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:
They link the actual study, I only have access to the abstract, but it gives some clues. Compromised mitochondrial function? Quote:
If you've followed and understood Peter at Hyperlipid's electron transport chain, proton pump stuff, congratulations. :lol: 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 the largest organ that clears blood sugar, maybe treating it as an organ for clearing blood sugar is a problem... |
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. |
Thanks. I haven't read Stan the Heretic in a while. Good to see his high fat diet hasn't killed him yet. :D
|
Hi, Teaser. :) Thanks for the chuckle.
|
All times are GMT -6. The time now is 13:08. |
Copyright © 2000-2024 Active Low-Carber Forums @ forum.lowcarber.org
Powered by: vBulletin, Copyright ©2000 - 2024, Jelsoft Enterprises Ltd.