|LETTER TO EDITOR
|Year : 2022 | Volume
| Issue : 4 | Page : 265-266
Cerebral edema: Role of insulin and insulin signaling pathways in the brain
Tariq Janjua1, Luis Rafael Moscote-Salazar2
1 Department of Critical Care Medicine, Physician Regional Medical Center, Naples, FL, USA
2 Department of Research, Colombian Clinical Research Group in Neurocritical Care, Bogota, Colombia
|Date of Submission||16-Jun-2022|
|Date of Acceptance||25-Jun-2022|
|Date of Web Publication||31-Oct-2022|
Dr. Luis Rafael Moscote-Salazar
Colombian Clinical Research Group in Neurocritical Care, Bogota
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Janjua T, Moscote-Salazar LR. Cerebral edema: Role of insulin and insulin signaling pathways in the brain. Indian J Med Spec 2022;13:265-6
|How to cite this URL:|
Janjua T, Moscote-Salazar LR. Cerebral edema: Role of insulin and insulin signaling pathways in the brain. Indian J Med Spec [serial online] 2022 [cited 2022 Dec 9];13:265-6. Available from: http://www.ijms.in/text.asp?2022/13/4/265/360048
Cerebral edema is defined as the increase in the net content of water at the cerebral level that leads to an increase in the volume of the brain tissue. In the progression from the initial injury and with the subsequent development of cerebral edema, complex mechanisms have been linked at the cellular, structural, and microcirculation levels. Intracranial hypertension is one of the situations that occur with the worsening of cerebral edema.
Insulin has some interesting functions at the level of the mammalian brain; the receptor for insulin is distributed in the synaptic endings. The specific areas in the animal model are shown to be in the external median eminence and the hypothalamic arcuate nucleus. Insulin crosses the blood–brain barrier through an insulin receptor-specific and vesicle-mediated process across brain endothelial cells. There is more to central insulin besides control of food intake, central response to hypoglycemia, and impact of hyperglycemia/hypoglycemia-induced cerebral changes. Insulin-like growth factor 1 impacts acute brain injury in vitro with a reduction in brain cells' water content, infarct volume reduction, and reduced apoptosis. An experimental model shows that pretreatment with insulin-like peptide 1 reduces oxidative stress, blood–brain barrier breakdown, cerebral edema formation, and cell injury. Intranasal insulin can act as a neuroprotective agent in Alzheimer's disease and acute ischemic stroke. In vitro model, intranasal insulin significantly reduced hematoma volume and brain edema after induced cerebral hemorrhage. Also was seen decreased blood–brain barrier permeability, neuronal degeneration damage, reduced neurobehavioral deficits, and improved survival rate in mice. Insulin reduced the lactate/pyruvate ratio and increased interstitial fluid glucose levels in subarachnoid hemorrhage in vitro. Other changes seen were improved neurological dysfunction, blood–brain barrier damage, and brain edema.
The same effect can be inferred in the case of traumatic brain injury (TBI)-induced cerebral edema. Further work will be required in human trials to see the impact and any true benefit in preventing cerebral edema. The question is still there if the blood glucose control protocol used with insulin therapy in neurointensive care and trauma units has any impact on TBI-induced cerebral edema. Hypoglycemic episodes with this protocol can mitigate any impact of this approach.
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Conflicts of interest
There are no conflicts of interest.
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