Fasting effect on mitochondria bio-genesis in E4s?
by Janelle » Sun Jan 26, 2014 5:07 pm I came across this discussion, and it made me
wonder about the potential benefits of short-term fasting for E4s? I
can't find backing research, but you guys seem to be better at this kind
of thing, so I thought I would ask. Have you guys heard about any
research on this front?
http://blog.trackyourplaque.com/2011/08 ... t-all.html
Would
one of you guys mind translating this too? It sounds like he's
suggesting that fasting would help burn up the protein fragments in our
cytoplasm?
wonder about the potential benefits of short-term fasting for E4s? I
can't find backing research, but you guys seem to be better at this kind
of thing, so I thought I would ask. Have you guys heard about any
research on this front?
http://blog.trackyourplaque.com/2011/08 ... t-all.html
ApoE4
degrades easiest of all ApoE forms, leaving protein fragments in cell’s
cytosol which then can affect a mitochondria’s lipid binding region
impairing the performing of tasks. In addition ApoE4 fragments diminish
gene PPAR gamma expression; and this depresses the desirable bio-genesis
of mitochondria. The affects on mitochondria may be why high levels of
dietary fat is problematic for ApoE4 individuals; there may be too
sparse output of viable mitochondria and mitochondria membranes are
involved in how efficiently we burn fat or glucose.
In light of
these ApoE4 nuances it is interesting to know that fasting raises free
fatty acid levels (from fats in the body and not loose fats from recent
food); and then those free fatty acids upregulate gene for PPAR gamma in
the liver. Fasting makes one put out ketones because of the extra PPAR
gamma programing and this ketogenesis is also one way that activating
more PPAR gamma improves insulin sensitivity. This suggests to me that
individuals with ApoE4 may (?) find some benefit from modified fasting;
possibly something like decidedly fewer meals in a day and also simply
not grazing on snacks (ie: in addition to just trying to select what
foods to eat) between meals that are regularly spaced apart (ie: very
early breakfast to let meal times spread put more evenly)
Would
one of you guys mind translating this too? It sounds like he's
suggesting that fasting would help burn up the protein fragments in our
cytoplasm?
Janelle
- Contributor
- Posts: 14
- Joined: Fri Jan 24, 2014 2:49 pm
Re: Fasting effect on mitochondria bio-genesis in E4s?
by Juliegee » Sun Jan 26, 2014 5:19 pm LOL, Janelle, I won't even try to translate that passage. I'll leave THAT for the scientists among us 
But, I did want to share that my neurologist strongly advises in favor
of both caloric restriction and fasting as an Alzheimer's prevention
tool. He also advises a low carb diet in order to generate ketones for
fuel. This is a controversial dietary strategy for E4's as benefits have
yet to be proven.
I maintain a low BMI, typically eat twice a
day, and often let 16+ hours go between meals. Many of us practice
caloric restriction (CR) and intermittent fasting (IF.)
But, I did want to share that my neurologist strongly advises in favor
of both caloric restriction and fasting as an Alzheimer's prevention
tool. He also advises a low carb diet in order to generate ketones for
fuel. This is a controversial dietary strategy for E4's as benefits have
yet to be proven.
I maintain a low BMI, typically eat twice a
day, and often let 16+ hours go between meals. Many of us practice
caloric restriction (CR) and intermittent fasting (IF.)
Juliegee
- Mod
- Posts: 468
- Joined: Sat Oct 26, 2013 5:36 pm
Peroxisome proliferator-activated receptor gamma - Wikipedia, the free encyclopedia
PPAR-gamma has been implicated in the pathology of numerous diseases
including obesity, diabetes, atherosclerosis, and cancer. PPAR-gamma agonists have been used in the treatment of hyperlipidaemia and hyperglycemia.[18] PPAR-gamma decreases the inflammatory response of many cardiovascular cells, particularly endothelial cells.[19] PPAR-gamma activates the PON1 gene, increasing synthesis and release of paraoxonase 1 from the liver, reducing atherosclerosis.[20]
PPARG regulates fatty acid storage and glucose metabolism. The genes activated by PPARG stimulate lipid uptake and adipogenesis by fat cells. PPARG knockout mice fail to generate adipose tissue when fed a high-fat diet.[6]
Deletion of PPARgamma in adipose tissues of mice protects against high fat diet-induced obesity and insulin resistance.
Jones JR, Barrick C, Kim KA, Lindner J, Blondeau B, Fujimoto Y, Shiota M, Kesterson RA, Kahn BB, Magnuson MA.
Abstract
Peroxisome
proliferator-activated receptor gamma (PPARgamma) plays a crucial role
in adipocyte differentiation, glucose metabolism, and other
physiological processes. To further explore the role of PPARgamma in
adipose tissues, we used a Cre/loxP strategy to generate
adipose-specific PPARgamma knockout mice. These animals exhibited marked
abnormalities in the formation and function of both brown and white
adipose tissues. When fed a high-fat diet, adipose-specific PPARgamma
knockout mice displayed diminished weight gain despite hyperphagia, had
diminished serum concentrations of both leptin and adiponectin, and did
not develop glucose intolerance or insulin resistance. Characterization
of in vivo glucose dynamics pointed to improved hepatic glucose
metabolism as the basis for preventing high-fat diet-induced insulin
resistance. Our findings further illustrate the essential role for
PPARgamma in the development of adipose tissues and suggest that a
compensatory induction of hepatic PPARgamma may stimulate an increase in
glucose disposal by the liver.
proliferator-activated receptor gamma (PPARgamma) plays a crucial role
in adipocyte differentiation, glucose metabolism, and other
physiological processes. To further explore the role of PPARgamma in
adipose tissues, we used a Cre/loxP strategy to generate
adipose-specific PPARgamma knockout mice. These animals exhibited marked
abnormalities in the formation and function of both brown and white
adipose tissues. When fed a high-fat diet, adipose-specific PPARgamma
knockout mice displayed diminished weight gain despite hyperphagia, had
diminished serum concentrations of both leptin and adiponectin, and did
not develop glucose intolerance or insulin resistance. Characterization
of in vivo glucose dynamics pointed to improved hepatic glucose
metabolism as the basis for preventing high-fat diet-induced insulin
resistance. Our findings further illustrate the essential role for
PPARgamma in the development of adipose tissues and suggest that a
compensatory induction of hepatic PPARgamma may stimulate an increase in
glucose disposal by the liver.
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