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ARS Home » Research » Publications at this Location » Publication #83629


item Kahl, Stanislaw - Stass
item Rosebrough, Robert
item Elsasser, Theodore

Submitted to: Nutrition Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/16/1998
Publication Date: N/A
Citation: N/A

Interpretive Summary: Excess fat production in the modern broiler accounts for an annual loss to the poultry industry of 800 to 950 million dollars annually. The original source of this problem relates to selection genetic practices that emphasized rapid growth at the expense of other carcass characteristics. The literature is of limited value in determining methods to depress fat synthesis and allow lean tissue synthesis to remain at an elevated rate. A strain male chicks noted for its rapid growth was used to study the effects of dietary protein and triiodothyronine on the ability of chicks to synthesize fat. The line of chicks selected for rapid growth provided liver tissue that, when put into a culture system, exhibited a high rate of lipid synthetic ability. When lines of chickens were fed higher fat diets, they exhibited a decrease in the ability to produce fat. Likewise, including the hormone triiodothyronine in the diets also decreased fat synthesis. These regimens may be of value if the slight growth-depressing effect of triiodothyronine can be overcome.

Technical Abstract: The conversion of thyroxine (T4) to the metabolically active thyroid hormone, triiodothyronine (T3), is catalyzed by iodothyronine 5'-monodeiodinase (EC; 5'D). Indian River male broiler chickens from 7 to 28 d of age were used in a 3 x 2 factorial to determine the effect of dietary energy from fat and T3 supplementation on hepatic 5'D activity and plasma concentration of T4 and T3. Chickens were fed diets (13.1 MJ/kg diet) containing 1.25 (LF), 2.5 (MF) and 5.00 (HF) MJ from fat/kg diet + 0 or 1 mg T3/kg diet. Blood and liver samples were collected on d 28. Hepatic 5'D was affected by fat x T3 interaction (P<0.01). with no added T3, MF and HF increased 'D 25 (P<0.01) and 16% (P<0.05) as compared to LF (1.5 nmoles/mg protein); however no changes in 5'D were found when T3 was added (1.42, 1.35 and 1.36 for LF, MF and HF, respectively). Diets with T3 increased plasma T3 (5.1 vs. 18.1 nmol/L, P<0.001) and decreased plasma T4 (12.4 vs. 7.9 nmol/L, P<0.001). Dietary fat did not affect plasma T3 and T4. The data indicate that the hepatic generation of T3 is stimulated by increased dietary fat intake. This effect of fat, however, is inhibited by dietary T3 supplementation.