Journal
DRUG DESIGN DEVELOPMENT AND THERAPY
Volume 4, Issue -, Pages 279-290Publisher
DOVE MEDICAL PRESS LTD
DOI: 10.2147/DDDT.S10180
Keywords
diabetes mellitus; incretin; glucagon-like peptide; insulin resistance
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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 epsilon-amino group of lysine (at position 26) using a gamma-glutamic acid spacer. Liraglutide has demonstrated glucose-dependent insulin secretion, improvements in beta-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 beta-cell function, weight loss, and prevention of chronic diabetic complications.
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