| Summary: | 碩士 === 中興大學 === 動物科學系所 === 99 === Genetic selection for rapid growth is accompanied by a loss of satiety regulation and energy homeostasis leading to a propensity of hyperphagia and obesity in modern broiler chickens. Obesity results in excessive fatty acid accumulation in non-adipose tissues leading to inflammatory responses, oxidative damage due to excessive β-oxidation, and bioactive lipid derivatives may cause cell dysfunction or apoptosis. This phenomenon is called “lipotoxicity”. In contrast to mammals, birds are characterized by hyperglycemia, hyperinsulinemia, and insulin resistance. Chronic hyperglycemia without diabetic conditions in birds has puzzled scientists for decades. Chicken pancreatic beta-cells are relatively insensitive to glucose stimulation in insulin secretion. Cytotoxin treatment such as alloxan or streptozotocin (STZ) for chemical pancreatectomy in chickens failed to cause glucose intolerance and alter basal plasma insulin concentrations or glucose-induced insulin secretion. Stimulation of pancreatic islets with glucose induces phospholipid hydrolysis, which amplifies the glucose-induced Ca2+ entry into islet β-cells to trigger insulin secretion. In addition, phospholipid synthesis is required to replenish lipid loss during the hydrolysis and insulin secretion. Phosphatidylcholine (PC) is a major component of the phospholipid fractions of islet cells. Increased PC synthesis or exogenous PC treatment has been known to rescue cell death. Thus, the synthesis of PC is an important regulatory process in β-cell function and insulin release. In this study, we hypothesized that the insensitivity of chicken pancreas may sperat through a cytoprotective mechanism against glucose and lipid insults. Broiler breeder hens were fed ad libitum or restricted feeding and examined the effect of body composition and physiological response. Results showed that body weight, absolute and relative abdominal fat weight were higher in ad libitum hens than their restricted counterparts, but absolute and relative pancreas weight were higher in restricted hens, suggesting that chickens fed ad libitum has developed into obesity. Plasma glucose levels were higher in hens fed ad libitum for 21 days, but plasma NEFA levels were higher in restricted hens. Plasma insulin levels were increased in restricted hens after one hour refeeding but this re-feeding induced increased of plasma insulin level was absent in hens fed ad libitum. Ad libitum feeding for 7 days or 21 days also promoted pancreatic TG, IL-1β, ceramide, but suppressed AKT activition, suggesting susceptible lipotoxicity and dysregulations in the hens under voluntary feeding. However, pancreatic phosphatidylcholine (PC) contents were higher in hens under ad libitum feeding for 21day. Expression of CTP1, the key enzyme for PC de novo synthesis was not affected by ad libitum feeding. Moreover, PEMT mRNA expression was higher in hens fed ad libitum for 7 days, but lower under ad libitum feeding for 21days, when compared to those of restricted hens. In combination with unchanged plasma insulin levels one hour after refeeding and pancreatic insulin mRNA levels in hens fed ad libitum, the results suggested that pancreas may protect cells against lipotoxicity through increasing pancreatic PC content. Pancreatic SPT mRNA expression was increased in hens under ad libitum feeding for both 7 days and 21days, but SMase expression was suppressed after ad libitum feeding for 21 days when compared to restricted hens. These results were consistent with pancreatic sphingomyelin and ceramide content in the hens under voluntary feeding regimen. Pancreatic SOD activity was promoted after ad libitum feeding for 7 days but resumed to no change after 21 days, and meanwhile GSH content was increased after 21-day ad libitum feeding. Taken together, these results suggest that prolong voluntary feeding in hens results in obesity and susceptible lipotoxicity in the pancreas. This lipotoxic development is likely to be ameliorated in the pancreas of chickens against excessive fuel insults, theory operation to increase glutathione and SPM content and PC synthesis, and decrease the sensitivity if insulin secretion and ROS generation.
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