Heart failure, mitochondria, and diabetes
https://www.sciencedaily.com/releas...80105135241.htm
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Interesting that the new imaging technique shows mitochondrial fragmentation in the heart, at least, to be an artifact of conventional electron microscopy. Quote:
This part, not so much. Athletes get fattier muscles, paired with an increase in muscle insulin sensitivity. Type II diabetics and people with insulin resistance get fattier muscles, paired with a decrease in muscle insulin sensitivity. Aside from that, there's a big difference from any organ taking in lots of free fatty acids and lots of glucose, and an organ taking in free fatty acids and lower amounts of glucose. If your heart's main fuel is fat, but most of what you eat is glucose, that's a far cry from being on a low carb diet and burning mostly fat. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5284490/ More about mitochondria form and function in diabetes. Quote:
https://newatlas.com/fasting-increa...-harvard/52058/ And a bit on fasting's effects on mitochondria. Quote:
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Teaser it's a little bit over my head. When they say excess fat, do they mean body fat or dietary fat?
People with hypothyroidism are more prone to dying of heart disease also. Would it be because we can't burn free fatty acids when the thyroid levels are low. I've also read that once thyroid levels are restored there's a period of time before the mitochondria normalize. Is this article saying that can be facilitated by fasting? |
Whatever they actually meant, I think they should have meant body fat, with what constitutes "excess" varying from person to person. Past a certain level of storage in fat tissue itself, excess fat starts to accumulate in all sorts of lean tissue, muscle, liver, heart, pancreas. With the exception of some increase fat in muscle in athletes, it's generally a bad deal and interferes with mitochondrial function etc.
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I have seen suggestions that for people with heart failure, reduced energy due to hypothyroidism could make things worse. You could see a vicious cycle, heart failure reduces oxygenation of blood, higher fat vs. carbohydrate increases reliance on oxygen for energy supply. A ketogenic diet is different vs. a diet that's just high in both fat and carbohydrate, Dominic D'Agostino's work on the ketogenic diet started with the observation that people and animals were more resilient in low oxygen conditions when ketones were elevated. Hypothyroid also seems to increase risk of atherosclerosis, and there seems to be some effect on vasodilation. I've only skimmed through this, but it's interesting; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4318631/ "Thyroid and the Heart." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4590606/ Quote:
I haven't really looked into thryoid's effects on mitochondria. There's just so much of this stuff. This looks relevant, I haven't read it, just sticking this here to read later and in case anybody else is interested. |
Thanks teaser great papers. I skimmed and found this interesting tidbit in the mito one.
Taken together, our data demonstrate that T3 maintains increased hepatic metabolic activity by promoting turnover of the intracellular pool of mitochondria through increased rates of mitophagy and mitochondrial synthesis. Thus, induction of mitophagy by intracellular ROS derived from increased mitochondrial energy production can help prevent the accumulation of damaged mitochondria as well as promote cellular health and function in hypermetabolic states. Mitochondrial function and its quality control are important factors in metabolic diseases such as diabetes and nonalcoholic fatty liver disease as well as aging.51,52 Our studies thus suggest that T3 or its analogs may be beneficial for treating these conditions by promoting mitochondrial turnover.53 Lastly, our finding that T3 stimulation of mitophagy occurs via a pathway involving increased ROS production; intracellular Ca2+ increase; CAMKK2, PRKAA1/AMPK, and ULK1 activation now provides several new therapeutic targets for maintaining mitochondrial number and function that could lead to novel treatments for metabolic and aging-related diseases.54 |
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