Abstract
Glucagon-like peptide-1 (GLP-1), an insulinotropic gastrointestinal peptide that is primarily produced by intestinal endocrine L-cells, stimulates satiety. Ghrelin, a hormone that is produced predominantly by the stomach stimulates hunger. There are two forms of ghrelin: active ghrelin and inactive des-acyl ghrelin. After depriving mice of food for 24 h, we demonstrated that the systemic administration of liraglutide (100 μg/kg), a human GLP-1 analog that binds to the GLP-1 receptor, increased (1.4-fold) the plasma levels of active GLP-1 and suppressed the plasma levels of active and des-acyl ghrelin after 1 h. Despite the elevated plasma levels of active GLP-1 (11-fold), liraglutide had no effect on the plasma levels of active or des-acyl ghrelin after 12 h. These findings demonstrated that liraglutide suppresses the plasma levels of active and des-acyl ghrelin independently of active GLP-1 levels in fasted mice, suggesting a novel in vivo biological effect of liraglutide beyond regulating plasma GLP-1.
Highlights
Hunger is stimulated by ghrelin, a hormone that is primarily produced by the P/D1 cells that line the fundus of the stomach [1]
Liraglutide (100 μg/kg) significantly decreased the plasma levels of active (0.35-fold) and des-acyl (0.28-fold) ghrelin (Figures 1(b) and 1(c)). These findings suggested that liraglutide acutely suppressed the plasma levels of active and des-acyl ghrelin, which was associated with a small increase in circulating GLP-1in mice that were fasted for 24 h
The intraperitoneal injection of liraglutide (100 μg/kg) did not significantly affect the plasma levels of active or des-acyl ghrelin at 12 h (Figures 2(b) and 2(c)). These findings suggested that despite the remarkable elevated levels of active Glucagon-like peptide-1 (GLP-1), systemic liraglutide did not affect the plasma levels of active or desacyl ghrelin in mice
Summary
Hunger is stimulated by ghrelin, a hormone that is primarily produced by the P/D1 cells that line the fundus of the stomach [1]. Plasma ghrelin levels increase during fasting and decrease after ingesting glucose or lipids but not protein [1]. The ghrelin that is secreted in the stomach stimulates the afferent vagus nerve and promotes food intake [1]. Ghrelin exists in both inactive (des-acyl ghrelin) and active forms. The effects of liraglutide on the plasma levels of active GLP-1, active ghrelin, and des-acyl ghrelin in fasted mice have not yet been evaluated. To determine the effects of liraglutide on the plasma levels of active GLP-1 and active and des-acyl ghrelin in vivo, we treated mice that were deprived of food for 24 h with an intraperitoneal injection of liraglutide. To determine whether the effects of liraglutide on the plasma levels of active and des-acyl ghrelin resulted from the increased plasma levels of active GLP-1 in vivo, we measured the plasma levels of active GLP-1 and active and des-acyl ghrelin in mice 12 h after an intraperitoneal injection of liraglutide
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