Ohm20 posted this just recently:
Sometimes I run across things that make me wonder.
Quote:
Ozempic adds 'saving kidneys, hearts and lives' to its list of benefits
An international clinical trial led by researchers from the University of New South Wales (UNSW) Sydney found that a low weekly dose of semaglutide improved kidney function and reduced the risk of death in people with type 2 diabetes and chronic kidney disease.
They found that semaglutide reduced the risk of ‘major kidney disease events’ by 24%. Kidney events included a combination of the onset of kidney failure requiring dialysis or organ transplantation and at least a 50% reduction in kidney function. The risk of death from any cause was 20% lower. The risk of cardiovascular events such as heart attack and stroke was 18% lower for those taking semaglutide, and the drug slowed the loss of kidney function, lowered systolic blood pressure, and reduced participants’ body weight. However, 49.6% of participants suffered serious adverse events from taking semaglutide, but this was lower than in the placebo group (53.8%).
https://newatlas.com/medical/ozempic-kidney-d...eath-risk/
We know that CCR5 blockade also has positive effects on kidney disease, diabetes, stroke and heart disease. Ozempic's mechanism of action is binding to GLP-1 receptors and activating them. So I wondered if CCR5 blockade had any effect on GLP-1.
I ran across a study that looked at met-RANTES blockade of CCR1. The study is a bit misguided because at the same time met-RANTES was blocking CCR1 it was also blocking CCR5. CCR5 is expressed massively compared to CCR1 so the effect is mostly attributable to CCR5. So leronlimab can do what Ozempic does without the side effects.
Quote:
Type 2 diabetes is associated with elevated circulating levels of the chemokine RANTES and with decreased plasma levels of the incretin hormone glucagon-like peptide 1 (GLP-1). GLP-1 is a peptide secreted from intestinal L-cells upon nutrient ingestion. It enhances insulin secretion from pancreatic β-cells and protects from β-cell loss but also promotes satiety and weight loss. In search of chemokines that may reduce GLP-1 secretion we identified RANTES and show that it reduces glucose-stimulated GLP-1 secretion in the human enteroendocrine cell line NCI-H716
These data show that RANTES is involved in altered secretion of glucagon-like peptide hormones most probably acting through SGLT1, and our study identifies the RANTES-receptor CCR1 as a potential target in diabetes therapy.
https://journals.physiology.org/doi/full/10.1...00329.2013
I just took a look at the leronlimab regulator list because this all seemed really familiar. I forgot that I had already looked at other studies and already had GLP-1 [+] on the list. Now I'm wondering why I forgot that.
Investors Hangout: https://investorshangout.com/post/view?id=669...z8e5a2XKFv
Sometimes I run across things that make me wonder.
Quote:
Ozempic adds 'saving kidneys, hearts and lives' to its list of benefits
An international clinical trial led by researchers from the University of New South Wales (UNSW) Sydney found that a low weekly dose of semaglutide improved kidney function and reduced the risk of death in people with type 2 diabetes and chronic kidney disease.
They found that semaglutide reduced the risk of ‘major kidney disease events’ by 24%. Kidney events included a combination of the onset of kidney failure requiring dialysis or organ transplantation and at least a 50% reduction in kidney function. The risk of death from any cause was 20% lower. The risk of cardiovascular events such as heart attack and stroke was 18% lower for those taking semaglutide, and the drug slowed the loss of kidney function, lowered systolic blood pressure, and reduced participants’ body weight. However, 49.6% of participants suffered serious adverse events from taking semaglutide, but this was lower than in the placebo group (53.8%).
https://newatlas.com/medical/ozempic-kidney-d...eath-risk/
We know that CCR5 blockade also has positive effects on kidney disease, diabetes, stroke and heart disease. Ozempic's mechanism of action is binding to GLP-1 receptors and activating them. So I wondered if CCR5 blockade had any effect on GLP-1.
I ran across a study that looked at met-RANTES blockade of CCR1. The study is a bit misguided because at the same time met-RANTES was blocking CCR1 it was also blocking CCR5. CCR5 is expressed massively compared to CCR1 so the effect is mostly attributable to CCR5. So leronlimab can do what Ozempic does without the side effects.
Quote:
Type 2 diabetes is associated with elevated circulating levels of the chemokine RANTES and with decreased plasma levels of the incretin hormone glucagon-like peptide 1 (GLP-1). GLP-1 is a peptide secreted from intestinal L-cells upon nutrient ingestion. It enhances insulin secretion from pancreatic β-cells and protects from β-cell loss but also promotes satiety and weight loss. In search of chemokines that may reduce GLP-1 secretion we identified RANTES and show that it reduces glucose-stimulated GLP-1 secretion in the human enteroendocrine cell line NCI-H716
These data show that RANTES is involved in altered secretion of glucagon-like peptide hormones most probably acting through SGLT1, and our study identifies the RANTES-receptor CCR1 as a potential target in diabetes therapy.
https://journals.physiology.org/doi/full/10.1...00329.2013
I just took a look at the leronlimab regulator list because this all seemed really familiar. I forgot that I had already looked at other studies and already had GLP-1 [+] on the list. Now I'm wondering why I forgot that.
Investors Hangout: https://investorshangout.com/post/view?id=669...z8e5a2XKFv
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