Central alarin ameliorated insulin resistance of adipocytes in type 2 diabetic rats
- 1Department of Endocrinology, Clinical Medical College, Yangzhou University, Nantong West Street No. 98, Yangzhou, Jiangsu 225001, China
2Medical College, Research Institute of Combined Chinese Traditional and Western Medicine, Yangzhou University, Yangzhou, Jiangsu 225001, China
3Department of Physiology, Hanlin College, Nanjing University of Chinese Medicine, Taizhou, Jiangsu 225300, China
4Department of Physical Education, Chuzhou College, Chuzhou, Anhui Province 239012, China
- Correspondence should be addressed to Z Zhang or P Bo; Emails: shimyyz{at}126.com or yzzzw{at}medmail.com.cn
Abstract
Alarin, a regulatory peptide, belongs to the galanin family and plays the same regulatory roles as galanin in orexigenic activity and energy metabolism. Our previous studies had found that galanin might facilitate insulin sensitivity via activation of its central receptors. To date, little is known about whether central alarin may exert similar effects on insulin sensitivity. In order to investigate this, alarin and its specific antagonist, alarin 6–25Cys, were administered into the cerebral ventricles of type 2 diabetic rats (T2DR) to evaluate the changes in insulin resistance. The results indicated that central treatment with alarin significantly increased the body weight of animals, the 2-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-2-deoxyglucose uptake, the plasma adiponectin levels, the glucose infusion rates in hyperinsulinemic–euglycemic clamp tests, the vesicle-associated membrane protein 2 as well as glucose transporter 4 (GLUT4 (SLC2A4)) protein and mRNA levels, and the ratios of GLUT4 contents in plasma membranes to total cell membranes in adipocytes, but reduced blood glucose and plasma retinol-binding protein 4 levels. These effects of alarin may be inhibited by pretreatment with alarin 6–25Cys. The above-mentioned results suggest that the central alarin projective system may facilitate insulin sensitivity and glucose uptake via the increase in GLUT4 content and GLUT4 translocation from intracellular pools to plasma membranes in T2DR.
- Received in final form 3 September 2014
- Accepted 18 September 2014
- Made available online as an Accepted Preprint 19 September 2014
- © 2014 Society for Endocrinology