BACKGROUND/AIM: Liraglutide, a glucagon-like peptide-1 analog, induces weight loss. We investigated whether liraglutide affects gastric accommodation and satiation by measuring the intragastric pressure (IGP) during nutrient-drink consumption and using the barostat technique.METHODS: Ten healthy volunteers (HVs) were tested after placebo, 0, 0 or 1 mg liraglutide administration. IGP was studied during intragastric nutrient-drink (1 kcal ml(-1)) infusion (60 ml min(-1)), while the HVs scored their satiation on a graded scale until maximal satiation. In a separate session, isobaric distentions were performed using the barostat with stepwise increments of 2 mm Hg starting from minimal distending pressure, although HVs scored their perception; gastric volume was monitored 30 min before and until 60 min after ingestion of 200 ml of nutrient drink. Data are presented as mean±s. e.m. comparisons were performed with ANOVA (P<05 was significant).RESULTS: During nutrient-drink infusion, IGP decreased with 4±0, 3±0, 2±0 and 2±0 mm Hg (placebo, 0, 0 and 1 mg liraglutide, respectively; P<05). The maximum-tolerated volume was not different, except after treatment with 1 mg liraglutide (695±135 ml) compared with placebo (1008±197 ml; P<05); however, 1 mg liraglutide induced nausea in all volunteers. In the barostat study, liraglutide did not affect the perception or compliance, but significantly decreased gastric accommodation to the meal (168±27 vs 78±36 ml after treatment with placebo and 0 mg liraglutide, CONCLUSION: Although no effect on perception, compliance or satiation was observed, liraglutide inhibited gastric accommodation. Whether this effect is involved in the anorectic effect of liraglutide remains to be determined. Albiglutide: a review of its use in patients with type 2 diabetes mellitus.is a glucagon-like peptide (GLP)-1 receptor agonist approved for the treatment of type 2 diabetes mellitus in several countries. Albiglutide has a longer half-life than native GLP-1, since it is resistant to degradation by the dipeptidyl peptidase-4 enzyme. As an incretin mimetic, albiglutide enhances glucose-dependent insulin secretion, suppresses inappropriate glucagon secretion, delays gastric emptying and reduces food intake. Several phase III clinical trials have demonstrated the efficacy of albiglutide in terms of improving glycaemic control in patients with inadequately controlled type 2 diabetes, including its use as monotherapy or add-on therapy to other antidiabetic agents (e.g. metformin, sulfonylureas, thiazolidinediones and insulins). In addition to improving glycaemic control, albiglutide had beneficial effects on bodyweight. These improvements in glycaemic control and reductions in bodyweight were maintained during long-term treatment (up to 3 years). Albiglutide was generally well tolerated in clinical trials, with mild to moderate gastrointestinal adverse events seen most commonly. Albiglutide has a convenient once-weekly administration regimen and a low risk of hypoglycaemia (except when used in combination with agents that may be associated with hypoglycaemia, such as sulfonylureas or insulin). Thus, albiglutide is an effective and generally well tolerated treatment option for patients with inadequately controlled type 2 diabetes.N-terminal acetylation protects glucagon-like peptide GLP-1-(7-34)-amide from DPP-IV-mediated degradation retaining cAMP- and insulin-releasing capacity.Since its discovery glucagon-like peptide-1 (GLP-1) is investigated as a treatment for type II diabetes based on its major function as insulin secretagogue. A therapeutic use is, however, limited by its short biological half-life in the range of minutes, predominantly caused via degradation catalyzed by dipeptidyl peptidase IV (DPP-IV). Therefore, Endocrine function drugs aimed to design a GLP-1 analogue exhibiting resistance against DPP-IV-catalyzed inactivation while retaining its biological activity. By means of matrix-assisted laser desorption/ionization mass spectrometry (MALDI MS) we have studied the stability of the N-terminally blocked new analogue Ac-GLP-1-(7-34)-amide against DPP-IV and compared it with both unblocked GLP-1-(7-34)-amide and the major naturally occurring form GLP-1-(7-36)-amide. GLP-1-(7-36)-amide and the C-terminally two amino acid residues shorter GLP-1-(7-34)-amide rapidly generated peptide fragments truncated by the N-terminal dipeptide. In contrast, the N-terminal blocked Ac-GLP-1-(7-34)-amide was not degraded in the presence of DPP-IV over a period of at least two hours. Ac-GLP-1-(7-34)-amide induced glp 1 meds -dependent increase of intracellular cAMP production and insulin release from rat insulinoma RIN-m5F cells to an extent comparable to that found for the N-terminally unblocked peptides GLP-1-(7-34)-amide and GLP-1-(7-36)-amide. Ac-GLP-1-(7-34)-amide may thus have the potential to act as a new long-acting GLP-1 analogue with significant resistance against DPP-IV and retained biological activity in vitro. Further research is required to investigate whether Ac-GLP-1-(7-34)-amide also exhibits its characteristics in The Effect of Transplacental Administration of Glucagon-Like Peptide-1 on Fetal Lung Development in the Rabbit Model of Congenital Diaphragmatic Hernia.
Endocrine function drugs|glp 1 meds
