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Post by peppy on Feb 24, 2016 7:04:38 GMT -5
Might be too much scientific jargon, but did a quick search and found an article from 2002!!! (amazing how much was known back then about GLP-1) It's pretty descriptive and does a good job explaining how it works if anyone is interested. diabetes.diabetesjournals.org/content/51/suppl_3/S434.fullThank you stevil. I tried to read it. I liked the discussion of ions and their charge, positive/negative.
For me a good read on why to avoid these meds.
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Post by mnholdem on Feb 24, 2016 8:21:02 GMT -5
Some excerpts from the abstract: The ability of GLP-1 to enhance insulin secretion in a glucose-dependent manner remains perhaps its most promising characteristic from a clinical perspective. The recent discovery that GLP-1 is able to promote β-cell mass expansion has added to the clinical promise of this peptide, or more likely a molecule that activates one or all of GLP-1’s signaling pathways.
GLP-1 is proposed to modulate glucose-stimulated insulin secretion (GSIS) by regulating the activity of several ion channels involved in KATP-dependent insulin secretion as well as steps distal to channel modulation.
The physiological consequences of GLP-1-facilitated KATP channel closure would be to 1) augment the excitability of cells already above the threshold for insulin release and 2) increase the percentage of β-cells actively secreting insulin at glucose concentrations normally subthreshold for the release of insulin.
With respect to GLP-1 therapy, it is unlikely that it will gain widespread acceptance in the diabetes community when effective oral agents are available. However, one can anticipate that a small molecule that holds some or all of the properties of native GLP-1 will eventually be developed.
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It seemed odd to me that the abstract made no mention, whatsoever, comparing GLP-1 therapy to insulin therapy. Then again, it's purpose is to help the reader better understand how GLP-1 works, and there are several physiological functions that the authors themselves state are still not understood.
While promising, the primary issue I have with GLP-1 is that it signals the pancreas to produce MORE insulin when, in fact, early diabetes often results from deteriorating insulin production caused by exhausted β-cells. GLP-1 augments the excitability of β-cells, triggering them to produce more insulin even though the β-cells are already depleted and unable to keep up with insulin demand, whereas a monomer insulin (ie Afrezza) simply provides needed insulin which enables the depleted β-cells to recuperate.
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I found the linked abstract to be an interesting read. Nonetheless, I believe that rather than usurping the body's natural functions by manipulating β-cells channels, which the authors themselves readily admit is not clearly understood and needs more study, it is better to provide something that the body normally uses but simply cannot produce enough of: human insulin.
Afrezza monomer human insulin serves two purposes here. First, if a patient's pancreas β-cells are overtaxed, inhaling monomer insulin helps take the load off the β-cells in the pancreas, enabling them to heal and regenerate greater amounts of insulin over time, possibly to a point where exogenous administration of insulin may no longer be necessary (aka remission). Second, if a patient's pancreas has been damaged beyond repair, exogenous insulin is required anyway. Afrezza promises unprecedented control, largely because of its speed. A GLP-1, however, would be largely ineffective at stimulating any remaining β-cells that are still able to produce insulin.
Arguably because monomer insulin is more natural, it offers the better treatment with the least amount of side effects.
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BTW, good luck with your upcoming exams. I hope you do well.
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