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Type 1.5/LADA Diabetes
C peptide test and Medication
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<blockquote data-quote="Oldvatr" data-source="post: 2613051" data-attributes="member: 196898"><p>OK Now that I have digested the info on the GLP-1 RA medication, I feel a need to refine an answer I gave to the OP earlier.</p><p></p><p>While the medication is still active in the blood then it will override the normal operation of the intrinsic GLP-1 / Glucagon control regime. That will still have some effect but the medication will probably flood the GLP-1 receptors with tha agonist versions. These agonists will remain for at least the half life of the medicaton, and probably longer since they are designed to be impervious to attack by the DPP-4 hormones that usually remove the natural GLP-1R within 11 minutes. so the beta cells will remain primed and ready to go for much longer than we are designed to operate with.</p><p></p><p>Once primed, then it seems that while glucose levels are above 5 mmol/l then insulin will be generated and released. if the glucose level is 20 mmol/l or above then the pancreas will be running at maximum output and being thrashed. If Insulin resistance is high then this high level of insulin will persist way past the point where glucagon would naturally terminate the glucose / glucagon cycle by reducing and removing the GLP-1 enable.</p><p></p><p>The effect of the sulphonylurea meds I believe is to shift the voltage scale that controls the pulsing of the pump in the Beta Cells, and so the glucose level 'seen' by the beta cell appears to be higher than it really is, so again, the pancreas will overdrive the insulin output.</p></blockquote><p></p>
[QUOTE="Oldvatr, post: 2613051, member: 196898"] OK Now that I have digested the info on the GLP-1 RA medication, I feel a need to refine an answer I gave to the OP earlier. While the medication is still active in the blood then it will override the normal operation of the intrinsic GLP-1 / Glucagon control regime. That will still have some effect but the medication will probably flood the GLP-1 receptors with tha agonist versions. These agonists will remain for at least the half life of the medicaton, and probably longer since they are designed to be impervious to attack by the DPP-4 hormones that usually remove the natural GLP-1R within 11 minutes. so the beta cells will remain primed and ready to go for much longer than we are designed to operate with. Once primed, then it seems that while glucose levels are above 5 mmol/l then insulin will be generated and released. if the glucose level is 20 mmol/l or above then the pancreas will be running at maximum output and being thrashed. If Insulin resistance is high then this high level of insulin will persist way past the point where glucagon would naturally terminate the glucose / glucagon cycle by reducing and removing the GLP-1 enable. The effect of the sulphonylurea meds I believe is to shift the voltage scale that controls the pulsing of the pump in the Beta Cells, and so the glucose level 'seen' by the beta cell appears to be higher than it really is, so again, the pancreas will overdrive the insulin output. [/QUOTE]
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