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Besides its typical role as an amino acid in protein synthesis, methionine is an important intermediate in methylation reactions. In addition, it can also be converted to cysteine and hence plays a role in the defence against oxidative stress. The present study was conducted to investigate further the role of DL-methionine (DLM) and its hydroxy analogue, DL-2-hydroxy-4-methylthiobutanoic acid (DL-HMTBA), on zootechnical performance and oxidative status of broiler chickens. Male broiler chickens were reared on two diets differing in crude protein (CP) content (low-protein, 18·3 % v. high-protein, 23·2 % CP) and were supplemented either with 0·25 % DLM or 0·25 % DL-HMTBA. Reducing the dietary protein content resulted in an impaired body weight gain (P < 0·0001). However, supplementation of DL-HMTBA to the low-protein diet partially alleviated these negative effects (P = 0·0003). This latter phenomenon could be explained by the fact that chickens fed DL-HMTBA-supplemented diets displayed a better antioxidant status as reflected in lower lipid peroxidation probably as a consequence of their higher hepatic concentrations of total and reduced glutathione compared with their DLM counterparts. On the other hand, within the high protein levels, uric acid might be an important antioxidant to explain the lower lipid peroxidation of high-protein DL-HMTBA-supplemented chickens. Hepatic methionine sulfoxide reductase-A gene expression was not significantly affected by the dietary treatments. In conclusion, the present study indicates that there are interactions between dietary protein content and supplementation of methionine analogues with respect to broiler performance and antioxidant status, also suggesting a causal link between these traits.

The endogenous ligand for the growth hormone (GH) secretagogue receptor ghrelin is a peptide secreted by the stomach of mammals and stimulates food intake and enhances adiposity. In avian species, ghrelin is mainly produced by the proventriculus but reduces food intake whereas its effect on lipogenesis in different tissues is unknown. We therefore investigated the effects of a single intravenous injection of 2.8 microg (1 nmol per chick) recombinant chicken ghrelin in neonatal broiler chicks. Besides food intake and plasma corticosterone levels, mRNA levels of the key lipogenic enzyme fatty acid synthase (FAS) and its related transcription factors sterol regulatory element binding protein-1 (SREBP-1) and peroxisome proliferator-activated receptor-gamma (PPARgamma) were determined in diencephalon, liver and quadriceps femoris muscle before, and 15, 30, and 60 min after injection. Chicken ghrelin administration induced a significant short-term (<30 min) reduction in food intake and markedly elevated plasma corticosterone levels. In diencephalon, FAS, SREBP-1 and PPARgamma mRNA levels were significantly increased within 15 min after ghrelin injection. These observations suggest that central fatty acid metabolism is involved in the anorectic effects of ghrelin. In contrast, hepatic mRNA levels of FAS and both transcription factors were significantly reduced within 30 min after ghrelin injection. In muscle, FAS and transcription factor gene expression was very low and not affected by ghrelin. Overall, our results indicate that ghrelin has opposite effects on FAS and transcription factor mRNA amounts with increased levels in diencephalon (central anorectic effect) and decreased levels in liver (peripheral anti-lipogenic effect) in chickens.

The objective of the present study was to evaluate the potential effects of dietary L-carnitine supplementation on acute phase protein response upon a lipopolysaccharide (LPS) challenge of male broiler chickens receiving a commercial broiler diet supplemented with 15 or 100 mg L-carnitine/kg or an unsupplemented (control) diet from 14 days of age onwards. At 28 days of age, eight chickens per dietary treatment were weighed and subcutaneously injected with 300 microg LPS from E. coli (100 microg LPS/ml saline) or 3 ml saline (unsupplemented group only). During the next 10 days, blood samples were taken repeatedly and analysed for their hemopexin (HX) and alpha-1 acid glycoprotein (AGP) levels. Extra dietary L-carnitine did not affect broiler performance. At day 1 postinjection, plasma HX and AGP levels were significantly increased in all treatment groups. However, the elevations in circulating HX and AGP levels were more pronounced in the L-carnitine supplemented chickens, especially in the 100mg L-carnitine group. It is concluded that extra L-carnitine in the diet of broiler chickens enhances or advances the acute phase protein response. The exact mode of action needs to be elucidated but seems to be consistent with a glucocorticoid mimicking effect.

While there have been many studies in various species examining the mode of central leptin action on food intake, there is however a paucity of data in birds. We have, therefore, addressed this issue in broiler chickens because this strain was selected for high growth rate, hence high food intake. Continuous infusion of recombinant chicken leptin (8 microg/kg/h) during 6 h at a constant rate of 3 ml/h resulted in a significant reduction (49-57%) of food intake in 3-week-old broiler chickens (P < 0.05). The effect of leptin within the central nervous system (CNS) was mediated via selective hypothalamic neuropeptides. Leptin significantly decreased the expression of its receptor (Ob-R), neuropeptide Y (NPY), orexin (ORX), and orexin receptor (ORXR) (P < 0.05), but not that of agouti-related protein (AgRP) (anabolic/orexigenic effectors) in chicken hypothalamus. However, the catabolic/anorexigenic neuropeptides namely proopiomelanocortin (POMC) and corticotropin-releasing hormone (CRH) mRNA levels remained unchanged after leptin treatment. Despite the absence of leptin effect on AgRP (the antagonist of melanocortin receptor MCR) and POMC (the precursor of alpha-melanocyte stimulating hormone which is a potent agonist for MCR), leptin significantly decreased the expression of MCR-4/5 gene in chicken hypothalamus (P < 0.05) suggesting that leptin acts directly (as ligand) or indirectly (via other ligands) on MCRs to regulate food intake in birds. Additionally, leptin down-regulated the expression of fatty acid synthase (FAS) gene in chicken hypothalamus, indicating an additional pathway of leptin action on food intake such as described for FAS inhibitors. These findings provide new insight into the mechanism of leptin control of food intake in chickens.

During their relatively short commercial lifespan of six weeks, broiler chickens undergo very pronounced age- or body weight-related changes in metabolic rate and body composition. The present study was aimed to assess the age-related changes in glucose oxidation rate of broiler chickens by using 13C-labeled glucose. The methodology for this breath test needed to be established first. Broiler chickens aged from two to six weeks were placed in open-circuit respiration cells and received a single intubation of U-13C6-glucose, followed by breath sampling for 4 hours and mass spectrometric analysis of 13C: 12C ratio in the exhaled air. Simultaneously, CO2 concentration in the respiration cell air was continuously monitored in order to calculate the cumulative percentage dose recovery (CPDR). With respect to the methodology, an oral dose of 2 mg U-13C6-glucose per kg body weight while maintaining a CO2 in the concentration of 0.4 to 0.5% was considered to be optimal. The three-parameter Gompertz curve fitted the CPDR values very well. Pronounced age-related changes in exogenous glucose oxidation rates in rapidly growing meat-type chickens were assessed. Young broiler chickens spend only a relatively low percentage of ingested glucose for immediate oxidation. In contrast, broiler chickens approaching the age of maximal absolute growth rate oxidize a greater proportion of the recently ingested glucose relative to the non-oxidative disposal pathways. This shift in the exogenous partitioning is discussed in relation to age-dependent changes in glucose turnover, lipid oxidation and deposition and metabolic heat production., (Copyright 2004 Elsevier Inc.)