Eggs are a highly nutritious food and an excellent source of carotenoids, lutein and zeaxanthin, which contribute to antioxidant defenses and ocular health. However, eggs have been viewed skeptically because of their impact on serum cholesterol levels. This review summarizes the evidence from clinical trials, observational studies, and worldwide ecological studies relating egg consumption to serum lipid profiles, antioxidant status, and cardiovascular outcomes. Recent meta-analyses on egg consumption have reported an increase in serum cholesterol but limited or no impact on atherosclerosis and cardiovascular disease risk. Clinical studies have reported that the additional consumption of an egg per day for 4 weeks improved high-density lipoprotein-cholesterol levels and decreased oxidized low-density lipoprotein levels. Most recently, a cross-sectional study of Japanese patients who underwent coronary angiography reported no significant association between egg intake and the prevalence of coronary artery disease or multi-vessel disease. Among patients not receiving lipid-lowering drugs, moderate egg intake (3–4 eggs/week) was associated with a lower prevalence of multi-vessel disease. Furthermore, worldwide ecological analyses have identified a significant negative association between egg intake and the incidence and mortality of ischemic heart disease. Given their high nutritional value, relatively low cost, and the evidence presented, eggs could contribute to healthy diets in many countries worldwide.

In layer chicks, central administration of insulin and refeeding promote the phosphorylation of AKT and extracellular signal-regulated kinase (ERK) in the medulla oblongata. Broiler chicks consume more feed than layer chicks, suggesting distinct feeding regulation. This study aimed to clarify the involvement of medullary AKT and mitogen-activated kinases (MAPKs: ERK, c-Jun N-terminal kinase (JNK), and p38 MAPK) in regulating feeding of broiler chickens. The phosphorylation of AKT and p38 MAPK, but not that of ERK and JNK, was significantly higher in the medulla oblongata of broilers refed for 1 h after a 24-h fasting. Intracerebroventricular (ICV) administration of insulin significantly enhanced AKT phosphorylation in the medulla oblongata, but had no significant effect on the phosphorylation of MAPKs. Oral administration of glucose increased plasma glucose and the phosphorylation of AKT and p38 MAPK, but not ERK and JNK, in the medulla oblongata. ICV administration of the p38 MAPK activator anisomycin strongly induced the phosphorylation of p38 MAPK, but not JNK, without affecting feed intake. These findings suggest that medullary AKT contributes to insulin-induced suppression of feed intake in broiler chicks, while medullary p38 MAPK is phosphorylated in response to postprandial elevation of blood glucose, but is not involved in feeding regulation.

When facing dehydration, birds use body fat and proteins as a source of endogenous water. Recently, we found that osmotic stress triggered protein catabolism in skeletal muscles of chicks. In the present study, we investigated whether osmotic stress also affected fat metabolism. Twelve 21-day-old male chicks were allocated to two groups based on body weight. The chicks received either saline (0.15 M NaCl) or hypertonic saline (1.5 M NaCl) intraperitoneally (5 mL/kg body weight). After 1 h of feed and water deprivation, the chicks were euthanized by decapitation. Blood, breast muscle (pectoralis major), abdominal adipose tissue, liver, and kidney samples were collected, followed by analysis of plasma components and gene expression. Hypertonic saline significantly increased the plasma levels of non-esterified fatty acids (NEFA); adipose triglyceride lipase (ATGL) mRNA in adipose tissue; pyruvate dehydrogenase kinase 4 (PDK4) mRNA in breast muscle, adipose tissue, and liver; phosphoenolpyruvate carboxykinase 1 mRNA in the liver; and atrogin-1 mRNA in breast muscle. It also increased the plasma content of the hormone vasotocin. Subsequent intravascular administration of vasotocin significantly elevated plasma NEFA, but not ATGL or PDK4 mRNA in adipose tissue. Collectively, our findings suggest that osmotic stress alters nutrient metabolism in the peripheral tissues of chicks and that vasotocin may be partly involved in fatty acid mobilization.

Inflammation often accompanies the development of liver diseases in humans, but appears to be repressed in geese. This study investigated the role of MAP3K7 C-terminal-like (MAP3K7CL) in goose fatty liver formation. Sixteen healthy 70-day-old male geese were randomly divided into control and overfed groups. Additionally, the transcriptome analysis after MAP3K7CL overexpression and lipopolysaccharide (LPS) treatment were performed in goose primary hepatocytes. The results showed that the MAP3K7CL mRNA expression was increased in the liver of overfed treatment compared to control group. Overexpression of MAP3K7CL in primary goose hepatocytes identified differentially expressed genes enriched in the mitogen-activated protein kinase (MAPK) signaling pathway. Specifically, DNA damage-inducible transcript 3 (DDIT3), insulin-like growth factor 1 receptor (IGF1R), neurofibromin 1 (NF1), and platelet-derived growth factor subunit B (PDGFB) were significantly downregulated upon MAP3K7CL overexpression, whereas heat shock protein family B member 1 (HSPB1) was significantly upregulated. Furthermore, transfection of goose hepatocytes with the MAP3K7CL overexpression vector lowered the expression of lipopolysaccharide-induced TNF factor (LITAF) and cysteinyl aspartate-specific proteinase-3, which are associated with inflammation and apoptosis, respectively. In accordance with these findings, DDIT3 and LITAF were downregulated in the overfed group, whereas HSPB1 was upregulated. Compared with the control, LPS treatment significantly decreased MAP3K7CL expression, while promoting that of LITAF and interleukin-6 (IL-6). Moreover, the combination of lipopolysaccharide and MAP3K7CL overexpression upregulated MAP3K7CL while downregulating LITAF and IL-6 with respect to LPS alone and empty vector control groups. Therefore, MAP3K7CL may inhibit the inflammatory response in goose fatty liver.

From an animal welfare perspective, thirst avoidance is an important criterion for the poultry industry. Neuropeptide Y (NPY) and α−melanocyte-stimulating hormone (α-MSH) play critical roles in regulating food intake, which is closely related to water intake in mammals and chickens. This study aimed to clarify the role of appetite-regulating neuropeptides in controlling thirst in chicks. In Experiment 1, 7-day-old male chicks were allocated to two groups and deprived of water for 24 h. Chicks were intracerebroventricularly injected with saline or the peptide. Water intake was measured at 60 and 120 min after injection under feed-deprived conditions. α-MSH significantly suppressed thirst-induced water intake, whereas NPY exhibited no effect. In Experiment 2, 8-day-old male chicks were allocated to two groups and intracerebroventricularly injected with either saline or peptide under ad libitum drinking conditions. NPY significantly increased water intake, whereas α-MSH had no effect. In Experiment 3, 8-day-old male chicks were allocated to two groups and euthanized after 0 or 3 h of water deprivation. Diencephalon mRNA levels of NPY and proopiomelanocortin (the gene encoding α-MSH) were not affected by water deprivation. Our findings suggest that chick NPY and α-MSH function as thirst-inducing and thirst-quenching peptides, respectively. Both control water intake through post-translational regulation.