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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The action of insulin on plasma cyclic nucleotide concentrations in normal human subjects has been studied after intravenous injection, alone and in combination with glucagon. 2. After injection of insulin alone there was an initial small, though not significant, decrease in plasma cyclic AMP at 15 min followed by an increase to more than twice the initial concentration at 30 min. The increase was absent when hypoglycaemia was lessened by infusion of glucose after insulin injection. 3. Injection of insulin caused no significant change in plasma cyclic GMP concentration, whether or not glucose was infused after the hormone. 4. Glucagon (3-300 nmol, 10-1000 mug), caused a dose-dependent increase in plasma cyclic AMP concentration. The rise in plasma cyclic AMP produced by 3 or 30 nmol of glucagon was not significantly modified by simultaneous injection of insulin (44 nmol; 6 units).
Clin Sci Mol Med 1976 Jun
PMID:The effect of insulin on adenosine 3':5'-monophosphate and guanosine 3':5'-monophosphate concentrations in human plasma. 17 51

1. Young Wistar rats were used as an experimental model to determine the effects of protein-energy malnutrition on glucose tolerance and insulin release. 2. Malnourished rats presented some of the features commonly found in human protein-energy malnutrition, such as failure to gain weight, hypoalbuminaemia, fatty infiltration of the liver and intolerance of oral and intravenous glucose loads. 3. The rate of disappearance of glucose from the gut lumen was greater in the malnourished rats but there was no significant difference in portal blood glucose concentration between normal and malnourished rats 5 and 10 min after an oral glucose load. 4. Insulin resistance was not thought to be the cause of the glucose intolerance in the malnourished animals since these rats had a low fasting plasma insulin concentration with a normal fasting blood glucose concentration and no impairment in their hypoglycaemic response to exogenous insulin administration. Furthermore, fasting malnourished rats were unable to correct the insulin-induced hypoglycaemia despite high concentrations of hepatic glycogen. 5. Malnourished rats had lower peak plasma insulin concentrations than normal control animals after provocation with oral and intravenous glucose, intravenous tolbutamide and intravenous glucose plus aminophyllin. This was not due to a reduction in the insulin content of the pancreas or potassium deficiency. Healthy weanling rats, like the older malnourished rats, had a diminished insulin response to intravenous glucose and intravenous tolbutamide. However, their insulin response to stimulation with intravenous glucose plus aminophyllin far exceeded that of the malnourished rats. Thus the impairment of insulin release demonstrated in the malnourished rats cannot be ascribed to a 'functional immaturity' of the pancreas.
Clin Sci Mol Med 1976 Mar
PMID:Glucose tolerance and insulin release in malnourished rats. 81 69

1. Gastric juice was collected at regular intervals during electrical stimulation of the vagus in anaesthetized cats and during insulin hypoglycaemia in both anaesthetized and conscious cats. The total amounts of acid and pepsin secreted were similar in the three groups. 2. Pepsins were examined by agar-gel electrophoresis. Resting juice contained two pepsins, and up to nine pepsins could be detected after stimulation. Three patterns of pepsin secretion were found. 3. The most noticeable feature was the variation in the proportion of total pepsin attributable to the pepsin which migrated most rapidly during electrophoresis (pepsin 1). In response to insulin hypoglycaemia, anaesthetized cats secreted only a small proportion of total pepsin 1 and conscious cats secreted a large proportion as pepsin 1. During direct electrical stimulation of the vagus, the proportion of pepsin 1 rose. 4. The possibility of a dependence of pepsin 1 secretion on vagal stimulation is discussed and the relevance of this to peptic ulcer and to vagotomy is considered.
Clin Sci Mol Med 1975 Apr
PMID:Variation in the proportions of individual pepsins secreted by the cat in response to vagal stimulation and hypoglycaemia. 109 18

1. Intravenous glucose tolerance test were performed in fourteen patients with mild or moderate liver damage due to paracetamol overdose. 2. In patients managed conservatively there was glucose intolerance associated with a diminished early insulin response to glucose, suggesting inadequate nutrition in the period between the overdose and the glucose tolerance test. 3. Patients given intravenous glucose supplements to maintain nutrition were also glucose intolerant and, in these, insulin responses to glucose were normal. The decreased fractional disappearance rate was partly due to an increase in glucose distribution space and partly due to a decrease in absolute glucose disappearance rate. 4. Impaired gluconeogenesis was suggested by mild fasting hypoglycaemia in four patients and raised fasting blood lactate concentrations. Serum growth hormone concentrations showed a paradoxical increase after glucose. 5. All these variables had returned to normal in four patients re-tested after recovery.
Clin Sci Mol Med 1975 Nov
PMID:Disturbances in glucose metabolism in patients with liver damage due to paracetamol overdose. 119 5

To further evaluate whether transsynaptic mechanisms account for stress-induced changes in adrenomedullary preproenkephalin mRNA (ppEnk mRNA), neonatal rats were made hypoglycemic at a time when synapses are non-functional (less than 10 days postnatal age). While ppEnk mRNA in medullae from adult rats increased as much as 60-fold in this paradigm (insulin 10 U/kg), ppEnk mRNA levels in the newborn increased only 1.6-fold (insulin 20 U/kg). To evaluate whether postsynaptic cholinergic pathways of the neonatal adrenal medulla were functional, we treated 5-day-old pups with cholinergic agonists (nicotine [1 mg/kg, s.c., q 12 h] + carbachol [1.7 mumol/kg, s.c., q 12 h x 4 days]). Combined cholinergic agonist treatment augmented enkephalin prohormone and peptide levels up to 3-fold (P less than 0.05). To determine whether the blunted response to hypoglycemia in the newborn resulted from a deficiency in functional transsynaptic activity, synapses were matured using thyroid hormone pretreatment (postnatal days 2 and 3) before hypoglycemic stress. Hypoglycemia now caused a 40-fold increase in adrenomedullary ppEnk mRNA levels only in the T3/insulin treated group. To exclude other secondary effects of hypoglycemia (eg. hormonal, or insulin treatment-dependent), intracellular glycopenia was produced in the presence of secondary hyperglycemia by injecting adult rats or pups with 2-deoxyglucose (500 mg/kg). Similar to the insulin-hypoglycemia group, a large increase in adrenomedullary ppEnk mRNA resulted in the adult but not in the 5-day-old neonatal adrenal medullae. We conclude that enkephalin biosynthesis, like co-stored catecholamines, is induced by a transsynaptic process.(ABSTRACT TRUNCATED AT 250 WORDS)
Brain Res Mol Brain Res 1992 Apr
PMID:Regulation of adrenomedullary preproenkephalin mRNA: effects of hypoglycemia during development. 131 92

Primary cortisol receptor resistance has been reported in 6 patients and 14 asymptomatic family members. We observed an additional 6 patients (2 males and 4 females). The male patients presented with hypertension. The female patients presented with acne, hirsutism and irregular menstruations. Dexamethasone therapy (1-1.5 mg/day) was of considerable clinical benefit. All 6 patients showed insufficient suppression of cortisol after 1 mg dexamethasone. The diurnal rhythm of ACTH and cortisol was intact, albeit at an elevated level. There was a normal increase of ACTH, cortisol, and GH to insulin-induced hypoglycemia, while cortisol production was (slightly) elevated. Adrenal androgen levels were increased in all patients. Glucocorticoid receptors measured in a whole cell dexamethasone binding assay in mononuclear leukocytes showed a lowered affinity in 1, and lowered numbers of receptors in 4 patients. In 1 patient no abnormalities were found. As a "bioassay" for glucocorticoid action dexamethasone suppressibility of mitogen-stimulated incorporation of [3H]thymidine in mononuclear leukocytes was measured. In this last patient dexamethasone suppressibility of [3H]thymidine incorporation was significantly lowered. Twelve months' treatment with 200 mg RU 486 per day in meningioma patients induced a similar biochemical picture as observed in primary cortisol receptor resistance. Partial cortisol receptor resistance might be less rare than previously thought. In the 6 patients presented at least 3 different forms can be recognized. Therapy with dexamethasone was successful in female patients with acne and hirsutism, as the secondary overproduction of adrenal androgens was effectively controlled. Chronic therapy with RU 486 causes a biochemical picture similar to primary cortisol receptor resistance.
J Steroid Biochem Mol Biol 1992 Oct
PMID:Familial and iatrogenic cortisol receptor resistance. 139 Feb 87

1. Rats which survived hypoglycemia by insulin, hypoxia by 10% O2, or ischemia by carotid ligation and hypotension to 40 mm Hg, evidenced no changes in cerebrospinal fluid (CSF) uridine. Animals which died soon after the above interventions or as a result of KCl-induced cardiac arrest had elevated CSF uridine concentrations. 2. Injection of whole blood or the soluble contents of lysed blood cells into the lateral ventricle of rats reduced CSF uridine to less than one-half normal at 24 hrs but values returned to normal 3 days later. Changes in hypoxanthine resembled those of uridine, but were less dramatic, whereas xanthine concentrations were largely unaltered. Intraventricular injection of plasma or saline did not alter CSF uridine. 3. It seems most likely that low CSF uridine concentrations previously reported in head injury patients may be secondary to the effects of blood cell contents in the cerebrospinal fluid, rather than responses to altered metabolism in neurons or glia cells.
Cell Mol Neurobiol 1990 Sep
PMID:Opposite alterations in cerebrospinal fluid uridine after severe cerebral ischemia or intrathecal blood injection. 225 61

The pancreases of three patients with hyperinsulinemic hypoglycemia were studied: one of these patients was a child born to a diabetic mother, the other two were adults with insulinomas. All the patients had nesidioblastosis, namely the presence of a number of pancreatic endocrine cells spread throughout the exocrine tissue singly or clustered in small groups. In the hypoglycemic child the endocrine cells scattered in the acinar tissue were mostly A cells, whereas in the patients with insulinomas both A and B cells were found with a similar frequency. Intermediate cells (acinar-islet cells) were found in all the cases. These findings suggest that nesidioblastosis and the de novo formation of intermediate cells are associated phenomena. Possible mechanisms for the genesis of the islet cell types spread throughout the exocrine parenchyma and of the intermediate cells are discussed and their possible clinical implications are suggested.
Virchows Arch B Cell Pathol Incl Mol Pathol 1985
PMID:Nesidioblastosis and intermediate cells in the pancreas of patients with hyperinsulinemic hypoglycemia. 285 37

The adrenals of 14-day-old control and hypothyroid rats have been stimulated by insulin-induced hypoglycaemia, and the subsequent induction in dopamine beta-hydroxylase (DBH) has been studied. In control rats, DBH induction was maximum 48 h after insulin administration. Hypothyroidism completely suppressed DBH induction.
Mol Cell Endocrinol 1986 Apr
PMID:Adrenal dopamine beta-hydroxylase induction in the young rat: influence of thyroid hormones. 351 57

We studied the influence of the thyroid hormones on the development of the ability of the adrenal glands to release epinephrine after stimulation by insulin-induced hypoglycaemia in the young rat. In animals rendered hypothyroid from birth, this development is delayed as compared to control rats. Administration of thyroxin to these animals restores the ability of the adrenals to deplete epinephrine. These results may indicate an influence of the thyroid hormones on the development of the functional innervation of the adrenal medulla in the young rat.
Mol Cell Endocrinol 1983 May
PMID:Adrenal epinephrine depletion after insulin-induced hypoglycaemia in young hypothyroid rats. 634 58


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