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  #1   ^
Old Mon, Apr-23-18, 05:00
teaser's Avatar
teaser teaser is offline
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Plan: mostly milkfat
Stats: 190/152.4/154 Male 67inches
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Default Active young adults with Type 1 diabetes have muscle complications

https://www.sciencedaily.com/releas...80418092042.htm

https://www.sciencedaily.com/releas...80418092042.htm

Quote:
Active young adults with Type 1 diabetes have muscle complications
Changes in muscles could impair ability to manage blood sugar

A new study from McMaster and York universities has found that poor muscle health may be a complication of Type 1 diabetes, even among active twenty-somethings.

The research team analyzed muscle biopsies of young adults with and without Type 1 diabetes who exceed Diabetes Canada's recommended weekly levels for physical activity.

The researchers found structural and functional changes in the power generation parts of the cell, or mitochondria, of those with diabetes. Not only were the mitochondria less capable of producing energy for the muscle, they were also releasing high amounts of toxic reactive oxygen species, related to cell damage.

These changes could result in reduced metabolism, greater difficulty controlling blood glucose and, if left unchecked, an accelerated rate of developing disability. The study findings add poor muscle health to the list of better-known complications of Type 1 diabetes, including nerve damage, heart disease and kidney disorders.

"Now we know that even active people with diabetes have changes in their muscles that could impair their ability to manage blood sugar," said Thomas Hawke, corresponding author of the study and a professor of pathology and molecular medicine at McMaster. "Knowing in the long term that this could contribute to faster development of disability, we can start to address it early on."

The paper was published today in Diabetologia, the journal of the European Association for the Study of Diabetes.

Christopher Perry, study co-senior author and an associate professor in kinesiology and health sciences and the Muscle Health Research Centre at York University, added: "Skeletal muscle is our largest metabolic organ and is the primary tissue for clearing blood sugar after eating a meal, so we need to keep muscle as healthy as possible."

With regular aerobic exercise, the amount of mitochondria in muscle increases, thereby helping muscle cells to use more glucose and become more efficient. Given this new data, Perry added that their study suggests that current guidelines for Type 1 diabetics may also need to be revised.

"We believe these dysfunctional mitochondria are what's causing the muscle to not use glucose properly and to also damage muscle cells in the process. We were surprised to see the muscles were this unhealthy in young adults with Type 1 diabetes who were regularly active."

Researchers say while further study is needed, revising evidence-based exercise guidelines, specific for those with Type 1 diabetes, may be required to keep them in the best health.

The team included researchers at York University, the University of Windsor and the German Center for Neurodegenerative Diseases as well as McMaster's departments of pathology and molecular medicine, pediatrics and kinesiology. Both Hawke and Perry are on the Board of Directors for the Canadian Society for Exercise Physiology.



They link the actual study, I only have access to the abstract, but it gives some clues. Compromised mitochondrial function?

Quote:
Mitochondrial oxidative capacity was significantly lower in participants with type 1 diabetes vs the control group, specifically at Complex II of the electron transport chain, without differences in mitochondrial content between groups.


If you've followed and understood Peter at Hyperlipid's electron transport chain, proton pump stuff, congratulations.

One thing he goes on an on about is fat vs. carbohydrate and their effect on dominance of the various complexes. Complex II is more active for metabolism of fat.

An interesting add on for a ketogenic diet--metabolism of acetoacetate requires conversion back to the acetyl-CoA it's produced from in the first place. Succinyl-CoA and succinate are two intermediates of the citric acid cycle, the second produced from the first. There's an "alternate" pathway for production of succinate from succinyl-CoA where that "CoA" from succinyl-CoA is donated to produce acetyl-CoA from acetoacetate. And if you look at a diagram of Complex II, it involves the production of fumarate from succinate. So we have a complex more involved in fat metabolism, that needs a metabolite, succinate, that ketone metabolism provides, and this is the complex that this study suggests is lacking in type I diabetics.

Quote:
"Skeletal muscle is our largest metabolic organ and is the primary tissue for clearing blood sugar after eating a meal, so we need to keep muscle as healthy as possible."


Skeletal muscle is the largest organ that clears blood sugar, maybe treating it as an organ for clearing blood sugar is a problem...
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  #2   ^
Old Mon, Apr-23-18, 05:06
SilverEm SilverEm is offline
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Plan: LC RPAH/FailSafe
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This is a most interesting subject. Thanks for bringing up the topic.

Stan Bleszynski wrote a blog post related to this, a few years ago.

http://stan-heretic.blogspot.com/20...ochondrial.html

Here is the first part:

Tuesday, October 4, 2011
Is t2 diabetes result of mitochondrial destruction?
.

1. A hypothesis:

- Metabolic syndrome and diabetes t2 results from mitochondrial destruction caused by overfeeding with glucose (and fructose but only in the liver), taking place over many years. An individual mitochondrion has (hypothetical assumption!) a fixed maximal total energy yield out of the two main energy sources: glucose (or glucose+fructose in the liver) plus fatty acids.

There is a self-clamping regulatory mechanism preventing mitochondrial overfeeding by fatty acids, by means of Malonyl-CoA/CPT1 feedback (see Peter’s discussion), but there are no very effective self-regulation feedbacks for glucose, only a partial mechanism reducing the glucose transport into in the cells! This partial mechanism is mediated by insulin regulating the transport of glucose into a cell through the cellullar membrane. This regulatory mechanism is not always effective or fast because the insulin secretion is not local to the cell, rather it is produced in the pancreas whose rate of secretion is regulated by the autonomous nervous system and pancreating glucose concentration involving many factors other than some particular mitochondria overload. Furthermore, the insulin regulation (blocking) of glucose can be overriden by high glucose concentration.

2. Conclusions.

A straight conclusion would be that a high carbohydrate diet can indeed be healthy and avoid diabetes as long as it restricts calories to prevent mitichondrial overfeeding. What is the limit? In my guesstimate (based on published literature) - probably around 25kcal/kg for women and 30kcal/kg for men.

A second straight conclusion is that a high fat low carb diet automatically avoids mitochondrial deterioration and thus diabetes among other degenerative diseases, by its built-in biochemical overfeeding protection mechanism. (note: my daily caloric intake on a high animal fat diet, is and has been around 20-25kcal/kg since 1999).

A third conclusion concerns a situation of the cells with the insufficient number of or worn-out mitochondria. Having lower total mitochondrial energy throughput, such cells may be forced to over-rely upon and and over-utilize the Penthose Phosphate Pathway (PPP) (also called the Penthose Shunt) which takes place in the cytosol volume outside of the mitochondria. This has originally been proposed by Dr. Jan Kwasniewski, the author of Optimal Diet in the 1970-ties. I found his idea fascinating, largely because there was no easy or obvious way of proving it at the time, and last but not least - it flew right against the medical dogma! Interestingly the PPP is mainly a synthesis pathways resulting in lipids and lipoproteins manufactured inside the cells, in-situ. Such as the infamous "cholesterol" plaque perhaps? Out of glucose? Like suggested by R.W. Stout in his 1968 and 1969 Lancet papers?


I found it well worth reading the rest of the blog post, the comments, and reading the references he cites.

This is one of his posts that has always stayed in my thoughts.
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  #3   ^
Old Mon, Apr-23-18, 05:32
teaser's Avatar
teaser teaser is offline
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Posts: 15,075
 
Plan: mostly milkfat
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Thanks. I haven't read Stan the Heretic in a while. Good to see his high fat diet hasn't killed him yet.
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  #4   ^
Old Mon, Apr-23-18, 05:54
SilverEm SilverEm is offline
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Plan: LC RPAH/FailSafe
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Hi, Teaser. Thanks for the chuckle.
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