Effect of liraglutide on food consumption, appetite sensations and eating behaviours in overweight people with type 1 diabetes.

AIMS: To investigate the effects of 24 weeks of treatment with liraglutide added to basal/bolus insulin on energy intake, appetite sensations and eating behaviours in overweight/obese participants with type 1 diabetes (T1D). METHODS: In a double-blinded crossover fashion, 15 participants were randomly assigned (1:1) to receive placebo or liraglutide for 24 weeks including a 1-month titration period from 0.6 to 1.2 to 1.8 mg, in addition to their insulin. The treatment was followed by a 1-month wash-out period. Participants were then assigned to the other treatment for another 24 weeks. Food intake was measured, visual analogue scales and Three-Factor Eating Questionnaires were completed. Paired rank tests were used to compare the variables. RESULTS: When treated with liraglutide, participants modified their ad libitum food consumption with decreased total intake and % fat and increased carbohydrates. Their appetite sensations were modified: fasting desire to eat, hunger and prospective food consumption were significantly reduced. The sensation of fullness was prolonged for a few hours after a standardized breakfast. Restraint and disinhibition were significantly reduced by liraglutide. CONCLUSIONS: In this randomized clinical trial, the addition of liraglutide to basal/bolus insulin therapy for 24 weeks in overweight/obese individuals with T1D significantly improved their food consumption, appetite sensations and eating behaviours.

Beyond glycaemic control: A cross-over, double-blinded, 24-week intervention with liraglutide in type 1 diabetes.

AIMS: To investigate the effects of 24 weeks of treatment with liraglutide added to basal/bolus insulin on anthropometric and metabolic parameters in overweight participants with type 1 diabetes. METHODS: In a double-blinded cross-over fashion, 15 participants were randomly assigned (1:1) to receive placebo (saline solution) or liraglutide for 24 weeks including a 1-month titration period from 0.6 to 1.2 to 1.8 mg, in addition to their insulin. The treatment was followed by a 1-month wash-out period. Participants were then assigned to the other treatment for another 24 weeks. Paired rank tests were used to compare the metabolic parameters. RESULTS: There was no treatment effect on HbA1c nor on insulin dose. Heart rate was increased by about 8 beats per minute with liraglutide. There were significant reductions in metabolic measures: weight, body mass index, waist and hip circumferences, body fatness, computed tomography scan abdominal and mid-thigh measurements, systolic and diastolic blood pressures (all P ≤ .05). There was no increase in time spent in hypoglycaemia with liraglutide. CONCLUSIONS: The addition of liraglutide to basal/bolus insulin therapy for 24 weeks in overweight/obese individuals with type 1 diabetes improved the anthropometric and metabolic profiles without an increase in hypoglycaemia. Clinical Trials.gov No: NCT01787916.

Increased ET-1 and reduced ET(B) receptor expression in uremic hypertensive rats.

The endothelin-1 (ET-1) system has been implicated in cardiovascular disease associated with chronic renal failure. We investigated the expression and localization of ET-1 and the ET(B) and ET(A) receptors in vascular and renal tissues of uremic hypertensive rats. Uremia was induced by renal artery branches ligation. At week 6, blood and renal parameters, and plasma and urine ET-1 levels were evaluated. The ET-1, and the ET(B) and ET(A) receptors expression and localization were determined by Northern and Western blotting, and by immunofluorescence, respectively. Blood pressure, serum creatinine, proteinuria, and urinary ET-1 were increased in uremic rats. The ET-1 expression was increased in the aorta, mesenteric arteries, and the renal cortex of uremic rats, whereas the ET(B) receptor expression was reduced. Immunofluorescence analysis using the thoracic aorta revealed that the endothelial ET-1 levels were increased 4-fold in uremic rats. In contrast, the ET(B) receptor expression, which was localized exclusively in the endothelium, was markedly reduced. The ET(A) receptor expression, however, was increased 1.6-fold and was detected in the media only. Similar changes in ET-1 and ET(B) receptor expression were observed in renal cortex vessels and glomeruli of uremic rats. This study reveals that ET-1 levels are augmented in the vascular endothelium of uremic rats, whereas the ET(B) receptor expression is reduced which may play a major role in hypertension and renal failure progression.