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OBJECTIVES: Emerging evidence shows that non-nutritive sweeteners might induce glucose intolerance
This study aims to determine the effects of chronic exposure to sucralose on glycemic response, insulin secretion and sensitivity, and glucagon-like peptide-1 (GLP-1) release in healthy subjects.METHODS: Healthy volunteers who did not use non-nutritive sweeteners and were normoglycemia after oral glucose tolerance test (OGTT) were recruited. Subjects underwent a 75-g OGTT on two separate occasions, preceded by blindly consuming pills containing either 200 mg sucralose or placebo for 4 wk in a randomized crossover trial. Plasma glucose, insulin, and active GLP-1 levels were obtained after ingesting 75-g glucose. On the following day, intravenous glucose tolerance test (IVGTT) was performed to evaluate the acute insulin response RESULTS: Fifteen participants (11 females, age 31 ± 10 y, body mass index 23 ± 3 kg/m2) participated in the study. AIR was lower after exposure to sucralose than placebo (58 ± 481 versus 694 ± 731 µU/mL, P < 001).

Whole-body insulin sensitivity (estimated using the Matsuda index) was lower in sucralose than placebo (49 ± 17 versus 51 ± 26, P < 005). AUC of active GLP-1 was significantly higher in the sucralose than placebo (236 ± 186 versus 18 ± 222 pmol/L ⋅ 120 min, P < 001).CONCLUSIONS: The continuous exposure to sucralose reduced AIR, decreased insulin sensitivity, and enhanced GLP-1 release in healthy subjects. However, the clinical significance of these results needs to be investigated in longer In taste cells, taste receptors, their coupled G proteins and downstream signalling elements mediate the detection and transduction of sweet, bitter and umami compounds. In some intestinal endocrine cells, taste receptors and gustducin contribute to the release of glucagon-like peptide 1 (GLP-1) and other gut hormones in response to glucose and non-energetic sweeteners. Conversely, taste cells have been found to express multiple hormones typically found in intestinal endocrine cells, e.g.

GLP-1, glucagon, somatostatin and ghrelin. In the present study, by immunohistochemistry, multiple subsets of taste cells were found to express GLP-1. The release of GLP-1 from 'endocrine taste cells' into the bloodstream was examined. In wild-type mice, even after oesophagectomy and vagotomy, oral stimulation with glucose induced an elevation of GLP-1 levels in the bloodstream within 10 min. glipizide used for of taste cell explants from wild-type mice with glucose led to the release of GLP-1 into the medium. Knocking out of the Tas1r3 gene did not eliminate glucose-stimulated GLP-1 release from taste cells in vivo. The present results indicate that a portion of the cephalic-phase rise in circulating GLP-1 levels is mediated by the direct release of GLP-1 from Conflict of interest statement: The authors declare that they have no conflicts Transfer of liraglutide from blood to cerebrospinal fluid is minimal in patients University of Copenhagen, Hellerup, Denmark.

Sciences, University of Copenhagen, Copenhagen, Denmark.Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Treatment with liraglutide leads to weight loss. glipizide used for investigated whether blood-to-cerebrospinal fluid (CSF) transfer of liraglutide occurs, and if so, whether it associates with clinical weight loss following liraglutide treatment in humans. We performed lumbar puncture and blood sampling in eight patients with type 2 diabetes (mean (range)): age 63 (54-79) years; actual body weight: 90 (75-118) kg treated with 1 mg liraglutide for 14 (5-22) months and with a treatment-induced weight loss of 8 (7-11) kg. We measured liraglutide in plasma and CSF with a radioimmunoassay specific for the N-terminus of the GLP-1 moiety of liraglutide. Mean plasma liraglutide was 31 (range: 21-63) nmol l(-1). The mean CSF-liraglutide concentration was 6 (range: 0-13) pmol l(-1).

Ratio of CSF: plasma-liraglutide concentrations was 02 (range: 07-002)% and plasma liraglutide did not correlate with CSF-liraglutide levels (P=07). Body weight loss tended to correlate with plasma-liraglutide levels (P=06), but not with CSF-liraglutide levels (P=09). In conclusion, we measured very low concentrations of liraglutide in CSF, and the levels of CSF liraglutide did not correlate with the actual clinical weight loss in these patients. The amount of liraglutide in plasma tended to correlate with the clinical weight loss.Is liraglutide a useful addition to diabetes therapy?OBJECTIVE: To evaluate liraglutide as an antidiabetic agent.METHODS: The pertinent English-language medical literature was reviewed for the period from 1985 to April 2010 with use of data from MEDLINE.RESULTS: Liraglutide is a glucagonlike peptide-1 receptor analogue that stimulates insulin secretion, reduces postprandial glucagon release, causes a mild delay in gastric emptying, and may slightly decrease appetite.

Mean reductions in hemoglobin A1c levels with liraglutide therapy range from 1% to 1% in comparison with baseline and are 1% and 1% in comparison with placebo. Head-to-head trials suggest that liraglutide may be more effective than glimepiride, rosiglitazone, insulin glargine, and exenatide.
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