Talk:Liraglutide

Pharmacology Mid‑importance

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Medicine Mid‑importance

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Ideal sources for Wikipedia's health content are defined in the guideline Wikipedia:Identifying reliable sources (medicine) and are typically review articles. Here are links to possibly useful sources of information about Liraglutide.

PubMed provides review articles from the past five years (limit to free review articles)
The TRIP database provides clinical publications about evidence-based medicine.
Other potential sources include: Centre for Reviews and Dissemination and CDC

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Link to CAS

The link does not work. It is unclear whether the CAS number has changed or whether the website is not functioning correctly. The CAS number reported seems to be correct, however. — Preceding unsigned comment added by 2606:6000:CD8C:E600:39EA:CC7F:78DB:75B5 (talk) 19:48, 27 September 2016 (UTC)[reply]

BBC Article

BBC Article - [1] --33rogers (talk) 12:14, 23 October 2009 (UTC)[reply]

Intro needs work

Intro needs placing inline citations [1-5] in more appropriate places.

Also note US FDA approval closely followed Japanese approval in Jan 2010. Rod57 (talk) 03:08, 7 April 2010 (UTC)[reply]

Black Box Versus Boxed Warning

We need a definitive ruling regarding this nomenclature. —Preceding unsigned comment added by 173.3.169.0 (talk) 17:55, 28 February 2010 (UTC)[reply]

I agree, and I've made the change. (I would have hoped this issue would have been laid to rest long ago, but some people continue to use the colloquial "black box warning," probably because it sounds more sinister). DoctorEric (talk) 21:26, 11 October 2013 (UTC)[reply]

Overall Improvements to the Article

This article has a lot of issues. A LOT! I hope to tackle several of them in the near future, including:

Restoring article to NPOV standards.

Making sure that the language in the article reflects the content of the cited sources (one of my biggest pet peeves is when editors use out-of-context and cherry-picked verbiage to distort the meaning of the source they are purportedly citing).

Reordering the sections of the article (putting the pharmacodynamics/-kinetics sections, because they deal with defining characteristics of a drug, before discussions of possible adverse effects) — Actually, I'm going to do that last one now.

I'll be back when I have some more time to make the other corrections. DoctorEric (talk) 22:05, 11 October 2013 (UTC)[reply]

Does it cross the blood brain barrier and enable peripheral insulin sensitization in the brain ?

Several journal articles have mentioned this class of medications for possible (initially off-label use but also for studies) use in Alzheimer's due to recent research indicating decreased insulin sensitivity in the brains of Alzheimer's patients, and initial work suggesting potential benefits from intranasal insulin. (The advantage of intranasal insulin (over normal administration) in this context is that it more readily crosses the blood brain barrier resulting in increased insulin levels (and activity) more specifically in the brain without dramatically increasing insulin levels throughout the body. Presumably, the use of insulin sensitizers in this context would similarly need to promote LOCAL insulin sensitivity (Eg. in the brain)). Please discuss & goto PUBMED if you need to add some references. Thanks.

Wheight Loss?

This is being marketed as a weight loss drung, any comments? — Preceding unsigned comment added by Alessio.aguirre (talk • contribs) 17:35, 30 November 2014 (UTC) Not true I went to the fda website and it says it's only for diabetes type 2 A8v (talk) 16:03, 27 December 2014 (UTC)[reply]

FDA approved for this purpose about a week ago. Formerly 98 (talk) 16:07, 27 December 2014 (UTC)[reply]

It is used as a weight loss drug and it works Rustygecko (talk) 09:35, 1 September 2022 (UTC)[reply]

Pls help: can anyone reconcile suppression of prandial glucagon secretion with promotion of prandial satiety to end meals?

I noticed that the book by Goldstein that we cite, and also Handbook of Biologically Active Peptides edited by Abba Kastin, cite this 1982 study of rats, which found that that antagonizing circulating glucagon during meals increased meal size, implicating prandial glucagon secretion in normal meal-ending satiation. Our article reports that these GLP-1 receptor agonists suppress prandial glucagon secretion, which should presumably have a similar effect, yet we also report that they promote satiety. Any ideas? Layzeeboi (talk) 08:36, 18 January 2015 (UTC)[reply]