Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma insulin dynamics were evaluated in 10 patients with primary hyperparathyroidism before and after parathyroidectomy and correction of hypercalcemia. Before surgery fasting plasma insulin concentrations and insulin responses to administered glucose, tolbutamide, and glucagon were significantly greater than postoperative values. Hyperinsulinemia was not associated with altered glucose curves during glucose or glucagon tolerance tests, but a relatively greater insulin response to tolbutamide resulted in an increased hypoglycemic effect following its administration. The glucose-lowering action of intravenous insulin was slightly impaired before treatment. Intramuscular injections of parathormone to six normal men for 8 days induced mild hypercalcemia and hypophosphatemia and reproduced augmented plasma insulin responses to oral glucose and intravenous tolbutamide. 4-hr intravenous infusions of calcium to another group of six normal men raised serum calcium concentrations above 11 mg/100 ml. This did not alter glucose or insulin curves during oral glucose tolerance but markedly accentuated insulin responses to tolbutamide and potentiated its hypoglycemic effect. When highly purified parathormone was incubated with isolated pancreatic islets of male rats, glucose-stimulated insulin secretion was unaffected. These findings suggest that chronic hypercalcemia of hyperparathyroidism sustains a form of endogenous insulin resistance that necessitates augmented insulin secretion to maintain plasma glucose homeostasis. This state is insufficient to oppose tolbutamide-induced hypoglycemia because of an additional direct, selective enhancement of hypercalcemia on pancreatic beta cell responsiveness to the sulfonylurea. The possible direct role of parathormone in these events has not been established.
 ...
PMID:Plasma insulin disturbances in primary hyperparathyroidism. 512 11

Pharmacological treatment of hypertension can cause clinically significant alterations in endocrine function through effects on glucose homeostasis, thyroid and parathyroid hormones, adrenal steroid metabolism and reproductive/pituitary physiology. Long term use of thiazide diuretics causes deterioration in glucose tolerance, probably secondary to potassium depletion. Hypoglycaemic complications of beta-blockers (mainly the non-selective compounds) can be dramatic, especially in type I diabetics. Clonidine, diazoxide and calcium antagonists have all been associated with deterioration in glucose tolerance and their long term use should be avoided in type II diabetics if possible. Propranolol lowers T3 levels by decreasing the conversion of T4 to T3. Prazosin causes elevations in T4 and thyroid-stimulating hormone, while sodium nitroprusside use may result in hypothyroidism. Numerous agents are associated with sexual dysfunction, including methyldopa, reserpine, clonidine and spironolactone. Thiazide diuretics may cause hypercalcaemia, particularly in patients with hyperparathyroidism, by decreasing urinary calcium as well as directly influencing bone and gut calcium handling. Conversely, propranolol may decrease circulating parathyroid hormone levels and correct the hypercalcaemia seen in hyperparathyroidism. Awareness of drug-induced changes in endocrine function will facilitate the rational management of the hypertensive patient.
 ...
PMID:Effects of antihypertensive drugs on endocrine function. 614 2

Carbohydrate metabolism was investigated in 9 patients with symptomatic primary hyperparathyroidism. Before and after parathyroidectomy intravenous and oral glucose tolerance test, tolbutamide test, arginine infusion test and insulin tolerance test were performed. During intravenous and oral glucose tolerance tests, patients with primary hyperparathyroidism exhibited hyperinsulinemia and impaired glucose tolerance without normalization after surgery. Tolbutamide-induced induced insulin release did not differ pre- or postoperatively. After restoration of normocalcemia and normocalcemia and normophosphatemia we found significantly lower glucose and insulin levels following arginine infusion and a significantly increased hypoglycemic response to parenterally administered insulin, probably indicating partial improvement of glucose tolerance after surgery. Our findings suggest that biochemical abnormalities associated with primary hyperparathyroidism, like hypercalcemia, hypophosphatemia, and elevated parathyroid hormone levels may cause and sustain a form of endogenous insulin resistance, which consequently leads to hyperinsulinemia and to impaired glucose tolerance. Since hyperinsulinemia as well as impaired glucose tolerance seem to be only slowly and partially reversible in symptomatic primary hyperparathyroidism, these data could be considered as an additional argument for early surgical intervention in this disorder.
 ...
PMID:Peripheral insulin resistance in primary hyperparathyroidism. 634 5

Clinical and biochemical data are presented on 18 children with severe hyperinsulinaemic hypoglycaemia born to non-diabetic mothers. Thirteen presented within three days of birth, three by 20 months and two aged nine years. Diagnosis of hyperinsulinism (HI) was made in a single blood sample by showing inappropriate plasma insulin levels (23 +/- 3 mU/l) for glycaemia (1.2 +/- 0.1 mmol/l), with low blood ketone body, lactate, alanine and glycerol levels. All children showed increased glucose disappearance rates (KG 7.6% +/- 0.06) and glucose requirement (range, 9-25 mg/kg/min) and an exaggerated glycaemic response to glucagon when hypoglycaemic. Confirmatory tests included measurement of plasma insulin levels during leucine and arginine tolerance tests, during hypercalcaemia and after fish insulin. Coeliac angiograms were performed in three cases. Clinical progress could be divided into five categories. Four cases recovered normal insulin control spontaneously (transient neonatal HI); two children responded and remain on diazoxide therapy, two responded to diazoxide after partial pancreatectomy (diazoxide responsive HI); in three cases resolution of hypoglycaemia resulted from resection of isolated adenoma (insulinoma); total pancreatectomy was needed in five cases (nesidioblastosis) and two children were victims of drug administration (drug induced HI). This analysis allows the definition of a practical approach to diagnosis and management of this major clinical problem.
 ...
PMID:Hyperinsulinaemic hypoglycaemia in infancy and childhood: a practical approach to diagnosis and medical treatment based on experience of 18 cases. 639 78

To determine the impact of induced hypo- and hypercalcemia on TRH (400 micrograms)-stimulated TSH and PRL release, healthy subjects (n = 11) were infused with 5% glucose in water (n = 11), disodium EDTA (n = 11), or calcium gluconate (n = 7). TRH was given as an iv bolus 60 min (5% glucose and EDTA) and 120 min (calcium) after initiation of the respective infusion. Basal plasma concentrations of TSH remained unchanged during induced hypo- and hypercalcemia, whereas those of PRL fell during the latter (P less than 0.05). The mean sum of increments (0-90 min) in PRL and TSH was considerably greater during hypocalcemia than during hypercalcemia (PRL, P less than 0.002; TSH, P less than 0.005). The increments in the plasma hormone concentration above basal after iv TRH were increased compared to those in normocalcemia (PRL, 98.4 +/- 37.9 ng/ml; TSH, 38.9 +/- 11.8 microU/ml) during hypocalcemia [PRL, 128 +/- 47.8 ng/ml (P less than 0.002); TSH, 46.7 +/- 12.8 microU/ml; (P less than 0.005)], but were impaired during hypercalcemia [PRL, 70.1 +/- 27 ng/ml (P less than 0.002); TSH, 28.9 +/- 8.5 microU/ml (P less than 0.025)]. The mean sum of increments in PRL was related to concentrations of both serum calcium (r = -0.59; P less than 0.01) and PTH (r = 0.51; P less than 0.05). A relation was also seen between the incremental responses of TSH and serum calcium (r = -0.52; P less than 0.05), PTH (r = 0.55; P less than 0.01), and phosphorus (r = -0.55; P less than 0.01). We conclude that in healthy man, TRH-mediated release of both PRL and TSH are inversely related to serum calcium concentrations in such a manner that hormone secretion is enhanced by acute hypocalcemia, but blunted by hypercalcemia.
 ...
PMID:Effects of disodium EDTA and calcium infusion on prolactin and thyrotropin responses to thyrotropin-releasing hormone in healthy man. 640 62

The effect of mild hypercalcaemia on the growth hormone (GH), C-peptide and glucose responses to arginine infusion in patients with insulin-dependent idiopathic diabetes mellitus (ID) was compared with that observed in patients whose diabetes was secondary to idiopathic haemochromatosis (IH) and chronic pancreatitis (CP). The summated GH responses to arginine infusion alone were similar in all three groups. Mild hypercalcaemia significantly diminished the GH response to arginine in patients with secondary diabetes, but not in those with ID. As the blood glucose and C-peptide responses were similar in the presence of a normal or raised serum calcium, the differences in GH response could not be ascribed to changes in blood glucose levels or to alterations in endogenous insulin release. For reasons as yet unknown, hypercalcaemia appears to have more of a stabilizing effect on the pituitary somatotrophic granules of those with secondary diabetes than in those with ID.
 ...
PMID:The effect of acute hypercalcaemia on arginine induced growth hormone release in diabetic man. 653 33

Biochemical and other parameters in VX-2 carcinoma in rabbits were evaluated. VX-2 carcinoma not only produced hypercalcemia but also hypophosphatemia and 25-OH-vitamin D deficiency. An increased turnover of 25-OH-vitamin D seems likely. Serum parathyroid hormone and urinary cyclic AMP did not increase. Hypokalemia occurred in association with hypophosphatemia and lowered blood glucose within 1 week after tumor transplantation. At the end of the experiment glucose and insulin were both below the control range. It is concluded that VX-2 carcinoma in rabbits yields much more complex biochemical alterations than reported before on calcium metabolism.
 ...
PMID:Electrolyte and glucose metabolism in VX-2 carcinoma of the rabbit. 668 51

Gastric inhibitory polypeptide (GIP) is a candidate hormone for an incretin which stimulates or potentiates insulin secretion. We elucidated that, in five patients with hyperparathyroidism, GIP and insulin responded remarkably to glucose ingestion, and that hypercalcaemia appeared to have a stimulatory effect on glucose-induced GIP release as well as on insulin release. In nine healthy subjects a 2% calcium solution was continuously infused intravenously and a hypercalcaemic state was maintained. This caused GIP to respond significantly more to glucose ingestion. In spite of GIP being considered an incretin in the normoglycaemic state, GIP does not markedly stimulate insulin secretion. However, in the hypercalcaemic state in healthy subjects, glucose-induced GIP and insulin secretion is significantly greater than in the normocalcaemic state. The potentiated response of insulin to glucose may be caused, in part, by GIP.
 ...
PMID:Release of gastric inhibitory polypeptide (GIP) during calcium infusion and in hyperparathyroidism. 675 Jul 3

The present investigation was carried out in 16 healthy subjects in order to study whether calcium antagonism would affect the hypoglycemic response to insulin, and/or whether it would affect the insulin and glucose responses to glucagon. For this purpose verapamil, a potent calcium-blocking agent, was used. Verapamil infused alone did not affect the basal insulin or glucose concentrations. However, such infusion reduced the hypoglycemic response to insulin. Furthermore, the glucose response to glucagon was augmented by simultaneous infusion of verapamil, whereas the insulin response to glucagon was unaffected. When healthy volunteers were simultaneously infused with both calcium and verapamil the glucose response to glucagon was no longer augmented. The insulin response to glucagon also remained unaffected. These findings indicate that intravenous verapamil has hyperglycemic effects, unrelated to insulin, under certain conditions. They also imply that exogenous hypercalcemia counteracts the augmentative effect of verapamil on the glucose response to glucagon.
 ...
PMID:Effect of verapamil on glucose response to intravenous injection of glucagon and insulin in healthy subjects. 699 47

Insulin secretion in response to an oral glucose challenge during acute hypercalcaemia was studied. Oral glucose tolerance tests (OGTT) were performed in 12 non-diabetic, non-obese human volunteers, aged 20-28 years. Blood samples were collected for calcium, glucose and insulin determination. The next day the same volunteers received a 4 h infusion of calcium gluconate (15 mg/kg/4 h) and were administered glucose 1 h after starting the infusion. Serum calcium, glucose and insulin concentrations were measured again. Infusion of calcium gluconate resulted in an increase in serum calcium concentration of 5 mg/100 ml over 4 h. During these infusions no significant changes in glucose concentrations were noted. On the other hand, the total mean insulin concentration, expressed as the area under the 3 h glucose tolerance curve, and the insulin peak at 30 min were significantly increased during hypercalcaemia (P < 0.001). These data indicate that acute hypercalcaemia does not affect carbohydrate tolerance but increases insulin secretion in human beings.
 ...
PMID:Effect of acute hypercalcaemia on glucose tolerance and insulin release in human beings. 699 45


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