Nutrition-Physiology-Gene Interactions in the Chicken

Nutrition entails the sum of processes involved in the ingestion of foods, digestion, absorption, transport of nutrients, intermediary metabolism, underlying anabolism and catabolism, and excretion of unabsorbed nutrients and metabolites. Research at the Animal Nutrition Laboratory is concerned with the identification of nutritional characteristics in several animal species with the aid of comparative biochemistry and molecular biology. This mini-review provides an overview of the nutritional regulation of metabolism, physiological functions and gene expression in avian species

Mitochonic Acid 5 (MA-5) Facilitates ATP Synthase Oligomerization and Cell Survival in Various Mitochondrial Diseases

Mitochondrial dysfunction increases oxidative stress and depletes ATP in a variety of disorders. Several antioxidant therapies and drugs affecting mitochondrial biogenesis are undergoing investigation, although not all of them have demonstrated favorable effects in the clinic. We recently reported a therapeutic mitochondrial drug mitochonic acid MA-5 (Tohoku J. Exp. Med., 2015). MA-5 increased ATP, rescued mitochondrial disease fibroblasts and prolonged the life span of the disease model “Mitomouse” (JASN, 2016). To investigate the potential of MA-5 on various mitochondrial diseases, we collected 25 cases of fibroblasts from various genetic mutations and cell protective effect of MA-5 and the ATP producing mechanism was examined. 24 out of the 25 patient fibroblasts (96%) were responded to MA-5. Under oxidative stress condition, the GDF-15 was increased and this increase was significantly abrogated by MA-5. The serum GDF-15 elevated in Mitomouse was likewise reduced by MA-5. MA-5 facilitates mitochondrial ATP production and reduces ROS independent of ETC by facilitating ATP synthase oligomerization and supercomplex formation with mitofilin/Mic60. MA-5 reduced mitochondria fragmentation, restores crista shape and dynamics. MA-5 has potential as a drug for the treatment of various mitochondrial diseases. The diagnostic use of GDF-15 will be also useful in a forthcoming MA-5 clinical trial

Mechanisms underlying the Effects of Heat Stress on Intestinal Integrity, Inflammation, and Microbiota in Chickens

Poultry meat and egg production benefits from a smaller carbon footprint, as well as feed and water consumption, per unit of product, than other protein sources. Therefore, maintaining a sustainable production of poultry meat is important to meet the increasing global demand for this staple. Heat stress experienced during the summer season or in tropical/subtropical areas negatively affects the productivity and health of chickens. Crucially, its impact is predicted to grow with the acceleration of global warming. Heat stress affects the physiology, metabolism, and immune response of chickens, causing electrolyte imbalance, oxidative stress, endocrine disorders, inflammation, and immunosuppression. These changes do not occur independently, pointing to a systemic mechanism. Recently, intestinal homeostasis has been identified as an important contributor to nutrient absorption and the progression of systemic inflammation. Its mechanism of action is thought to involve neuroendocrine signaling, antioxidant response, the presence of oxidants in the diet, and microbiota composition. The present review focuses on the effect of heat stress on intestinal dysfunction in chickens and the underlying causative factors. Understanding these mechanisms will direct the design of strategies to mitigate the negative effect of heat stress, while benefiting both animal health and sustainable poultry production

Crucial role of membrane potential in heat stress-induced overproduction of reactive oxygen species in avian skeletal muscle mitochondria.

Heat stress is an environmental factor that causes oxidative stress. We found previously that acute heat stress stimulates the production of reactive oxygen species (ROS) in the skeletal muscle mitochondria of birds, and that this was accompanied by an increase of the mitochondrial membrane potential (ΔΨ) due to increased substrate oxidation by the electron transport chain. We also showed that avian uncoupling protein (avUCP) expression is decreased by the heat exposure. The present study clarifies whether ΔΨ is a major determinant of the overproduction of ROS due to acute heat stress, and if the decrease in avUCP expression is responsible for the elevation in ΔΨ. Control (24°C) and acute heat-stressed (34°C for 12 h) birds exhibited increased succinate-driven mitochondrial ROS production as indicated by an elevation of ΔΨ, with this increase being significantly higher in the heat-stressed group compared with the control group. In glutamate/malate-energized mitochondria, no difference in the ROS production between the groups was observed, though the mitochondrial ΔΨ was significantly higher in the heat-stressed groups compared with the control group. Furthermore, mitochondria energized with either succinate/glutamate or succinate/malate showed increased ROS production and ΔΨ in the heat-stressed group compared with mitochondria from the control group. These results suggest that succinate oxidation could play an important role in the heat stress-induced overproduction of mitochondrial ROS in skeletal muscle. In agreement with the notion of a decrease in avUCP expression in response to heat stress, proton leak, which was likely mediated by UCP (that part which is GDP-inhibited and arachidonic acid-sensitive), was reduced in the heat-exposed group. We suggest that the acute heat stress-induced overproduction of mitochondrial ROS may depend on ΔΨ, which may in turn result not only from increased substrate oxidation but also from a decrease in the mitochondrial avUCP content

Progressive Changes in the Physiological Responses of Heat-stressed Broiler Chickens

The present experiment was designed to study progressive changes in the physiological responses of broiler chickens (Gallus gallus) exposed to different durations of acute heat stress. Male broiler chickens (n=8) at 16 days of age, were exposed to acute heat stress of 34°C for 6, 12 or 18h while control chickens were kept at 25°C. Exposure to different durations of heat stress resulted in significant decreases in the levels of blood HCO3- and pCO2, while pH and pO2 were not changed. Hemoglobin, hematocrit and Na+ values were reduced after 6h while no such change was observed after 12 or 18h of heat stress. In contrast, K+ levels were lowered by 6 or 12h of heat stress and no differences in blood calcium levels were observed between the control and heat-stressed groups. In conclusion, there is evidence that exposure of broiler chickens to different durations of acute heat stress resulted in distinct time-dependent physiological responses. Data set from this experimental model could provide an overview of physiological state in the typical acute heat-stressed birds

Differences in Breast Muscle Mitochondrial Respiratory Capacity, Reactive Oxygen Species Generation, and Complex Characteristics between 7-week-old Meat- and Laying-type Chickens

The skeletal muscle growth rate is a major feature differentiating meat- and laying-type chickens. A large amount of ATP is required during skeletal muscle synthesis, in which mitochondrial energy production capacities play a significant role. Additionally, mitochondria may participate in muscle protein degradation via reactive oxygen species generation. To investigate the differences in mitochondrial energetic characteristics between chickens exhibiting different growth rates, this study evaluated respiratory capacities in response to different types of respiratory substrate, protein abundances, assembly of individual respiratory complexes (I–V) and supercomplexes, and reactive oxygen species generation rates. These characteristics were compared between mitochondria from the breast muscle (M. pectoralis superficialis) of seven-week-old meat- and laying-type male chickens. Blue native polyacrylamide gel electrophoresis analysis revealed that meat-type chickens exhibited a significantly lower protein abundance of complex III (cytochrome bc1 complex), complex V (F0F1 ATP synthase), and total amount of supercomplexes than did laying-type chickens. There were no differences between chicken types in the respiration rate of mitochondria incubated with either pyruvate/malate or succinate, each of which drives complex I- and complex II-linked respiration. Carnitine palmitoyltransferase-1-dependent and -independent respiration during ATP synthesis and carnitine palmitoyltransferase-2 enzymatic activity were significantly lower in meat-type chickens than in layingtype chickens. For mitochondria receiving pyruvate/malate plus succinate, the reactive oxygen species generation rate and its ratio to the oxygen consumed (the percentage of free radical leak) were also significantly lower in meat-type chickens than in laying-type chickens. These results suggested that the mitochondrial energetic capacities of the breast muscle of meat-type chickens could be lower than those of laying-type chickens at seven weeks of age. Furthermore, the lower reactive oxygen species generation rate in meat-type chickens might have implications for rapid muscle development, which is possibly related to their lower muscle protein degradation rates