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

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.

Recent advances in the understanding of how neuropeptide Y andα-melanocyte stimulating hormone function in adipose physiology

“…66 It is unclear if birds are similar to humans in regards to metabolic differences between adipose tissue depots, although we have reported that there are differences in gene expression between adipose depots in chickens. [66][67][68] In addition to the differences we have reported in meat-type broiler chickens, we have also found adipose depot differences in a line of chickens selected for high and low body weight, the Virginia lines of chickens, which have undergone divergent selection for either low (LWS) or high (HWS) juvenile body weight at 56 days of age for 58 generations. This selection has resulted in a 10-fold difference in body weight at age of selection, with associated physiological and behavioral differences in feeding, adiposity, development, and body composition, with the LWS being lean and hypophagic, while the HWS are obese and hyperphagic as juveniles.…”

“…67 HWS chickens expressed more NPY and NPYR 1 and 5 mRNA in the abdominal fat, 67 while LWS chicks expressed more NPY and NPYR 2 and 5 in the hypothalamus. 149 Additionally, expression of NPY5R in the hypothalamus is regulated differently between the fed vs fasted state, where in the fed state, NPY5R was more highly expressed in the LWS, and the magnitude of difference between the LWS and HWS was lessened by fasting.…”

“…122 The NPY5R is most similar to NPY1R in amino acid sequence identity, 123 and is co-localized with NPY1R in many areas of the nervous system where NPY5R is expressed. 124 Adipose-specific production of NPY5R remains debated, as it has been detected in the adipose of rodents 125,126 and chickens, 67 but at other times is undetectable. 127,128 Additionally, NPY2R was expressed in human, 10 mouse 10 and chicken preadipocytes, 11 while in another study NPY2R was not detected in mouse preadipocytes.…”

Avian and Mammalian Facilitative Glucose Transporters

“…The encoded protein regulates bidirectional glucose transport across liver cells, pancreatic islet beta cells that store and release insulin, epithelial kidney cells and intestines. Similar to mammalian species, chickens have abundant GLUT2 expression in the liver [19], pancreatic beta cells, kidney and small intestine [20]. Due to its low affinity for glucose, GLUT2 may be a glucose sensor.…”

“…One study linked gout to GLUT9 deficiency in a population of Japanese males [38]. It is assumed that chicken GLUT9 mediates uric acid uptake, although substrate specificity for this GLUT transporter has not yet been identified [19]. Liver mRNA expression of GLUT9 was shown to be greater in obese chickens, possibly due to having a larger glucose uptake capacity with greater demand and glucose load in high bodyweight chickens [19].…”