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"Give with a free hand, but give only your own."
-- J.R.R. Tolkien The Children of Hurin
- Glucose Metabolism -
General
Information:
Names:
Wikipedia entry:
Dr. Ray Shahelien
entry:
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Observations:
Type III
Diabetes
See also Coconut Oil, Cinnamon, Methylene Blue
[Need more info-- research in
Canada-- Certain diabetes drugs help? -- Basic idea is that brain
cells don't metabolize sugar well, leading to build-up of AB
plaques. Also find info on recent research indicating that
pancreatic diabetes (types I & II) can be caused by
malfunctioning nerve cells in the pancrease. I wonder if
these two are related?]
Getting Diabetes Before 65 More Than
Doubles Risk For Alzheimer's Disease
ScienceDaily (Jan. 28, 2009)
"Diabetics have a significantly greater risk of dementia, both
Alzheimer's disease — the most common form of dementia — and other
dementia, reveals important new data from an ongoing study of
twins. The risk of dementia is especially strong if the onset of
diabetes occurs in middle age, according to the study..."
http://www.sciencedaily.com/releases/2009/01/090127152835.htm
Related article appearing
February 3, 2009 on ScienceDaily.com about AD as a "type 3
diabetes".
So, the question is, does cinnamon help with sugar metabolism, or
with preventing and reversing tau protein corruption? Or both? Is
there enough of the tau-buster chemical in the typical quantity of
cinnamon people have been taking (about 1/2 tsp) to be effective?
When the news about this "water-soluble component of common
cinnamon" first appeared last year, this was pretty much our only
option to fight tau corruption. Since then, we've learned about methylene blue and niacinamide. For improving sugar
metabolism, we now know about MCT oil and coconut oil. See
also Tau Busters.
Here's
the article:
Insulin Is
A Possible New Treatment For Alzheimer's
ScienceDaily (Feb. 3, 2009)
"A
Northwestern University-led research team reports that insulin,
by shielding memory-forming synapses from harm, may slow or
prevent the damage and memory loss caused by toxic proteins in
Alzheimer's disease. The findings, which provide additional new
evidence that Alzheimer's could be due to a novel third form of
diabetes, will be published online the week of Feb. 2 by the
Proceedings of the National Academy of Sciences (PNAS)..."
http://www.sciencedaily.com/releases/2009/02/090202174818.htm
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Diabetes
and Dementia
See also Metformin,
Cinnamon,
Substance
in Tangerines Fights Obesity and Protects Against Heart Disease,
Research Suggests
ScienceDaily
(Apr.
6, 2011) — New research from The University of Western Ontario has
discovered a substance in tangerines not only helps to prevent
obesity, but also offers protection against type 2 diabetes, and
even atherosclerosis, the underlying disease responsible for most
heart attacks and strokes... "The Nobiletin-treated mice were
basically protected from obesity. And in longer-term studies,
Nobiletin also protected these animals from atherosclerosis, the
buildup of plaque in arteries, which can lead to a heart attack or
stroke. This study really paves the way for future studies to see
if this is a suitable treatment for metabolic syndrome and related
conditions in people."
http://www.sciencedaily.com/releases/2011/04/110406161030.htm
Nobiletin Attenuates VLDL
Overproduction, Dyslipidemia, and Atherosclerosis in Mice With
Diet-Induced Insulin Resistance.
Diabetes.
2011 Apr 6.
Mulvihill
EE, Assini JM, Lee JK, Allister EM, Sutherland BG, Koppes JB,
Sawyez CG, Edwards JY, Telford DE, Charbonneau A, St-Pierre P,
Marette A, Huff MW.
Vascular Biology, Robarts Research Institute, London, Ontario,
Canada.
Abstract
OBJECTIVE Increased plasma concentrations of apolipoprotein B100
often present in patients with insulin resistance and confer
increased risk for the development of atherosclerosis. Naturally
occurring polyphenolic compounds including flavonoids have
antiatherogenic properties. The aim of the current study was to
evaluate the effect of the polymethoxylated flavonoid nobiletin on
lipoprotein secretion in cultured human hepatoma cells (HepG2) and
in a mouse model of insulin resistance and atherosclerosis.
RESEARCH DESIGN AND METHODS Lipoprotein secretion was determined
in HepG2 cells incubated with nobiletin or insulin. mRNA abundance
was evaluated by quantitative RT-PCR, and Western blotting was
used to demonstrate activation of cell signaling pathways. In LDL
receptor-deficient mice (Ldlr(-/-)) fed a Western diet
supplemented with nobiletin, metabolic parameters, gene
expression, fatty acid oxidation, glucose homeostasis, and energy
expenditure were documented. Atherosclerosis was quantitated by
histological analysis. RESULTS In HepG2 cells, activation of
mitogen-activated protein kinase-extracellular signal-related
kinase signaling by nobiletin or insulin increased LDLR and
decreased MTP and DGAT1/2 mRNA, resulting in marked inhibition of
apoB100 secretion. Nobiletin, unlike insulin, did not induce
phosphorylation of the insulin receptor or insulin receptor
substrate-1 and did not stimulate lipogenesis. In fat-fed
Ldlr(-/-) mice, nobiletin attenuated dyslipidemia through a
reduction in VLDL-triglyceride (TG) secretion. Nobiletin prevented
hepatic TG accumulation, increased expression of Pgc1α and Cpt1α,
and enhanced fatty acid β-oxidation. Nobiletin did not activate
any peroxisome proliferator-activated receptor (PPAR), indicating
that the metabolic effects were PPAR independent. Nobiletin
increased hepatic and peripheral insulin sensitivity and glucose
tolerance and dramatically attenuated atherosclerosis in the
aortic sinus. CONCLUSIONS Nobiletin provides insight into
treatments for dyslipidemia and atherosclerosis associated with
insulin-resistant states.
PMID: 21471511 [PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/21471511
Type-2 diabetes linked to
autoimmune reaction in study
APRIL 17, 2011
Stanford School of Medicine
...Nearly all type-2 diabetes drugs marketed today are designed to
control a patient’s high blood sugar levels — a symptom of the
body’s inability to respond properly to insulin. However, the
researchers found that anti-CD20, which targets and eliminates
mature B cells, could completely head off the development of
type-2 diabetes in laboratory mice prone to the disorder and
restore their blood sugar levels to normal. The researchers
believe that insulin resistance arises when the B cells and other
immune cells react against the body’s own tissues... Several years
ago, Daniel and Shawn Winer began to speculate that different
types of immune cells, including T cells and B cells, can cause
inflammation in the fatty tissue that surrounds and cushions
organs in the body. This inflammation occurs in mice fed a
high-fat, high-calorie diet when the rapidly growing fat cells
outstrip their blood supply and begin to die. (It’s also seen in
humans with type-2 diabetes.) The dying cells spew their contents,
and immune system cells called macrophages are summoned to clean
up the mess...
http://med.stanford.edu/ism/2011/april/engleman.html
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Known sources:
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Natural sources:
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References:
In Parkinson's Disease, Brain
Cells Abandon Mitochondria
ScienceDaily
(Oct.
8, 2010) — In a study that sheds new light on the causes of
Parkinson's disease, researchers report that brain cells in
Parkinson's patients abandon their energy-producing machinery,
the mitochondria. A shutdown in fuel can have devastating
effects on brain cells, which consume roughly 20 percent of the
body's energy despite making up only 2 percent of body weight...
researchers, now show that a root cause of Parkinson's disease
may lie in 10 gene sets related to energy production that spur
neurons in the brain to "divorce" their mitochondria and related
energy-producing pathways..."The most exciting result from our
study for me is the discovery of PGC-1alpha as a new therapeutic
target for early intervention in Parkinson's disease. PGC-1alpha
is a master switch that activates hundreds of mitochondrial
genes, including many of those needed to maintain and repair the
power plants in the mitochondria,"... FDA-approved medications [Actos, CoQ10] that activate
that PGC-1alpha are already available for widespread diseases
like diabetes. These medications may jumpstart the development
of new Parkinson's drugs; instead of having to start from
scratch, pharmaceutical companies may be able to dust off their
drug libraries and find look-alike drugs capable of targeting
PGC-1alpha in the brain. "As we wrap up our first year of
publishing the journal, the new study from Zheng et al.
exemplifies the goal of Science Translational Medicine, applying
knowledge and technology from different fields-such as
neuroscience, genomics and bioinformatics-to achieve new
discoveries,"...
http://www.sciencedaily.com/releases/2010/10/101006151557.htm
Study Dusts Sugar
Coating Off Little-Known Regulation in Cells
ScienceDaily (Apr. 16,
2012) — In Alzheimer's disease, brain neurons become
clogged with tangled proteins. Scientists suspect these
tangles arise partly due to malfunctions in a
little-known regulatory system within cells. Now,
researchers have dramatically increased what they know
about this particular regulatory system in mice. Such
information will help scientists better understand
Alzheimer's and other diseases in humans and could
eventually provide new targets for therapies... The
O-GlcNAc system likely adds another layer of control to
the proteins that serve as a brain cell's widgets and
gears -- control that might be muddled in Alzheimer's
brains known to have problems
in sugar metabolism...
http://www.sciencedaily.com/releases/2012/04/120416154048.htm
Tandem
mass spectrometry identifies many mouse brain O-GlcNAcylated
proteins including EGF domain-specific O-GlcNAc transferase
targets.
Alfaro JF, Gong CX, Monroe ME, Aldrich JT, Clauss TR, Purvine SO,
Wang Z, Camp DG 2nd, Shabanowitz J, Stanley P, Hart GW, Hunt DF,
Yang F, Smith RD.
Proc Natl Acad Sci U S A. 2012 May 8;109(19):7280-5. Epub 2012 Apr
19.
Source: Pacific Northwest National Laboratory, Richland, WA
99352, USA.
PMID: 22517741
[PubMed] PMCID:
PMC3358849 [Available on 2012/11/8]
http://www.ncbi.nlm.nih.gov/pubmed/22517741
[This may
mean that the “glucose hypometabolism” targeted by MCT oil
(ketoacids) is due to oligomers, not mitochondrial dysfunction.]
Amyloid-β and Tau Pathology of
Alzheimer's Disease Induced by Diabetes in an Animal Model.
Bitel
CL, Kasinathan C, Kaswala RH, Klein WL, Frederikse PH.
J
Alzheimers Dis. 2012 Jul 11. [Epub ahead of print]
Source:
Department of Pharmacology and Physiology and Rutgers-UMDNJ
Integrative Neurosciences Program, UMDNJ-New Jersey Medical
School, Newark, NJ, USA.
Abstract
Alzheimer's
disease (AD) is the major age-dependent disease of the brain,
but what instigates late-onset AD is not yet clear.
Epidemiological, animal model, and cell biology findings suggest
links between AD and diabetes. Although AD pathology is
accelerated by diabetes in mice engineered to accumulate
human-sequence amyloid-β (Aβ) peptides, they do not adequately
model non-inherited AD. We investigated AD-type pathology
induced solely by diabetes in genetically unmodified rabbits
which generate human-sequence Aβ peptides. After 15 weeks,
alloxan-treated diabetic rabbits with expected high blood
glucose showed ∼5-fold increase in Aβ40/Aβ42 in cortex and
hippocampus, and significantly, generated Aβ-derived assemblies
found in human AD. Deposits of these putative pathogenic toxins
were detected by Aβ/Aβ oligomer antibodies in brain parenchyma
and surrounding vasculature, also co-localizing with markedly
elevated levels of RAGE. Soluble brain extracts showed
diabetes-induced buildup of Aβ oligomers on dot-blots.
Phospho-tau also was clearly elevated, overlapping with
βIII-tubulin along neuronal tracts. Indications of retina
involvement in AD led to examination of AD-type pathology in
diabetic retinas and showed Aβ accumulation in ganglion and
inner nuclear cell layers using Aβ/oligomer antibodies, and RAGE
again was elevated. Our study identifies emergence of AD
pathology in brain and retina as a major consequence of
diabetes; implicating dysfunctional insulin signaling in
late-onset AD, and a potential relationship between Aβ-derived
neurotoxins and retinal degeneration in aging and diabetes, as
well as AD. AD-type pathology demonstrated in genetically
unmodified rabbits calls attention to the considerable potential
of the model for investigations of AD pathogenesis, diagnostics,
and therapeutics.
PMID:
22785400 [PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/22785400
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Updated: July 2, 2012
Inception: July 2, 2012