Dietary Nitrogen Intake Regulates Hepatic Malic Enzyme Messenger Ribonucleic Acid Expression

Abstract

Increased dietary protein intake rapidly (3 h) decreases malic enzyme and increases hepatic histidase mRNA expression. Experiments were conducted to determine the role that individual dispensable amino acids and nonprotein N sources might have in regulating the activity of these enzymes and to determine if the addition of a N supplement to a practical broiler diet during the entire rearing period would reduce abdominal fat accumulation in broilers. Broiler chicks were fed a basal diet containing 22% protein or this diet supplemented with 9.5% l-Glu, 5% Gly, 6% l-Ala, 5.08% ammonium bicarbonate, or 4.25% dibasic ammonium phosphate for 24 h. Each of the dietary supplements added 0.90% total N to the diet. Hepatic malic enzyme mRNA expression was significantly (P < 0.05) depressed in chicks fed any of the supplemented diets compared with chicks fed the basal diet. Histidase mRNA expression, however, was only significantly increased in the chicks fed the basal diet supplemented with Gly. Broilers fed practical corn-soybean meal starter and developer diets supplemented with 2.3, 4.7, or 9.5% Glu from 0 to 40 d of age had significantly smaller abdominal fat pads relative to BW than broilers fed the unsupplemented corn-soybean meal diets. Feeding the Glu supplements, however, reduced the overall BW gain of broilers by 100 to 150 g compared with broilers fed the unsupplemented diets. The results suggest that hepatic mRNA expression of malic enzyme may be regulated by total dietary N intake, whereas hepatic mRNA expression of histidase may be regulated by specific amino acids.

Meta-analysis of the effect of low-protein diets on the growth performance, nitrogen excretion, and fat deposition in broilers

“…Therefore, using AA-to-Lys ratios corresponding to the ideal protein profile limits fat deposition; however, this phenomenon still occurs, indicating that the effect of CP on fat deposition is not solely related to AA limitations. This is consistent with the results from Chendrimada et al (2007), which showed the inhibitory effect of protein with non-essential AA (i.e., Ala and Glu) and mineral N, on the malic enzyme involved in fat deposition.…”

Influential factor contributing to the isoform‐specific inhibition by ATP of human mitochondrial NAD(P)+‐dependent malic enzyme

“…m-NAD-ME is a unique isoform that has a multifaceted regulatory system for control of its catalytic activity [4,6,27,28,30,32,33]. It displays substrate cooperativity in l-malate, and the enzyme can be allosterically activated by fumarate [16,30,33].…”