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Fasting-Mimicking Diet Promotes Ngn3-Driven β-Cell Regeneration to Reverse Diabetes
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<blockquote data-quote="Hoping4Cure" data-source="post: 1437771" data-attributes="member: 393050"><p>I've definitely had a couple of hyper episodes, and not always on purpose. Time to cut off the "refeeding" I think. We just don't know what a good level of hyperglycemia is the ideal compromise between maximizing pressure for regeneration / maturation to occur, and avoiding overly stressing new or prior beta cells with extra workload and the harmful effects of glucotoxicity on top of that. There's also the new data posted here on d co uk about signalling being broken in beta cells which are capable of producing insulin but not of detecting elevated glucose levels to know when to activate themselves. This is what's meant by the "maturing step", and it seems less than optimal to build insulin production aspect prior to glucose detection aspect, since glucose detection in beta cells, when low, signals to alpha cells to start producing glucagon which will raise your blood sugars and avoid hypos. So if you see reduction in hypos there's a distinct chance that it's from more beta cells reaching the mature state, although alternate hypotheses such as less IR, like you said type 1s having type 2 symptoms and vice versa. These two diseases are both related to gut dysbios in some way, that's also known. And that means they both likely have a diet-driven component, if not necesserily for the initial cause of the disease but for its progression. I believe it's a feedback loop, some types of germs in the gut feed more on simple sugars and others more on fibers and complex nutrients, which in turn makes the IR and/or auto-immunity worse. This overlap is why, in retrospect, it doesn't seem odd at all that metformin and incretin mimetics work in both diseases. Apparently metformin doesn't even reduce IR, at least not directly, it helps by suppressing glucose production in the liver while simultaneously increasing healthy gut microbes in the lower gut, amongst other things! (like anti-aging).</p><p></p><p>I think it's becoming obvious that there's still a lot we don't know yet and the pieces of the puzzle are coming in every day. It's very exciting but also frustrating. I am so sick of this disease, enough already!</p></blockquote><p></p>
[QUOTE="Hoping4Cure, post: 1437771, member: 393050"] I've definitely had a couple of hyper episodes, and not always on purpose. Time to cut off the "refeeding" I think. We just don't know what a good level of hyperglycemia is the ideal compromise between maximizing pressure for regeneration / maturation to occur, and avoiding overly stressing new or prior beta cells with extra workload and the harmful effects of glucotoxicity on top of that. There's also the new data posted here on d co uk about signalling being broken in beta cells which are capable of producing insulin but not of detecting elevated glucose levels to know when to activate themselves. This is what's meant by the "maturing step", and it seems less than optimal to build insulin production aspect prior to glucose detection aspect, since glucose detection in beta cells, when low, signals to alpha cells to start producing glucagon which will raise your blood sugars and avoid hypos. So if you see reduction in hypos there's a distinct chance that it's from more beta cells reaching the mature state, although alternate hypotheses such as less IR, like you said type 1s having type 2 symptoms and vice versa. These two diseases are both related to gut dysbios in some way, that's also known. And that means they both likely have a diet-driven component, if not necesserily for the initial cause of the disease but for its progression. I believe it's a feedback loop, some types of germs in the gut feed more on simple sugars and others more on fibers and complex nutrients, which in turn makes the IR and/or auto-immunity worse. This overlap is why, in retrospect, it doesn't seem odd at all that metformin and incretin mimetics work in both diseases. Apparently metformin doesn't even reduce IR, at least not directly, it helps by suppressing glucose production in the liver while simultaneously increasing healthy gut microbes in the lower gut, amongst other things! (like anti-aging). I think it's becoming obvious that there's still a lot we don't know yet and the pieces of the puzzle are coming in every day. It's very exciting but also frustrating. I am so sick of this disease, enough already! [/QUOTE]
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