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  #16   ^
Old Sat, Jun-27-15, 18:19
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RawNut RawNut is offline
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I remember coming across this in my Promethase report:



I don't know if it's an up or down regulation of the enzyme but to hazard a guess, it's a downregulation consideringing it's associated with higher fasting insulin. About half the studied population are CC, which means that about 25 percent are TT, similar to the perentage who do well on low fat diets, according to Volek.

If this is the case, I think it'd be a grave mistake to inhibit this enzyme. It might work in the short-term to lower glucose, as does exogenous insulin, but will have negative ramifications in the long-term.

Last edited by RawNut : Sat, Jun-27-15 at 18:43.
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  #17   ^
Old Sat, Jun-27-15, 20:14
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teaser teaser is offline
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Yeah, my instinct is against rushing to market with some drug too. Anything that's really effective is liable to have magician's apprentice-type consequences of one type or another. Also, the stuff degrades insulin, amylin, and glucagon. What else does it degrade? These are just the things they checked for. It degrades amyloid plaque in the brain.... sounds like maybe it just targets peptides in general. Or at least a broad class of peptides. This is not a surgical strike, the probability of unintended consequences seems pretty high.
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  #18   ^
Old Tue, Nov-01-16, 07:08
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https://www.sciencedaily.com/releas...60419083245.htm

Quote:
Double advantage of potential new diabetes treatment

Blocking the hormone that raises sugar levels in the blood could increase insulin levels while keeping blood sugar levels down.

The findings in mice, to be published in eLife, point to a novel way to treat diabetes -- but only in some patients. They also challenge the benefits of the strategy in severely diabetic patients.

"Inhibiting the hormone glucagon has recently been explored as an alternative or supplement to insulin injection, but it has limitations," says lead author Pedro Herrera from the University of Geneva.

"Our research reveals why: the body needs to have some residual insulin production in order for a treatment blocking glucagon to work."

Other recent studies have suggested that diabetes is caused solely by an excess of glucagon rather than a deficiency of insulin. These studies found that blocking glucagon prevents excessively high blood glucose levels, despite a complete lack of insulin. They suggested that blocking glucagon rather than regularly injecting insulin could be a treatment for hyperglycemia.

However, the current findings indicate that the models used were not totally lacking in insulin and that just blocking glucagon was only effective if some insulin was still being produced. For the new research, the scientists used transgenic mice in which insulin could be more efficiently eliminated. These mice became severely diabetic.

Around three quarters of patients with type 1 diabetes possess a small number of the beta cells needed to produce insulin. In these patients, blocking glucagon, in addition to insulin replacement, could help keep blood sugar levels in check. It could also result in some glucagon-producing alpha cells converting into beta cells and producing more insulin.

Sugar accumulates in the blood after a meal, triggering the release of insulin from the pancreas to allow tissues to use and store it. During fasting or exercising, glucagon is released and opposes the action of insulin. The balance between the two pancreatic hormones keeps blood sugar levels steady.

Using insulin therapy and blocking glucagon as a combined treatment could in some cases provide a more effective and safer way to maintain a healthy balance and avoid the peaks and troughs of blood sugar levels. Beyond that, future therapies could focus on regenerating beta cells by reprogramming alpha cells.

The number of people with diabetes has risen from 108 million in 1980 to 422 million in 2014, affecting 8.5% of over-18s. Diabetes is a major cause of blindness, kidney failure, heart attacks, stroke, and lower limb amputation. Type 1 diabetes commonly starts in childhood and is caused by the body's own immune system, which attacks and destroys the insulin-producing cells in the pancreas.
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  #19   ^
Old Tue, Nov-01-16, 09:26
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Quote:
Originally Posted by RawNut
If this is the case, I think it'd be a grave mistake to inhibit this enzyme. It might work in the short-term to lower glucose, as does exogenous insulin, but will have negative ramifications in the long-term.


I completely agree. In the case of statins, they were totally wrong about the process, and statins might be the most toxic drug ever made, from what I've read.

In this case, they have the action right: but seem to have no clue what else might be going on. Considering that drug trials weed out anyone who exhibits side effects, this could lead to really messed up effects downstream.

One thing that really scares me is how I used to think drug side effects were temporary; stop taking the drug, and they would go away. But statins are capable of creating side effects which linger; and if they trigger ALS (in people with genetic susceptibility, that has been studied and supported) there's no going back.

I know of two others: Accutane (for acne) and Propecia (for male pattern baldness) are two drugs that seem capable of triggering a terrible cascade of effects which cannot be reversed.
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  #20   ^
Old Tue, Mar-14-17, 11:28
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This Sciencedaily article reminded me of this thread.

https://www.sciencedaily.com/releas...70308114706.htm

Quote:
Diabetes drug shows promise for safely treating, detecting Alzheimer's disease
First time tested in humans

Summary:
Treatment with the diabetes drug amylin (or pramlintide) safely improves learning and memory function in Alzheimer's disease (AD) patients and reduces the AD pathology in their brains. The findings also may lead to the development of a blood test for AD.

As the number of patients with Alzheimer's disease (AD) rapidly increases, new treatments as well as blood tests that are simple and can be easily performed in a doctor's office to diagnose are urgently needed.

A new study has found treatment with the diabetes drug amylin (or pramlintide) safely improves learning and memory function in AD patients and reduces the AD pathology in their brains. The findings, which appear in the Journal Translational Research and Clinical Interventions, also may lead to the development of a blood test for AD.

Currently, lumbar punctures to detect biomarkers in cerebrospinal fluid and positron emission tomography imaging scans are used to diagnose AD. Unfortunately many patients are fearful of these procedures and the high cost is prohibitive.

"A single injection of pramlintide into our patients was well tolerated and reduced the amyloid burden as well as lowered the concentrations of amyloid-β peptides, a major component of AD in the brain," explained corresponding author Wendy Qiu, MD, PhD, associate professor of psychiatry and pharmacology and experimental therapeutics at Boston University School of Medicine.

"Our study suggests a potential role for the creation of a blood test that relies on pramlintide, which could cross the blood-brain barrier and help to translocate the biomarkers related to AD pathology including amyloid-β peptides and neuroinflammation, from the brain into the bloodstream where they can be detected," added Qiu.


I think I've seen the idea that misfolded endogenous amylin might be an initiating factor in accumulation of amyloid type plaques outside of the pancreas, including in the brain. It would make sense if exogenous amylin reduced production of amylin in the pancreas--so a decrease in misfolded amylin protein could result.
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