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Liraglutide in the management of type 2 diabetes.

Wajcberg E, Amarah A - Drug Des Devel Ther (2010)

Bottom Line: Research has shown additional mechanisms, including incretin deficiency or resistance in the gastrointestinal tract.Liraglutide is a modified form of human glucagon-like peptide-1.Liraglutide has demonstrated glucose-dependent insulin secretion, improvements in β-cell function, deceleration of gastric emptying, and promotion of early satiety leading to weight loss.

View Article: PubMed Central - PubMed

Affiliation: Premier Nephrology and Hypertension, Internal Medicine Department, Trinitas Regional Medical Center, Elizabeth, New Jersey 07202, USA. ewajcberg@yahoo.com

ABSTRACT
The pathophysiology of type 2 diabetes has been attributed to the classic triad of decreased insulin secretion, increased insulin resistance, and elevated hepatic glucose production. Research has shown additional mechanisms, including incretin deficiency or resistance in the gastrointestinal tract. Liraglutide is a modified form of human glucagon-like peptide-1. Liraglutide was obtained by substitution of lysine 34 for arginine near the NH2 terminus, and by addition of a C16 fatty acid at the ɛ-amino group of lysine (at position 26) using a γ-glutamic acid spacer. Liraglutide has demonstrated glucose-dependent insulin secretion, improvements in β-cell function, deceleration of gastric emptying, and promotion of early satiety leading to weight loss. Liraglutide has the potential to acquire an important role, not only in the treatment of type 2 diabetes, but also in preservation of β-cell function, weight loss, and prevention of chronic diabetic complications.

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Related in: MedlinePlus

Liraglutide structure.
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f1-dddt-4-279: Liraglutide structure.

Mentions: Liraglutide (Victoza®; Novo Nordisk Inc, Bagsvaerd, Denmark) is a modified form of human GLP-1 (γ-Lglutamyl[ N-α-hexadenoyl]-Lys,26 Arg34-GLP-1 [7–37]). Native GLP-1 is a 30-amino acid peptide produced by cleavage of the transcription product of the preproglucagon gene.15 Liraglutide was obtained by substitution of lysine 34 to arginine near the NH2 terminus, and by addition of a C16 fatty acid at the ɛ-amino group of lysine (at position 26) using a γ-glutamic acid spacer, which allows noncovalent binding to albumin (see Figure 1).16 The resultant molecule shares 97% (36/37 amino acids) sequence identity with native human GLP-1.17 The high degree of homology of liraglutide to GLP-1 may in part explain the relatively low levels of antibodies produced in response to liraglutide. However, the clinical relevance of antibodies is not yet known.


Liraglutide in the management of type 2 diabetes.

Wajcberg E, Amarah A - Drug Des Devel Ther (2010)

Liraglutide structure.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2990388&req=5

f1-dddt-4-279: Liraglutide structure.
Mentions: Liraglutide (Victoza®; Novo Nordisk Inc, Bagsvaerd, Denmark) is a modified form of human GLP-1 (γ-Lglutamyl[ N-α-hexadenoyl]-Lys,26 Arg34-GLP-1 [7–37]). Native GLP-1 is a 30-amino acid peptide produced by cleavage of the transcription product of the preproglucagon gene.15 Liraglutide was obtained by substitution of lysine 34 to arginine near the NH2 terminus, and by addition of a C16 fatty acid at the ɛ-amino group of lysine (at position 26) using a γ-glutamic acid spacer, which allows noncovalent binding to albumin (see Figure 1).16 The resultant molecule shares 97% (36/37 amino acids) sequence identity with native human GLP-1.17 The high degree of homology of liraglutide to GLP-1 may in part explain the relatively low levels of antibodies produced in response to liraglutide. However, the clinical relevance of antibodies is not yet known.

Bottom Line: Research has shown additional mechanisms, including incretin deficiency or resistance in the gastrointestinal tract.Liraglutide is a modified form of human glucagon-like peptide-1.Liraglutide has demonstrated glucose-dependent insulin secretion, improvements in β-cell function, deceleration of gastric emptying, and promotion of early satiety leading to weight loss.

View Article: PubMed Central - PubMed

Affiliation: Premier Nephrology and Hypertension, Internal Medicine Department, Trinitas Regional Medical Center, Elizabeth, New Jersey 07202, USA. ewajcberg@yahoo.com

ABSTRACT
The pathophysiology of type 2 diabetes has been attributed to the classic triad of decreased insulin secretion, increased insulin resistance, and elevated hepatic glucose production. Research has shown additional mechanisms, including incretin deficiency or resistance in the gastrointestinal tract. Liraglutide is a modified form of human glucagon-like peptide-1. Liraglutide was obtained by substitution of lysine 34 for arginine near the NH2 terminus, and by addition of a C16 fatty acid at the ɛ-amino group of lysine (at position 26) using a γ-glutamic acid spacer. Liraglutide has demonstrated glucose-dependent insulin secretion, improvements in β-cell function, deceleration of gastric emptying, and promotion of early satiety leading to weight loss. Liraglutide has the potential to acquire an important role, not only in the treatment of type 2 diabetes, but also in preservation of β-cell function, weight loss, and prevention of chronic diabetic complications.

Show MeSH
Related in: MedlinePlus