ARS | Publication request: UNIQUE RESPONSES OF PANCREATIC PHOSPHOLIPID METABOLISM OF BROILER HENS IN RESPONSE TO INCREASED PLASMA GLUCOSE AND LIPID CONCENTRATIONS

Submitted to: Poultry Science
Publication Type: Abstract Only
Publication Acceptance Date: May 31, 2004
Publication Date: June 1, 2004
Citation: Chen, S.E., McMurtry, J.P., Walzem, R.L. 2004. Unique responses of pancreatic phospholipids metabolism of broiler hens in response to incresed plasma glucose and lipid concentration [abstract]. Poultry Science. 83(Suppl.1):111.

Technical Abstract: Higher caloric intake (twice the recommended 145 g/day/hen; T or free access to feed; F, n=15 for each) for 10 days in broiler hens (Cobb 500 Fast Feathering, age=35 wks) caused 500 grams body weight (BW) gain when compared with hens consuming recommended feed intakes (R, n=15) or with hens necropsied at the start of feeding trial as basal references (BR, n=15). Rapid BW gain was associated with an increase (p<0.05) of relative liver (50%) and abdominal fat weights (30%), and elevated preprandial plasma insulin (45-60%), NEFA (40%), glucose (43%), VLDL-TG (27%), and total cholesterol (TC) concentrations (60-80%) but a decreased HDL-TC (45%) concentration, suggesting metabolic dysregulations similar to those of mammalian obesity and type-II diabetes. Higher caloric intake also increased (p<0.05) relative pancreas weight (25-30%), pancreatic protein content (25%) and protein/DNA ratio (20%), and all classes of pancreatic phospholipids (average 35%), indicative of pancreatic hypertrophy. Notably, phosphatidylethanolamine increased 75% in concert with increased delta 9 desaturase activity (18:1n9/18:0, mol/mol) (15-30%) and a general enhancement of unsaturation in pancreatic PL fatty acids (12-35%) when compared with group R and PR hens. These observations indicate that specific changes in pancreatic lipid metabolism accompany the acceleration of endocrine/exocrine functions in response to food intake above the amount needed for optimal egg production. Hen pancreatic cells may mount specific metabolic responses to prevent cytotoxicity resulting from excessive glucose and saturated fatty acid availability. Key words: pancreas, hypertrophy, hyperinsulinemia, saturated fatty acids, lipotoxicity