R. Peresson

Dietary lysine deficiency greatly affects muscle and liver protein turnover in growing chickens

We analysed the respective influences of age and lysine deficiency on skeletal muscle and liver protein turnover. Growing male broilers were fed ad libitum on isoenergetic diets containing 200 g crude protein/kg which varied in their lysine content (7.7 or 10.1 g/kg). Fractional rates of protein synthesis (FSR) were measured in vivo in the liver and the pectoralis major muscle of 2-, 3- and 4-week-old chickens (flooding dose of L-[4-3H]phenylalanine). Fractional rates of proteolysis (FBR) were estimated for the same tissues as the difference between synthesis and growth. Over the 2-week period liver FSR and FBR were unchanged, whereas muscle FSR decreased with age. This developmental decline was related to the lower capacity for protein synthesis (Cs) without any modifications of the translational efficiency. Whatever the age, lysine deficiency resulted in significant decreases in body weight, tissue protein content and tissue protein deposition, apparently because of reduced amounts of proteins synthesized. We recorded a difference in the response of the two tissues to lysine deficiency, the pectoralis major being more sensitive than the liver. When comparing birds of the same age, liver FSR and FBR were not modified by the diet, whereas muscle FSR, Cs and FBR were higher in chicks fed on a lysine-deficient diet than in the controls. Conversely, when chicks of similar weights were compared, the main effect of the dietary deficiency was an increase in muscle FBR. The results suggest that lysine deficiency not only delayed chick development so that protein turnover was affected, but also induced greater changes in metabolism. Thus, the principal mechanism whereby muscle mass decreased appeared to be a change in FBR.

Relative responses of protein turnover in three different skeletal muscles to dietary lysine deficiency in chicks

1. The effect of lysine deficiency was analysed on muscle protein turnover in 2-, 3- and 4-week-old growing broilers. Protein fractional synthesis rates (FSR, in %/d) were measured by a reliable in vivo technique (flooding dose of L-[4-3H] phenylalanine) in the Pectoralis major (PM), the Anterior latissimus dorsi (ALD) and the Sartorius (SART) muscles. Protein fractional breakdown rates (FBR, in %/d) were estimated as the difference between the synthesis rates and the growth rates of tissue protein. 2. Lysine deficiency resulted in significant increases in muscle FSR and FBR. When expressed in absolute rates (g/d), tissue protein deposition was reduced whatever the tissue. This phenomenon was accompanied by decreased protein synthesis (ASR). 3. The protein turnover responsiveness to the lysine deficiency appeared to depend on the studied muscle, since the PM muscle was the most sensitive whereas the SART and ALD muscles presented a lower sensitivity.

Influence of orotic acid and estrogen on hepatic lipid storage and secretion in the goose susceptible to liver steatosis

Fatty liver in the goose results from an increased hepatic lipogenesis in response to overfeeding, together with a deficient secretion of triacylglycerol as very-low-density lipoproteins (VLDL). Orotic acid and estrogen, which both modify lipid metabolism in the liver, were used in male geese as tools to understand the alterations of liver lipids and plasma lipoproteins during the induction of liver steatosis. Liver lipids were analyzed after solvent extraction and plasma lipoproteins after separation by density gradient ultracentrifugation. Contrary to what is known in the rat, orotic acid (1% in food for 2 weeks) failed to induce liver steatosis. In force-fed geese, liver weight increased from approximately 100 g to approximately 800 g in 2 weeks, as a consequence of a specific accumulation of triacylglycerol. In both groups, VLDL contained less triacylglycerol (35%) than normal. Such an uncoupling of triacylglycerol synthesis and secretion, of which the precise reason is still unknown, may facilitate their accumulation when force-feeding increases hepatic lipogenesis. As with force-feeding, triacylglycerol synthesis was enhanced by estrogen, but their secretion as VLDL was very efficient and prevented liver steatosis almost completely. Since HDL concentrations were considerably decreased by estrogen, VLDL were the main lipoprotein species, with 48 g/l and 62% triacylglycerol. Where estrogen-treated geese were force-fed concomitantly, VLDL concentration was even higher (62 g/l), but triacylglycerol secretion could not prevent liver steatosis (liver weight 640 g). The data are discussed in relation to in vitro studies showing that channelling of triacylglycerol towards secretion as VLDL or hepatic storage depends on their residence time in the different intracellular compartments.