Scientists that astrocytes missing insulin receptors actually became less efficient over time in transporting glucose in

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progranulindefect
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Scientists that astrocytes missing insulin receptors actually became less efficient over time in transporting glucose in

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http://www.sciencealert.com/sugar-is-co ... tudy-finds


This news isn't specifically about apoe4 or alzheimers, but since we are concerned about glucose hypo-metabolism in the brain, I thought I'd post it here. The question that pops into my mind is do astrocytes somehow lose their insulin receptors, and if so, what causes the insulin receptors to be 'lost'.

We have talked about glucose hypo-metabolism in the brain being caused in women by a drop in estrogen, but what are other causes of glucose hypo-metabolism? What is the consensus about intranasal insulin? What have PET scans proven helps increase insulin sensitivity in the brain?
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Stavia
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Re: Scientists that astrocytes missing insulin receptors actually became less efficient over time in transporting glucos

Post by Stavia »

Thanks Pro.
The trouble with insulin is that its broken down by an enzyme (IDE) that is needed to break down amyloid thus extra insulin results in less available to clear amyloid. Insulin resistance doesnt do well with just giving more insulin.
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Stavia
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Re: Scientists that astrocytes missing insulin receptors actually became less efficient over time in transporting glucos

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http://www.ncbi.nlm.nih.gov/pubmed/23627981
Exercise can enhance brain and hypothalamic insulin sensitivity, but it is the option least preferred and/or continuously practiced by the general population. Pharmacological treatments that increase brain and hypothalamic insulin sensitivity may provide new insights into the prevention of dementia disorders, obesity, and type 2 DM
So here are some drugs that might be candidates.
http://diabetes.diabetesjournals.org/content/63/7/2253


Sigh. Our modern society is sooo broken. The cognitive dissonance....basically they know exercise works but lets try and find a drug instead.
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Re: Scientists that astrocytes missing insulin receptors actually became less efficient over time in transporting glucos

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here are pieces that don't fit:

1. brinton posits that glucose hypo-metabolism in the brain can cause hot flashes
2. studies show that exercise increases insulin sensitivity in the brain
3. logically, an increase in insulin sensitivity in the brain should lead to normal glucose metabolism in the brain

sooo....when i exercise the most regularly, i should be steadily increasing my brain's inulin sensitivity, normalizing my brain glucose metabolism, and ultimately i should experience fewer hot flashes

buuuuut.....the more strenuously i exercise, especially if i exercise fasted, the worse my hot flashes can be. when my hot flashes were just starting about 6 years ago (i still get pretty regular periods even now), they would always happen the night immediately following the morning i did sprints and weights fasted.

so why isn't exercising in my case not leading to fewer hot flashes, but rather more hot flashes??????
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Stavia
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Re: Scientists that astrocytes missing insulin receptors actually became less efficient over time in transporting glucos

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Because insulin sensitivity in the brain is only one of many possible causes of hot flushes/flashes.
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Re: Scientists that astrocytes missing insulin receptors actually became less efficient over time in transporting glucos

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...and the best way to improve insulin sensitivity in the brain is to do so peripherally. What's your A1c, fasting glucose and insulin, Pro? Exercise alone probably isn't enough to restore normal cerebral glucose metabolism for menopausal women- especially E4 women. (I know that's not you.)
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Re: Scientists that astrocytes missing insulin receptors actually became less efficient over time in transporting glucos

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Some day I going to have to go back and re-read "The Other Brain" by R Douglass Fields...


Amazon description:
Despite everything that has been written about the brain, a potentially critical part of this vital organ has been overlooked—until now. The Other Brain examines the growing importance of glia, which make up approximately 85 percent of the cells in the brain, and the role they play in how the brain functions, malfunctions, and heals itself.

Long neglected as little more than cerebral packing material, glia (meaning “glue”) are now known to regulate the flow of information between neurons and to repair the brain and spinal cord after injury and stroke. But scientists are also discovering that diseased and damaged glia play a significant role in psychiatric illnesses such as schizophrenia and depression, and in neurodegenerative diseases such as Parkinson’s and Alzheimer’s. Diseased glia cause brain cancer and multiple sclerosis and are linked to infectious diseases such as HIV and prion disease (mad cow disease, for example) and to chronic pain. The more we learn about these cells that make up the “other” brain, the more important they seem to be.

Written by a neuroscientist who is a leader in glial research, The Other Brain gives readers a much more complete understanding of how the brain works and an intriguing look at potentially revolutionary developments in brain science and medicine.
I read it long before any interest in APOE, so may have missed key useful insights. The big idea I walked away with, though, was that we are woefully inaccurate to equate the word "brain" with "neurons." The glial cells (including astrocytes) are not just packing material around the functional neuron system, but actually highly functional in their own right.

Anyone else aware of insightful reads on the subject that may be even more current?
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Re: Scientists that astrocytes missing insulin receptors actually became less efficient over time in transporting glucos

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Demetrius at Harvard works on the reverse Warburg effect. https://dash.harvard.edu/bitstream/hand ... sequence=1

This paper outlines the give and take between neurons and astrocytes.

"Several years ago, it was proposed that lactate formed and released by astrocytes in an excitatory
activity-dependent manner could provide an additional oxidative energy substrate for neurons . . . .This model, known now as the Astrocyte-Neuron Lactate Shuttle, describes a cellular and molecular mechanism (including lactate supply by astrocytes to neurons) . . . . "
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