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Insulin plus zinc induces a favorable biochemical response effects on oxidative damage and dopamine levels in rat brain.

08:00 EDT 27th March 2019 | BioPortfolio

Summary of "Insulin plus zinc induces a favorable biochemical response effects on oxidative damage and dopamine levels in rat brain."

The aim was to determine the effect of zinc (Zn) and insulin on oxidative stress and levels of dopamine in brain of rats. Wistar rats were treated either with zinc alone or combined with insulin during 10 days. After the last dose blood glucose was measured. Their brains were extracted to measure HO, Ca, Mg ATPase, glutathione (GSH), lipid peroxidation (Tbars) and Dopamine. Zn does not possess anti-glycemic effect like Insulin however, it is noticeable that the combination of Insulin plus Zn induces a major glucose reduction (p < 0.0001) than Insulin alone. In cerebellum/medulla oblongata, the groups treated with Insulin and Zn show a significantly increase in dopamine (p < 0.005). Insulin plus Zn reduced GSH level in cortex. Insulin plus Zn reduced level of HO in Striatum and in cerebellum/medulla oblongata. Lipid peroxidation was significantly reduced by the administration of Insulin as in the combination of Insulin and Zn in all regions (p < 0.0001). In cerebellum medulla oblongata, ATPase activity showed an increase only in the group treated with Insulin + Zn.
CONCLUSION:
These results suggest that the use of insulin plus Zn produce favorable changes on oxidative stress and this as consequence on the levels of dopamine.

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Journal Details

This article was published in the following journal.

Name: International journal of biological macromolecules
ISSN: 1879-0003
Pages:

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Medical and Biotech [MESH] Definitions

An intermediate-acting INSULIN preparation with onset time of 2 hours and duration of 24 hours. It is produced by crystallizing ZINC-insulin-PROTAMINES at neutral pH 7. Thus it is called neutral protamine Hagedorn for inventor Hans Christian Hagedorn.

An intermediate-acting INSULIN preparation with onset time of 2 hours and duration of 24 hours. It is produced by crystallizing ZINC-insulin-PROTAMINES at neutral pH 7. Thus it is called neutral protamine Hagedorn for inventor Hans Christian Hagedorn.

A forkhead box transcription factor that is a major target of INSULIN signaling and regulator of metabolic homeostasis in response to OXIDATIVE STRESS. It binds to the insulin RESPONSE ELEMENT (IRE) and the related Daf-16 family binding element (DBE). Its activity is suppressed by insulin and it also regulates OSTEOBLAST proliferation, controls bone mass, and skeletal regulation of GLUCOSE metabolism. It promotes GLUCONEOGENESIS in HEPATOCYTES and regulates gene expression in ADIPOSE TISSUE. It is also an important CELL DEATH regulator. Chromosomal aberrations involving the FOXO1 gene occur in RHABDOMYOSARCOMA.

A syndrome with excessively high INSULIN levels in the BLOOD. It may cause HYPOGLYCEMIA. Etiology of hyperinsulinism varies, including hypersecretion of a beta cell tumor (INSULINOMA); autoantibodies against insulin (INSULIN ANTIBODIES); defective insulin receptor (INSULIN RESISTANCE); or overuse of exogenous insulin or HYPOGLYCEMIC AGENTS.

Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS. It can be caused by the presence of INSULIN ANTIBODIES or the abnormalities in insulin receptors (RECEPTOR, INSULIN) on target cell surfaces. It is often associated with OBESITY; DIABETIC KETOACIDOSIS; INFECTION; and certain rare conditions. (from Stedman, 25th ed)

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