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Biomedical subjects

M Ui

Publications and source records attributed to M Ui.

At least 343 records · Page 19Linked to original sources
PubMed1976

Attenuation of epinephrine-induced increase in liver cyclic AMP by endogeneous insulin in vivo.

1. Epinephrine-induced increase in rat liver cyclic AMP in vivo was potentiated when the circulating insulin was suppressed by injection of anti-insulin serum or by induction of diabetes. Consequently, phosphorylase was activated, glycogen synthetase was inactivated and glycogen accumulation induced by glucose load was prevented by epinephrine in the insulin-deficient rats to a much larger extent than in normal rats. 2. Insulin lack was effective in potentiating epinephrine-induced increase in liver and muscule cyclic AMP even after the treatment of rats with theophylline; the potentiation could not be solely accounted for by the inhibition of cyclic AMP phosphodiesterase. Thus, it is likely that insulin lack enhaces epinephrine activation of adenylate cyclase. 3. Unlike epinephrine, glucagon increased liver cyclic AMP to essentially the same extent whether the rat was treated with anti-insulin serum or not. 4. Based on the difference in dose-response curves between normal and insulin-deficient rats, a possibility is discussed that there are two adenylate cylase in the liver with higher and lower affinities for epinephrine and that circulating insulin blocks the high affinity enzyme selectively.

Adenylyl Cyclases↗
PubMed1976

Accelerated turnover of blood glucose in pertussis-sensitized rats due to combined actions of endogenous insulin and adrenergic beta-stimulation.

1. Epinephrine-induced hyperglycemia was attenuated by the treatment of rats with pertussis vaccine, but this attenuation was abolished when endogenous insulin was suppressed by streptozotocin or anti-insulin serum. It was concluded that epinephrine-induced hyperglycemia was counterbalanced by the hypoglycemic action of insulin, the secretion of which was markedly potentiated in pertussis-sensitized rats. 2. Without epinephrine, no hypoglycemia developed in pertussis-sensitized rats despite the higher blood level of insulin. Tracer experiments with [14C,3H] glucose or [14C]bicarbaonate showed that, in pertussis-sensitized rats, more glucose was liberated into the blood from hepatic gluconeogenesis at the expense of hepatic glycogenesis, thereby accelerating the turnover of blood glucose. 3. Since this activation of hepatic glucose production was reduced by propranolol, a beta-adrenergic blocking agent, it is very likely that adrenergic beta-stimulation is, at least partly, responsible for the metabolic alterations observed in pertussis-sensitized rats.

Animals↗
PubMed1975

Activation and inactivation of phosphorylase and glycogen synthetase during perfusion of rat liver as influenced by epinephrine, glucagon and hydrocortisone.

1. The changes in phosphorylase activity and glycogen synthetase I (active form) activity during perfusion of rat liver were studied together with their responses to added epinephrine and glucagon. 2. Phosphorylase activity of the liver from fed or fasted rats fell rapidly during perfusion, regardless of whether the perfusate was added with glucose or not. The addition of epinephrine or glucagon at the start or at 60 min of perfusion caused a prompt restoration of the initial high activity. Both glycogen breakdown and glucose liberation proceeded in parallel with the changes in phosphorylase activity. 3. The I-form of glycogen synthetase in the liver from fed rats increased rapidly when the concentration of perfusate glucose was raised to near 10 mM. This increase was promptly prevented by the addition of epinephrine or glucagon. In contrast, glycogen synthetase of the liver from fasted rats responded to neither glucose nor epinephrine (or glucagon) during perfusion. 4. Phosphorylase in the liver of fasted, adrenalectomized rats did not respond to a low concentration of epinephrine (3 - 10(-8) M) or glucagon (5 - 10(-9) M), but was increased by higher concentrations of the hormones. The treatment of adrenalectomized rats with hydrocortisone restored the response of liver phosphorylase to the low concentrations of the hormones. Thus, glucocorticoid plays a "permissive" role by increasing the affinity of liver phosphorylase to epinephrine or glucagon.

Animals↗
PubMed1975

Carbohydrate metabolism and its response to catecholamines as modified in alkalotic rat.

Metabolic activities and their responses to catecholamines were studied in fasted rats exposed to simulated altitudes. Analysis of hepatic levels of gluconeogenic intermediates revealed the inhibition of gluconeogenesis between glyceric acid 3-P and fructose 6-P associated with a rise of the ratios of redox pairs such as lactate to pyruvate in livers of alkalotic rats. Inhibition of gluconeogenesis was indicated also by the suppressed incorporation of glutamate 14C into blood glucose. Since no activation was detected on glycolytic pathway of skeletal muscles, marked hyperlactacidemia during alkalosis appeared to result from the suppression of hepatic gluconeogenesis. Most of metabolic actions of epinephrine and isoproterenal known to be mediated via the beta receptor were significantly reduced but not completely abolished during alkalosis. Exceptionally, hyperinsulinemia induced by isoproterenol was completely reversed and replaced by hypoinsulinemia during alkalosis. Despite hypoinsulinemia, hyperglycemia induced by glucose load decreased more rapidly in alkalotic than in normal rats. In view of the fact that the adrenergic alpha receptor is involved in theinhibition of insulin secretion, the observed irregular modifications of catecholamine actions could be explained on the basis of a postulate that the adrenergic alpha-receptor functions are potentiated in alkalosis.

Alkalosis, Respiratory↗
PubMed1975

Hydrocortisone restoration of the pH-dependent metabolic responses to catecholamines.

Feeding NH4CL to fasted rats caused changes of blood levels of lactate, glycerol, and insulin, hepatic levels of glycogen and phosphorylase, and muscle levels of glycogen and glucose 6-P in the direction opposite to the changes induced by respiratory alkalosis. The effects of epinephrine and isoproterenol in vivo on these metabolic indices, which are classified as their function mediated via the adrenegic beta receptor, were potentiated by NH4CL feeding in contrast to their attenuation in alkalosis. The prior treatment of the rat with hydrocortisone was very effective in overcoming the alkalosis-induced inhibition of the beta-receptor-mediated metabolic actions of epinephrine and isoproterenol, such as the activation of liver phosphorylase, accumulation of muscle hexose phosphates, and stimulation of pancreatic secretion of insulin. Epinephrine sensitivity of the liver and muscle levels of cyclic AMP was not altered by the hydrocortisone therapy or inductions of alkalosis and acidosis. The mechanism for the hydrocortisone restoration of the adrenergic beta functions in alkalosis is discussed as related to its permissive effect.

Acidosis↗
PubMed1975

Metabolic background for glucose tolerance: mechanism for epinephrine-induced impairment.

Turnover rates of blood glucose in rats were calculated from the decay of [14C]glucose. A glucose load suppressed glucose appearance and this was reversed by epinephrine or glucagon. Incorporation of [14C]bicarbonate into liver glycogen and blood glucose demonstrated that these hormones did not alter gluconeogetic rate but, rather the proportion of glucose recovered in the two products. The glucose enhanced by glucagon, probably through increased insulin secretion. In contrast, epinephrine decreased peripheral glucose uptake.

Animals↗
PubMed1975

Adrenergic receptor and epinephrine-induced hyperglycemia and glucose tolerance.

Intravenous glucose tolerance in fasting rats was improved by phentolamine, an alpha-adrenergic blocking agent, and diminished by propranolol, a beta-adrenergic blocking agent. These effects of adrenergic blockers were dependent on the action of insulin, secretion of which is controlled by an adrenergic mechanism. Epinephrine caused by hyperglycemia and impaired glucose tolerance. Both actions of epinephrine were partly inhibited by either an alpha or beta blocker and completely abolished by combination of both blockers in normal rats. However, in rats treated with anti-insulin serum or 5-methoxyindole-2-carboxylic acid, a potent inhibitor of gluconeogenesis, both actions of epinephrine were blocked by propranolol alone, but not by phentolamine. It is concluded that beta-receptor-mediated inhibiton of peripheral glucose utilization is primarily responsible for epinephrine-induced hyperglycemia and impairment of glucose tolerance. Furthermore, the reduction of glycemic action of epinephrine observed after alpha blockade is due to the hypoglycemic action of insulin secreted by the stimulation of beta receptors in pancreatic beta cells.

Animals↗
PubMed1975

Potentiation of the adrenergic beta-receptor-mediated insulin secretion in pertussis-sensitized rats.

The increase in blood insulin level induced by adrenergic beta-stimulants, glucose and tolbutamide was strongly exaggerated in pertussis-sensitized rats. Moreover, the decrease in blood insulin caused by the alpha-receptor-mediated action of epinephrine in glucose- or tolbutamide-treated rats was effectively reversed by pertussis sensitization. The rise of blood insulin concentration due to adrenergic alpha-blockade was also enhanced by pertussis sensitization. It is concluded that the secretion of insulin resulting from the stimulation of adrenergic bate-receptor is enhanced by pertussis sensitization, probably due to activation of a process occurring in the chain of events leading to the discharge of insulin from the pancreatic beta-cell.

Animals↗