Search Results
You are looking at 1 - 1 of 1 items for
- Author: Bo Shi x
- Refine by access: Content accessible to me x
Search for other papers by Lili Guo in
Google Scholar
PubMed
Search for other papers by Penghua Fang in
Google Scholar
PubMed
Search for other papers by Mei Yu in
Google Scholar
PubMed
Search for other papers by Mingyi Shi in
Google Scholar
PubMed
Department of Endocrinology, Medical College, Department of Physiology, Department of Physical Education, Clinical Medical College, Yangzhou University, Nantong West Street No. 98, Yangzhou, Jiangsu 225001, China
Search for other papers by Ping Bo in
Google Scholar
PubMed
Search for other papers by Zhenwen Zhang in
Google Scholar
PubMed
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.
