I've seen quite a few diabetics on here. I hope this helps.


This has saved my life and has helped me to get off the mountain of pills the doctors were prescribing, that included all the side effects that came with them.

This helps with the production of insulin by the pancrius but stays dorment if none is needed (a smart hormone ). They have discovered why the brain and pancrius don't communicate, this is it. When was the last time you felt full after eating?

Diet and excersize are still essentail.

This does not work like insulin and will not help non-diabetics. It may how ever balance the insulin tolerance caused by HGH.


Liraglutide (NN2211), marketed under the brand name Victoza, is a long-acting glucagon-like peptide-1 (GLP-1) analog that has been developed by Novo Nordisk for the treatment of type 2 diabetes. The product was approved by the European Medicines Agency (EMA) on July 3, 2009, and by the U.S. Food and Drug Administration (FDA) on January 25, 2010.[1][2][3][4][5]

Liraglutide is marketed under the brandname Victoza in the U.S., India, Canada, Europe and Japan. It has been launched in Germany, Denmark, the Netherlands, the United Kingdom, Ireland, Sweden, Japan, Canada, the United States, France, Malaysia and Singapore.

Phase I trials of an oral variant of Victoza (NN9924) started in 2010.[6]

Contents [hide]
1 Cancer concerns
2 Pharmacodynamics
3 Pharmacokinetics
4 Controversy
5 Marketing
6 See also
7 References


[edit] Cancer concernsOn April 2, 2009, an FDA advisory panel reviewed the significance of malignant C-cell carcinoma and thyroid C-cell focal hyperplasia in rats and mice. Some[who?] say the tumors were caused by a nongenotoxic, specific receptor-mediated mechanism to which rodents are particularly sensitive, whereas nonhuman primates and humans are not.[7][8]

The Victoza label carries a Black Box Warning:

“ Because of the uncertain relevance of the rodent thyroid C-cell tumor findings to humans, prescribe Victoza only to patients for whom the potential benefits are considered to outweigh the potential risk.[9] ”

The FDA said serum calcitonin, a biomarker of medulliary thyroid cancer, was slightly increased in liraglutide patients, but still within normal ranges, and it required ongoing monitoring for 15 years in a cancer registry.[10]

Novo Nordisk has reminded healthcare professionals of the serious risks associated with the use of Victoza. Liraglutide causes dose-dependent and treatment-duration-dependent thyroid C-cell tumors in rats and mice. It is unknown whether Victoza causes thyroid C-cell tumors, including medullary thyroid carcinoma (MTC), in humans.[11]

[edit] PharmacodynamicsStudies to date suggest liraglutide improves control of blood glucose.[12]

It reduces meal-related hyperglycemia (for 12 hours after administration) by increasing insulin secretion, delaying gastric emptying, and suppressing prandial glucagon secretion.

Liraglutide is an acylated human glucagon-like peptide-1 (GLP-1) receptor agonist, with a 97% amino acid sequence identity to endogenous human GLP-1(7-37). GLP-1(7-37) represents <20% of total circulating endogenous GLP-1. Like GLP-1(7-37), liraglutide activates the GLP-1 receptor, a membrane-bound cell-surface receptor coupled to adenylyl cyclase by the stimulatory G-protein, Gs, in pancreatic beta cells. Liraglutide increases intracellular cyclic AMP (cAMP), leading to insulin release in the presence of elevated glucose concentrations. This insulin secretion subsides as blood glucose concentrations decrease and approach euglycemia. Liraglutide also decreases glucagon secretion in a glucose-dependent manner. The mechanism of blood glucose lowering also involves a delay in gastric emptying. GLP-1(7-37) has a half-life of 1.5–2 minutes due to degradation by the ubiquitous endogenous enzymes, dipeptidyl peptidase IV (DPP-IV) and neutral endopeptidases (NEP). Unlike native GLP-1, liraglutide is stable against metabolic degradation by both peptidases and has a plasma half-life of 13 hours after subcutaneous administration. The pharmacokinetic profile of liraglutide, which makes it suitable for once daily administration, is a result of self-association that delays absorption, plasma protein binding and stability against metabolic degradation by DPP-IV and NEP.[13]

Liraglutide may have advantages over current therapies:

It acts in a glucose-dependent manner, meaning it will stimulate insulin secretion only when blood glucose levels are higher than normal. Consequently, it shows negligible risk of hypoglycemia.
It has the potential for inhibiting apoptosis and stimulating regeneration of beta cells (seen in animal studies).
It decreases appetite and maintains body weight, as shown in a head-to-head study versus glimepiride.[14]
It lowers blood triglyceride levels.
It has only mild and transient side effects, mainly gastrointestinal.
[edit] PharmacokineticsLiraglutide is a once-daily GLP-1 derivative for the treatment of type 2 diabetes. GLP-1, in its natural form, is short-lived in the body (the half-life after intramuscular injection is approximately half an hour), so it is not very useful as a therapeutic agent. However, liraglutide has a half-life after subcutaneous injection of 11–15 hours, making it suitable for once-daily dosing (less frequent than the currently approved Byetta form of exenatide, which is twice daily, but considerably more frequent than the once weekly Bydureon form of exenatide, which received marketing approval from the FDA on January 27, 2012).

The prolonged action of liraglutide is achieved by attaching a fatty acid molecule at one position of the GLP-1 molecule, enabling it to bind to albumin within the subcutaneous tissue and bloodstream. The active GLP-1 is then released from albumin at a slow, consistent rate. Binding with albumin also results in slower degradation and reduced elimination of liraglutide from the circulation by the kidneys compared to GLP-1.[citation needed]