Influence of BioChrome on the response of metabolic hormones in PEMS-infected poults.
Poult enteritis and mortality syndrome (PEMS), a disease that affects turkeys between 7 and 28 d of age, causes a severe inflammation of the intestinal tract and is characterized in poults by severe diarrhea, high morbidity, mortality, and stunting. The PEMS-associated mortality and growth depression is related to malabsorption and decreased metabolic activity caused, in part, by a possible insulin deficiency or insensitivity. Insulin receptors are stimulated by the glucose tolerance factor (GTF) that incorporates Cr. Body Cr deficiency can be exacerbated by dietary deficiency and by increased excretion due to stress associated with a diarrheal disease such as PEMS. BioChrome (BC) contains natural, preformed GTF, the bioactive form of Cr. Experiments were conducted in which BC was blended into poult starter feed at 400 ppb during the first 21 d posthatch. Body weights were determined at 1, 7, 14, and 21 d of age, and weekly feed conversions were calculated for each treatment group (control, BC, PEMS, and BC+PEMS). At 6 d post-hatch, each PEMS-designated poult was given a 0.1-mL oral gavage of a 10% suspension of feces from PEMS-infected poults. Blood samples were taken via cardiac puncture from four birds per treatment group at 7, 10, 14, 17, and 21 d of age. Radioimmunoassays were conducted for plasma insulin, glucagon, thyroxine (T4), and triiodothyronine (T3). Plasma insulin levels were depressed in PEMS-infected poults from Days 10 through 17, but plasma glucagon levels in the PEMS-infected poults were significantly elevated at 14 and 17 d, after which they returned to control levels in both of the PEMS-infected groups. The T3 and T4 levels were depressed through Day 21 in PEMS-infected poults, but with BC treatment these blood hormone levels rebounded by Day 21. Body weights of PEMS-infected poults were increased significantly by the BC treatment but not to the level of noninfected controls.
Doerfler
R E
RE
Department of Poultry Science, North Carolina State University, Raleigh 27695-7635, USA.
Edens
F W
FW
McMurtry
J P
JP
Qureshi
M A
MA
Parkhurst
C R
CR
Havenstein
G B
GB
D000367:Age Factors; D000596:Amino Acids / Q000378:metabolism / Q000494:pharmacology; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight; D002857:Chromium / Q000378:metabolism* / Q000494:pharmacology / Q000627:therapeutic use; D004751:Enteritis / Q000188:drug therapy / Q000378:metabolism / Q000662:veterinary*; D005260:Female; D005934:Glucagon / Q000097:blood; D007328:Insulin / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D007335:Insulin-Like Growth Factor II / Q000032:analysis; D007422:Intestines / Q000503:physiopathology; D009539:Nicotinic Acids / Q000378:metabolism / Q000494:pharmacology; D011201:Poultry Diseases / Q000188:drug therapy / Q000378:metabolism* / Q000401:mortality; D011863:Radioimmunoassay / Q000662:veterinary; D011897:Random Allocation; D013577:Syndrome; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood; D014422:Turkeys
D000596:Amino Acids; D001786:Blood Glucose; D007328:Insulin; D009539:Nicotinic Acids; C015240:glucose tolerance factor; D014284:Triiodothyronine; D002857:Chromium; D007334:Insulin-Like Growth Factor I; D007335:Insulin-Like Growth Factor II; D005934:Glucagon; D013974:Thyroxine