Is there a trusted pharmacy that is typically used?
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See here:
- Buy Rapamycin Online - List of Reliable Pharmacies
- What Brands of Medications to buy: Generally Good Indian Pharma Companies
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Doing further research, I am wondering about drug interactions. For example, what if your version of poor glucose control does not result from any defect in beta cells GSIS, and since one way in which imeglimin works is that it “fixes” GSIS, you may surmise that imeglimin might not be for you. But what if you are also taking another drug, say, sirolimus, which longer term or with some protocols (daily dosing?) actually damages beta-cells GSIS? Now you might be adding this defect to your glucose control issues, and what if under those circumstances (i.e. you taking sirolimus) taking imeglimin might make sense, whereas without sirolimus it does not.
Evidence for Rapamycin Toxicity in Pancreatic β-Cells and a Review of the Underlying Molecular Mechanisms
Quote:
“Overall, the majority of these studies demonstrate significant effects of rapamycin on glucose homeostasis, and the combined evidence strongly suggests that rapamycin adversely affects GSIS from β-cells.”
Of course, GSIS from beta-cells can be impacted through various mechanisms, so it remains to be shown whether imeglimin can “fix” the damage sirolimus does to beta-cells. Again we need to take a closer look at the MOA of both drugs to guess at any possible interaction, and then test it. The research continues.
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“suppresses hepatic neoglucogenesis” “fixes GSIS”
Aren’t these good things? GSIS declines with age.
(Gemini)
"Yes, Imeglimin suppresses hepatic gluconeogenesis (the production of new glucose by the liver). It is a core part of its “dual-benefit” mechanism of action, which targets the liver, skeletal muscle, and pancreatic beta cells.
Mechanism in the Liver
Imeglimin reduces excessive glucose production through several mitochondrial-dependent pathways:
Mitochondrial Rebalancing: It acts on the mitochondrial respiratory chain by partially and competitively inhibiting Complex I and restoring the activity of Complex III.
Energy Regulation: This rebalancing lowers the ATP/ADP ratio and increases mitochondrial redox potential in hepatocytes, which reduces the driving force for gluconeogenesis."
"Age-Related Decline in GSIS
In humans, beta cell function generally declines with age, estimated at a rate of approximately 1% per year. This decline is often independent of peripheral insulin resistance or body mass index.
Reduced Stimulated Secretion: Islets from younger donors (<40 years) typically exhibit significantly higher GSIS than those from older donors.
Elevated Basal Secretion: Aging is often associated with an increase in basal (fasting) insulin secretion, which may represent a compensatory state but also reduces the cell’s “dynamic range” when stimulated by high glucose.
Mechanisms of Dysfunction."
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