmol l-1, postpartum: 4.7 +/- 0.1 mmol l-1, P less than 0.01), gut GLI (25 +/- 3 v. 33 +/- 2 pmol-eqv l-1, P less than 0.01), and PP (7.9 +/- 1.0 v. 13.0 +/- 1.2 pmol l-1, P less than 0.01) were decreased, gastrin and GIP unaltered, and insulin (90 +/- 9 v. 72 +/- 5 pmol l-1, P less than 0.05) and glucagon (17 +/- 1 v. 13 +/- 1 pmol l-1, P less than 0.01) increased. The gastrin, GIP and glucagon responses to the meal were unaffected by pregnancy, whereas the responses of gut GLI (integrated responses in pregnancy: 1217 +/- 325 pmol-eqv l-1, postpartum 2223 +/- 404 pmol-eqv l-1, P less than 0.05) and PP (9801 +/- 1440 v. 14,078 +/- 1543 pmol l-1, P less than 0.01) were impaired and the insulin response enhanced (27,973 +/- 6814 v. 11,409 +/- 3102 pmol l-1, P less than 0.01) in pregnancy. The physiological implications of these findings are at present not known in detail. They may, however, be important for the altered carbohydrate metabolism in pregnancy and also for the changes occurring during gestation in gastrointestinal physiology.

Adult↗
PubMed1981

Decreased plasma pancreatic polypeptide levels in pregnancy.

The pancreatic polypeptide (PP) response to oral glucose ingestion was determined in late pregnancy and post partum in 11 normal healthy women. Glucose tolerance was significantly impaired in pregnancy compared to post partum. Fasting plasma PP concentrations were reduced in pregnancy [7.6 +/- 1.2 vs. 12.6 +/- 1.2 pmol liter-1 (mean +/0- SE); P less than 0.01]. The levels of PP increased after glucose ingestion during pregnancy as well as post partum, but the PP response was significantly impaired in gestation (integrated PP responses: 548 +/- 331 vs. 1645 +/- 347 pmol liter-1 min-1; P less than 0.01). It is concluded that in pregnancy, PP levels after an overnight fast are decreased and the PP response to glucose is diminished compared to post partum.

Adult↗
PubMed1981

Influence of lactation on oral glucose tolerance in the puerperium.

The influence of endogenous hyperprolactinaemia on oral glucose tolerance in normal women post-partum was studied. An oral glucose tolerance test (OGTT) was performed 8 weeks after delivery in 23 women, 13 of whom were breastfeeding. The lactating women had significantly higher plasma prolactin values before and during the OGTT than the non-lactating women (P less than 0.005). Fasting values of serum FSH, LH, progesterone and plasma glucagon were similar in the two groups. The non-lactating women had higher fasting concentrations of serum oestradiol (P less than 0.0005), plasma glucose (P less than 0.05) and insulin (P less than 0.05) than the lactating women. After oral glucose no differences were found between lactating and non-lactating women in changes in plasma glucose, insulin and glucagon concentrations. It is concluded that lactating women 8 weeks post-partum do not have an impaired OGTT compared to non-lactating women despite elevated plasma prolactin levels.

Adult↗
PubMed1981

Gastrointestinal insulinotropic hormones in normal and gestational-diabetic pregnancy: response to oral glucose.

The responses of gastric inhibitory polypeptides (GIP), gut glucagon-like-immunoreactivity (gut GLI), insulin, and pancreatic glucagon to a 50-g oral glucose load were studied in late pregnancy and postpartum in 11 normal women, 10 normal weight gestational diabetics, and 10 overweight gestational diabetics. The GIP response to glucose was impaired in pregnancy in all three groups. In pregnancy, the GIP response was smaller in both groups of gestational diabetics than in normal women, whereas postpartum, the GIP response was lower than normal in the normal weight gestational diabetics only. In pregnancy, the gut GLI response to glucose was reduced in the overweight gestational diabetics and abolished in the normal women. The insulin response to glucose was increased in pregnancy in all three groups. Moreover, it was higher in the overweight gestational diabetics than in the other two groups in pregnancy and postpartum. In the normals, the suppression of glucagon levels after glucose ingestion was more marked in pregnancy than postpartum, whereas no such effect was seen in gestational-diabetic pregnancy. It is concluded that pregnancy--normal as well as gestational-diabetic--is accompanied by profound changes in the secretion of gastrointestinal insulinotropic hormones after glucose ingestion. These findings may be important for the understanding of changes in metabolism and gastrointestinal physiology in gestation.

Blood Glucose↗
PubMed1980

Hormonal polypeptides and amine metabolites in small cell carcinoma of the lung, with special reference to stage and subtypes.

To elucidate the ectopic hormonal pattern in patients with small cell carcinoma of the lung, plasma ACTH, serum calcitonin, serum gastrin, plasma glucagon, serum insulin, plasma secretin, plasma VIP, serum growth hormone, serum hCG/LH, the total of serum hCG and hCG-beta-subunit,serum alpha-subunit, serum human placental lactogen, urine ADH, urine 5-HIAA, urine VMA, urine HVA, and urine hCG-LH were measured prior to therapy in 75 patients. Twenty-two patients (29%) had elevated plasma ACTH, and 18 of these had concomitant increased values of corticosteroid in a 24-hour urine sample. Forty-eight patients (64%) were found to have elevated serum calcitonin, and one-third of the patients were diagnosed as having the ectopic ADH syndrome. Serum gastrin concentrations were increased in 20% of the patients, but the elevations were marginal in almost all cases. None of the remaining substances was found to be significantly elevated. Concentrations of plasma ACTH, serum calcitonin, and urine ADH were not found to be correlated with the stage of the disease, and no correlation of these substances with the histological subtypes of small cell carcinoma was disclosed.

Adrenocorticotropic Hormone↗
PubMed1980

Simultaneous recording of the gastro-entero-pancreatic hormonal peptide response to food in man.

The serum or plasma concentrations of gastrin, gastric inhibitory polypeptide (GIP), gut glucagon-like-immunoreactivity (gut GLI), secretin, vasoactive intestinal polypeptide (VIP), insulin, glucagon, and pancreatic polypeptide (PP) were recorded simultaneously following the ingestion of a normal, mixed meal in seven healthy, normal weight men. The concentrations of PP and gastrin increased within 10 min. Subsequently GIP, insulin, glucagon, and gut GLI increased in the order mentioned. The mean concentrations of secretin and VIP were not affected by the meal, athough transient decreases in secretion concentrations could be detected in all subjects. The concentrations of the other hormones remained elevated for 4 hr or more. Perhaps the period of observation following food stimulation of gastro-entero-pancreatic hormones should be extended.

Adult↗
PubMed1980

Effect of epidural analgesia on glucose tolerance during surgery.

Intravenous glucose tolerance tests were performed on 12 surgical patients the day before surgery and during surgery. Six patients were anesthetized with enflurane and six were operated on during an epidural lumbar blockade (Th8-S5). In the general anaesthesia group the plasma glucose concentration was significantly higher after the intraoperative glucose load than after the preoperative load. The pre- and intraoperative glucose tolerance tests were identical in the epidural group. Pre- and intraoperative glucose disappearance rates and plasma insulin responses were similar in the two groups, indicating that the observed differences in plasma glucose were caused by differences in hepatic glucose release, rather than differences in peripheral glucose utilization.

Aged↗
PubMed1980

Gastric inhibitory polypeptide and insulin: response to intraduodenal and intravenous glucose infusions in fetal and neonatal pigs.

The responses of gastric inhibitory polypeptide (GIP) and insulin to intraduodenal (OGTT) and iv (IVGI) glucose infusions were measured in 14 late fetal and 9 neonatal pigs. Basal plasma glucose (P < 0.01) and GIP (P < 0.001) concentrations were lower in the fetal than in the neonatal pigs, while basal plasma insulin was not significantly different in the two groups. In the fetal pigs, almost identical plasma glucose curves were obtained during the OGTT and the IVGI, but plasma insulin did not change during either test. In these pigs, plasma GIP increased 3-fold (P < 0.01) during the OGTT, whereas no significant changes in plasma GIP were observed during the IVGI. In the neonatal pigs, plasma glucose increased more during the OGTT than during the IVGI, but plasma insulin exhibited similar increments during both tests. Thus, the insulinogenic index of the IVGI was almost 3 times higher than that of the OGTT (P < 0.05). In contrast to the normal increment in plasma GIP observed in fetal pigs, plasma GIP decreased significantly during both tests in the neonatal pigs. It is concluded that beta-cells of fetal pigs are unresponsive to acute elevations of plasma glucose with or without a concomitant increase in plasma GIP. Conversely, beta-cells of neonatal pigs exhibit a significant response to hyperglycemia, but the enteroinsular axis is defective, since more insulin is released after iv than during intraduodenal glucose administration. The defective enteroinsular axis in neonatal pigs might be due to the observed fall in plasma GIP during the OGTT.

Animals↗
PubMed1980

Pancreatic glucoregulatory hormones in cirrhosis of the liver: portal vein concentrations during intravenous glucose tolerance test and in response to a meal.

We studied the relationship between the pancreatic glucoregulatory hormones, insulin and glucagon, and glucose intolerance through the response to food and intravenous glucose in 11 patients with verified hepatic cirrhosis. Blood samples were obtained from the portal vein and the superior vena cava. The results of the systemic vein hormone determinations were compared to results obtained from peripheral vein determination in 10 age-, sex- and weight-matched controls admitted to hospital for minor surgery and to results from ambulant, normal subjects. In the cirrhotics collateral shunting was elevated by transhepatic portography. The cirrhotics and the matched controls had similar glucagon levels and responses, but showed hyperresponsiveness to a meal compared to ambulant normal subjects. Compared to the matched controls the cirrhotics showed glucose tolerance and hyperinsulinism, but compared to normal subjects the hospitalized controls were also glucose intolerant and demonstrated hyperinsulinism. In the cirrhotics, the portal vein/vena cava ratio for insulin was negatively correlated to the degree of collateral shunting. No relationship was found between the degree of portosystemic shunting and fasting concentrations of glucagon and insulin, and the insulin response to glucose. The glucagon response to the meal, was correlated to severity of cirrhosis. The rate constant for glucose disappearance (K-value) was not related to the insulin response, to severity of disease or to degree of shunting. It was, however, correlated to the suppressibility of glucagon secretion as measured in the portal vein. Our results indicate that the glucoregulatory disturbances in compensated cirrhosis are partly caused by non-specific factors which are independent of cirrhosis; the portal-vein hormone responses, however, support the contention that glucagon secretion influences glucose tolerance in cirrhotics.

Adult↗
PubMed1979

Diminished gastric inhibitory polypeptide response to oral glucose in late human pregnancy.

It has been shown that the incretin effect - i.e. the gastrointestinal potentiation of the insulin response to oral glucose - is reduced in late normal pregnancy. As evidence points to gastric inhibitory polypeptide (GIP) as mediator of at least part of the incretin effect, the GIP response was determined following a 50 g oral glucose load in 6 normal women in the last trimester of pregnancy and again post partum. Compared to post partum the GIP response to oral glucose was significantly impaired in late pregnancy. It is concluded that the diminished GIP response to oral glucose in late pregnancy might at least partly explain the impaired incretin effect found in this condition.

Blood Glucose↗
PubMed1979

Decreased insulin binding to monocytes from normal pregnant women.

To ascertain whether the decrease of glucose tolerance in pregnancy might be mediated by changes in insulin receptors, we have studied insulin binding to monocytes in 12 normal women during late pregnancy and 14 healthy, young, normal weight, nonpregnant female controls. The pregnant women had significantly higher fasting insulin concentrations in plasma than the controsl (18 +/- 3.5 vs. 8 +/- 1.1 microU/ml; P less than 0.01). Fasting concentrations of glucose and ketone bodies in plasma were not significantly different in the two groups. Insulin binding to monocytes from pregnant women was about 35% lower at each insulin concentration tested compared to the nonpregnant controls (P less than 0.01 at tracer insulin concentrations). Changes in cellular insulin binding were due to changes of the receptor number per cell, whereas the receptor affinity was unaffected. Insulin binding was not significantly correlated with the fasting plasma insulin in either of the two groups (P less than 0.1). Our results suggest that the deterioration of glucose tolerance in normal late pregnancy might be explained by a decrease of insulin sensitivity caused by a reduction of the number of insulin receptors.

Adult↗
PubMed1979

Elevated serum proinsulin in beta cell nesidioblastosis. Report of a case in a newborn.

A newborn infant with severe hypoglycaemia and nesidioblastosis was subjected to subtotal pancreatectomy without any sign of improvement. In spite of very low plasma levels of glucose (i.e. less than 1 mmol/l) plasma insulin concentrations were high (i.e. greater than 700 pmol/l). Plasma proinsulin was considerably enhanced comprising 43% of the total insulin immunoreactivity. Plasma glucagon concentrations were normal. Postoperatively normal to subnormal plasma glucose levels could only be maintained by treatment with frequent meals, diazoxide and intramuscular injections of a long-acting glucagon preparation. With time, signs of mental retardation became obvious.

Adenoma, Islet Cell↗
PubMed1978

Diminished gastrointestinal potentiation of insulin secretion in human pregnancy.

In order to investigate whether an increased gastrointestinal potentiation of glucose-induced insulin release might be involved in the enhanced insulin response to oral glucose in pregnancy, seven normal women were subjected to an oral glucose tolerance test (OGTT) and an IV glucose infusion test (IVGI) in the last trimester of pregnancy and again four to ten weeks post-partum. The amount of glucose administered intravenously was adjusted to obtain plasma glucose concentrations similar to those of the preceding OGTT. By this technique it was possible to quantitate the amount of insulin release attributable to gastrointestinal factors. Contrary to expectations, the results revealed that the gastrointestinal potentiation of insulin secretion was reduced by more than 75% in late pregnancy (p less than 0.05). The hyperinsulinaemia of pregnancy is therefore not explained by an increased activity of the entero-insular axis. Moreover the results confirm a substantially increased beta cell sensitivity to a glycaemic stimulus in pregnancy.

Administration, Oral↗
PubMed1978

Effect of secretin on basal- and glucose-stimulated insulin secretion in man.

Plasma immunoreactive secretin and insulin concentrations were measured in fasting normal humans after intraduodenal infusions of hydrochloric acid, isotonic or hypertonic glucose. The effect of intraduodenal acidification or intravenous bolus injections of secretin on plasma insulin concentrations during infusions of glucose was also examined. The intraduodenal glucose load did not cause an increase in plasma secretin concentrations. Secretin concentrations rose after acid both in the fasting state and during infusions of glucose. A concomitant rise in insulin levels was however only observed during infusions of glucose. Intravenous injection of secretin in a dose which mimicked the response to intraduodenal acidification was without effect on the glucose-stimulated insulin release, while a 30 times higher dose caused a highly significant augmentation of the insulin release. The insulin response pattern to this high dose of secretin differed completely from that observed after intraduodenal infusion of acid. It is concluded and confirmed that the stimulating effect of secretin on insulin secretion is pharmacological and that secretin plays no significant role in the entero-insular axis.

Adult↗
PubMed1978

Mesenchymal tumor hypoglycemia: the effect of a tumor tissue extract on the insulin and glucagon secretion from the isolated perfused porcine pancreas.

Severe fasting hypoglycemia and hypoinsulinemia occurred in a sixty-six year old woman with an intrahepatic mesenchymal tumor. An extract from the tumor was potent in inhibiting the arginine-induced glucagon secretion from the isolated perfused porcine pancreas. This observation supports the theory recently advanced that mesenchymal tumor hypoglycemia in some cases is due to a still unknown factor secreted from the tumor, which directly inhibits pancreatic glucagon secretion.

Aged↗