Quantity of glucose transporter and appetite-associated factor mRNA in various tissues after insulin injection in chickens selected for low or high body weight

被引:42
作者
Zhang, Wei [1 ]
Sumners, Lindsay H. [1 ]
Siegel, Paul B. [1 ]
Cline, Mark A. [1 ]
Gilbert, Elizabeth R. [1 ]
机构
[1] Virginia Tech, Dept Anim & Poultry Sci, Blacksburg, VA USA
关键词
body weight chickens; gene expression; glucose transporters; insulin; NPY; NEUROPEPTIDE-Y; GENE-EXPRESSION; ADIPOSE-TISSUE; MURINE ADIPOCYTES; BROILER-CHICKENS; NPY RECEPTORS; FOOD-INTAKE; LONG-TERM; LINES; METABOLISM;
D O I
10.1152/physiolgenomics.00102.2013
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Chickens from lines selected for low (LWS) or high (HWS) body weight differ by 10-fold in body weight at 56 days old with differences in food intake, glucose regulation, and body composition. To evaluate if there are differences in appetite-regulatory factor and glucose transporter (GLUT) mRNA that are accentuated by hypoglycemia, blood glucose was measured, and hypothalamus, liver, pectoralis major, and abdominal fat collected at 90 days of age from female HWS and LWS chickens, and reciprocal crosses, HL and LH, at 60 min after intraperitoneal injection of insulin. Neuropeptide Y (NPY) and receptor (NPYR) subtypes 1 and 5 mRNA were greater in LWS compared with HWS hypothalamus (P < 0.05), but greater in HWS than LWS in fat (P < 0.05). Expression of NPYR2 was greater in LWS than HWS in pectoralis major (P < 0.05). There was greater expression in HWS than LWS for GLUT1 in hypothalamus and liver (P < 0.05), GLUT2 in fat and liver (P < 0.05), and GLUT9 in liver (P < 0.05). Insulin was associated with reduced blood glucose in all populations (P < 0.05) and reduced mRNA of insulin receptor (IR) and GLUT 2 and 3 in liver (P < 0.05). There was heterosis for mRNA, most notably NPYR1 (-78%) and NPYR5 (-81%) in fat and GLUT2 (-70%) in liver. Results suggest that NPY and GLUTs are associated with differences in energy homeostasis in LWS and HWS. Reduced GLUT and IR mRNA after insulin injection suggest a compensatory mechanism to prevent further hypoglycemia.
引用
收藏
页码:1084 / 1094
页数:11
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