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M Azam

Publications and source records attributed to M Azam.

10 recordsLinked to original sources
PubMed1992

Modulation of rat brain insulin receptor kinase activity in diabetes.

Insulin receptors from rat brain regions were studied for insulin binding and receptor associated kinase activity, in alloxan induced short-term and long-term diabetes, and insulin induced hypoglycemia. Insulin receptor activity was assessed by [125I]insulin binding, and basal as well as insulin stimulated kinase activity of the receptor, expressed as phosphorylation of the synthetic peptide poly (Glu-Tyr (4:1)). Regional distribution pattern elicited the highest binding and kinase activity in the olfactory bulb. Diabetes caused a significant increase in the kinase activity. The data suggests that brain insulin receptor kinase is regulated differently compared to peripheral tissues and supports the concept of an active brain insulin receptor in vivo.

Animals↗
PubMed1992

Effect of experimental diabetes on the catecholamine metabolism in rat brain.

The levels of epinephrine, norepinephrine, and dopamine and the activities of tyrosine hydroxylase and monoamine oxidase were estimated in four regions of rat brain during alloxan-induced hyperglycemia and insulin-induced hypoglycemia. Catecholamine levels were estimated by HPLC, and the insulin levels were quantified by radioimmunoassay. The results demonstrated significant increases in the activities of the metabolizing enzymes and levels of catecholamines during experimental conditions. The levels of catecholamines were highest in the cerebral hemispheres, the region associated with high activities of the metabolizing enzymes. Insulin-induced hypoglycemia caused a decrease in the activities of the metabolizing enzymes followed by their recovery within 2 h.

Animals↗
PubMed1991

Effect of hyperglycemia on acetylcholinesterase and catecholamine levels in rat brain and heart.

The effect of hyperglycemia due to experimental diabetes induced in rats, causes a decrease in the activity of Acetylcholinesterase in brain regions and heart; changes in the heart being more significant than the brain. Insulin administration reversed this effect in both the hear and the brain. Significant increase in the levels of catecholamines were also found in the brain regions in diabetes, which was reversed by insulin. The decreased activity of acetylcholinesterase observed in diabetes may be due to an early impaired glucose oxidation and glucose transport as a result of lack of insulin, which causes specific alterations in neurotransmitter levels, thereby effecting blood brain barrier transport, thus causing brain dysfunction.

Acetylcholinesterase↗
PubMed1991

Imipramine inhibits monoamine oxidase activity in hyperglycemic rat brain.

The effect of the chronic treatment of tricyclic antidepressants like Imipramine on the catecholamine metabolism of rat brain, in normal and hyperglycemic conditions was investigated. Imipramine was found to elevate the catecholamine levels in controls, while chronic treatment of hyperglycemic animals with the drug, failed to cause any change other than seen as a result of hyperglycemia. The activities of Monoamine oxidase on the other hand, decreases significantly as a result of the treatment, both in controls and in the hyperglycemic state. The results suggest that the drug apart from acting as an antidepressant, assumes the role of a monoamine oxidase inhibitor under pathological conditions.

Animals↗
PubMed1990

Purification and immunochemical interrelationship of insulin receptors from rat brain and liver.

Insulin receptors from rat brain and liver were purified. Brain purified receptor exhibited protein bands of apparent Mr = 135,000 and 95,000 molecular weight corresponding to alpha- and beta-subunits, retained a tyrosine specific protein kinase activity and demonstrated phosphorylation that is hormonally sensitive. Antisera were raised against both insulin receptor preparations and enzyme-linked immunosorbent assay was developed. The comparison of two insulin receptors was based on a displacement enzyme-linked immunosorbent assay where antisera were interchanged on predetermined optimal dilutions. This indicated that both insulin receptors possess some unique antigenic determinants thereby implying a structural difference.

Animals↗
PubMed1990

Effect of chronic administration of propranolol on acetylcholinesterase and 5-hydroxytryptamine levels in rat brain and heart.

The effect of chronic administration of propranolol on the rat brain and heart acetylcholinesterase was studied by administering propranolol (5mg/kg body weight) for 14 days. This treatment was found to substantially inhibit the enzyme activity. Levels of 5-hydroxytryptamine were measured in the brain and heart; in brain the levels of 5-hydroxytryptamine increased with propranolol administration, while in the heart there was no change. Effect of different concentrations of propranolol on acetylcholinesterase activity was also studied in vitro and a decreased activity of the enzyme was found in brain and heart homogenates. The significance of these results is discussed in terms of the therapeautic effects of the drug in the control of hypertension.

Animals↗
PubMed1990

Changes in the levels of catecholamines, hexokinase and glucose 6-phosphate dehydrogenase in red cell aging.

The activity of the enzymes hexokinase and glucose 6-phosphate dehydrogenase and the level of catecholamines were measured in isolated rat Red Blood Cells (RBC) during cellular aging. The results clearly showed a linear decline in the two enzyme profiles with corresponding increase in age of RBC. A decrease of 75-85% in the activities were found in the oldest cell fractions as compared to the youngest. The levels of glycosylated haemoglobin and catecholamines were found to increase with aging. A correlation can probably be established between the enzyme activities, the levels of glycosylated haemoglobulin and catecholamines during aging.

Animals↗