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<blockquote data-quote="SimonCrox" data-source="post: 2089918" data-attributes="member: 388174"><p>Semaglutide is really interesting because in SUSTAIN 6 it reduced adverse cardiovascualr outcomes:-</p><p></p><p><a href="https://www.nejm.org/doi/full/10.1056/NEJMoa1607141" target="_blank">https://www.nejm.org/doi/full/10.1056/NEJMoa1607141</a></p><p></p><p>This is of crucial importance since diabetic folk are at increased risk of heart attack and stroke.</p><p></p><p>Interestingly, semaglutide can be given orally (although not available yet) and reduces adverse events slightly - this was not so significant as in SUSTAIN 6, but the study was of far shorter duration.</p><p></p><p><a href="https://www.nejm.org/doi/10.1056/NEJMoa1901118" target="_blank">https://www.nejm.org/doi/10.1056/NEJMoa1901118</a></p><p></p><p>To put things in perspective, liraglutide and dulaglutide decrease adverse CV outcomes whaereas exenatide and lixesenatide do not. If you look at the names, -glutide drugs are good (derived from human GLP-1) and -natide drugs (derived from exendin 4 in gila maonster saliva) do not have the CV protection.</p><p></p><p>Some tablets, SGLT-2 inhibitors, and pioglitazone and probably metformin decrease CV events. It is handy that we have a large selection of drugs available if diet / lifestyle do not do the trick</p><p></p><p>Semaglutide has been on the UK market since early this year, I think, so would be interesting to hear peoples' experience of it.</p><p></p><p>One of the features of T2DM is that the body fails to suppress glucagon levels after meals whereas in non-diabetic people, the glucagon level drops a bit after meals - supplementing GLP-1 prevents the rise in glucoagon and supplements the rise in insulin after meals.</p><p></p><p>Thanks for pointing out about the retinopathy; Diabetic retinopathy complications occurred in 50 patients (3.0%) in the semaglutide group and 29 (1.8%) in the placebo group (hazard ratio, 1.76; 95% CI, 1.11 to 2.78; P=0.02). The cause of this was not clear, and the autohrs wondered if it might have been due to rapid improvement in HbA1c. Certainly something to be aware of. Conversely, I think that there was less nephropathy on the semaglutide . I don't think this was seen on the other agents' trials, but I will go and look them up</p><p></p><p>Thanks for interesting post</p><p></p><p>Best wishes</p></blockquote><p></p>
[QUOTE="SimonCrox, post: 2089918, member: 388174"] Semaglutide is really interesting because in SUSTAIN 6 it reduced adverse cardiovascualr outcomes:- [URL]https://www.nejm.org/doi/full/10.1056/NEJMoa1607141[/URL] This is of crucial importance since diabetic folk are at increased risk of heart attack and stroke. Interestingly, semaglutide can be given orally (although not available yet) and reduces adverse events slightly - this was not so significant as in SUSTAIN 6, but the study was of far shorter duration. [URL]https://www.nejm.org/doi/10.1056/NEJMoa1901118[/URL] To put things in perspective, liraglutide and dulaglutide decrease adverse CV outcomes whaereas exenatide and lixesenatide do not. If you look at the names, -glutide drugs are good (derived from human GLP-1) and -natide drugs (derived from exendin 4 in gila maonster saliva) do not have the CV protection. Some tablets, SGLT-2 inhibitors, and pioglitazone and probably metformin decrease CV events. It is handy that we have a large selection of drugs available if diet / lifestyle do not do the trick Semaglutide has been on the UK market since early this year, I think, so would be interesting to hear peoples' experience of it. One of the features of T2DM is that the body fails to suppress glucagon levels after meals whereas in non-diabetic people, the glucagon level drops a bit after meals - supplementing GLP-1 prevents the rise in glucoagon and supplements the rise in insulin after meals. Thanks for pointing out about the retinopathy; Diabetic retinopathy complications occurred in 50 patients (3.0%) in the semaglutide group and 29 (1.8%) in the placebo group (hazard ratio, 1.76; 95% CI, 1.11 to 2.78; P=0.02). The cause of this was not clear, and the autohrs wondered if it might have been due to rapid improvement in HbA1c. Certainly something to be aware of. Conversely, I think that there was less nephropathy on the semaglutide . I don't think this was seen on the other agents' trials, but I will go and look them up Thanks for interesting post Best wishes [/QUOTE]
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