BoredLawyer, This is a interesting line of rese
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Posted On: 05/21/2020 7:43:33 AM
Re: Bored Lawyer #34856
BoredLawyer,
This is a interesting line of research for us. The relationship between Diabetes Mellitus and HIV has been known for long time.
https://link.springer.com/article/10.1186/1744-8603-5-9
from,
https://dmsjournal.biomedcentral.com/articles...8-5996-3-2
And it seems that HAART therapy plays a good role in exacerbating it.
Obviously, the question is: Would Leronlimab have the same effect? worse?? Better ??
If we can improve the current status quo it will be another reason to go Leronlimab (go monotherapy, that is), and a good one due to the high prevalence of diabetes among HIV sufferers.
So ... we don't know for sure the answer at the moment, I guess more research needs to be done in humans , rather than in mice, but for sure, the other therapies are having a pronounced negative effect on the problem.
This is a interesting line of research for us. The relationship between Diabetes Mellitus and HIV has been known for long time.
https://link.springer.com/article/10.1186/1744-8603-5-9
from,
https://dmsjournal.biomedcentral.com/articles...8-5996-3-2
Quote:
A recent analysis has found that diabetes is four fold more common is HIV-infected men exposed to highly active anti retroviral therapy (HAART) than in HIV seronegative men. HAART is based on the use of a class of drugs known as protease inhibitors (PIs), which have been used extensively as antiretroviral agents. The various PIs used include atazanavir, darunavir, saquinavir and ritonavir.
PIs have been shown to increase insulin resistance and reduce insulin secretion, by interfering with GLUT-4 mediated glucose transport. Risk factors for development of diabetes with PI therapy include positive family history of diabetes, weight gain, lipodystrophy, old age and hepatitis C infection. PIs interfere with cellular retinoic acid-binding protein type 1 (CRABP 1) that interacts with peroxisomal proliferator-activated receptor (PPAR) γ. Inhibition of PPAR-γ promotes adipocyte inflammation, release of free fatty acids and insulin resistance. Hyperglycemia resolves in almost all patients when PIs are discontinued.
All PIs do not have the same metabolic effects. Indinavir induces insulin resistance with no effect on lipid metabolism, whereas lopinavir and ritonavir increase fasting triglycerides and free fatty acids, but do not worsen insulin sensitivity. Indinavir and retonavir both block GLUT -4, but no such effect is noted with amprenavir, and atazanzvir. HIV-infected patients treated for 12 weeks with nelfinavir, indinavir, liponavir or saquinavir, demonstrate alterations in first phase insulin release with a 25% reduction in β-cell dysfunction.
And it seems that HAART therapy plays a good role in exacerbating it.
Obviously, the question is: Would Leronlimab have the same effect? worse?? Better ??
If we can improve the current status quo it will be another reason to go Leronlimab (go monotherapy, that is), and a good one due to the high prevalence of diabetes among HIV sufferers.
So ... we don't know for sure the answer at the moment, I guess more research needs to be done in humans , rather than in mice, but for sure, the other therapies are having a pronounced negative effect on the problem.
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