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

Physiol Genomics. 2013 Nov 15;45(22):1084-94. doi: 10.1152/physiolgenomics.00102.2013. Epub 2013 Sep 17.

Abstract

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.

Keywords: NPY; body weight chickens; gene expression; glucose transporters; insulin.

MeSH terms

  • Abdominal Fat / metabolism
  • Animals
  • Appetite / genetics*
  • Blood Glucose / metabolism
  • Body Weight / genetics*
  • Chickens
  • Crosses, Genetic
  • Female
  • Forkhead Transcription Factors / genetics
  • Forkhead Transcription Factors / metabolism
  • Glucose Transport Proteins, Facilitative / metabolism*
  • Hybrid Vigor
  • Hypothalamus / metabolism
  • Insulin / pharmacology*
  • Liver / metabolism
  • Muscle, Skeletal / metabolism
  • Neuropeptide Y / genetics
  • Neuropeptide Y / metabolism
  • Organ Specificity
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism*
  • Receptor, Insulin / genetics
  • Receptor, Insulin / metabolism
  • Receptors, Neuropeptide / genetics
  • Receptors, Neuropeptide / metabolism*
  • Species Specificity

Substances

  • Blood Glucose
  • Forkhead Transcription Factors
  • Glucose Transport Proteins, Facilitative
  • Insulin
  • Neuropeptide Y
  • RNA, Messenger
  • Receptors, Neuropeptide
  • Receptor, Insulin