کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2022372 | 1542393 | 2014 | 8 صفحه PDF | دانلود رایگان |
• IGF-1 recovers the DM-induced alteration of the muscle thickness in rats.
• IGF-1 partly recovers the decrease of body weight and gastrointestinal transit rate in diabetic rats.
• The gastrointestinal transit rate was positively correlated with IGF-I level.
• IGF-1 inhibits the DM-induced colonic smooth muscle cells apoptosis, might be associated with the mitochondrial pathway.
• IGF-1 suppresses the isolated colonic SMCs apoptosis via PI3K/Akt and ERK/MAPK signaling pathways.
Cellular apoptosis and colonic dysmotility are involved in diabetes mellitus (DM) complications. Insulin-like growth factor-1 (IGF-1) is known to affect apoptosis and proliferation. Here, we demonstrated that the treatment of 1500 ng/kg IGF-1 partly recovers the decrease of the muscle thickness, body weight and gastrointestinal transit rate in DM rats. The gastrointestinal transit rate is positively correlated with the IGF-I level, but negatively correlated with the level of colonic cellular apoptosis. The DM-induced colonic apoptosis is also attenuated by the IGF-1 stimulation. Moreover, IGF-1 inhibits the apoptosis of the isolated colonic SMCs in vitro via the activation of PI3K/Akt and ERK1/2 signaling pathways. Taken together, our data indicated that IGF-1 inhibits the DM-induced colonic SMC apoptosis and might be involved in the alleviation of colonic dysmotility in diabetic rats.
Journal: Regulatory Peptides - Volumes 194–195, November 2014, Pages 41–48