Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/25079
標題: 任食引發肥胖改變白肉種雞胰臟磷脂代謝與胰島素分泌-細胞自我防護機制之探討
Obesity-associated alterations of pancreatic phospholipid metabolism and insulin secretion of broiler breeder hens under voluntary feed intake-a study of cell self-defensive mechanisms.
作者: 黃郁芬
Huang, Yu-Fen
關鍵字: Obesity
肥胖
Lipotoxicity
Broiler breeder hens
Pancreas
Phosphatidylcholine
脂肪中毒
白肉種雞
胰臟
磷脂醯膽鹼
出版社: 動物科學系所
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摘要: 現今的白肉雞因快速生長選拔,使得雞隻伴隨著食慾調節以及能量平衡調控的喪失,進而導致攝食過量 (hyperphagia) 與肥胖。肥胖使體內過多的脂肪堆積在非脂肪組織時,會造成細胞發炎反應、脂肪酸氧化形成活性氧以及一些具生物活性脂肪衍生物的產生,進而對細胞造成細胞毒性,使細胞功能異常甚至造成細胞死亡,這種現象稱為脂肪中毒 (lipotoxicity)。相較於哺乳類,禽類具有高血糖、高血酯、高胰島素血症以及胰島素低敏感性,且禽類胰臟β細胞對葡萄糖刺激較不敏感,長期處於高血糖狀態下,不會產生類似哺乳類糖尿病的現象。利用alloxan或streptozotocin (STZ) 等對胰臟細胞具有毒性的化學藥物處理雞隻,不會影響葡萄糖耐受性或是改變血液中胰島素濃度以及葡萄糖刺激之胰島素分泌。葡萄糖會誘發胰島中磷脂的水解,提高鈣離子進入細胞,增強胰島素分泌。胰臟β-cells磷脂的合成乃為了補充胞膜上磷脂水解與胰島素分泌時所減少之脂質,胰島中主要的磷脂為磷脂醯膽鹼 (PC),研究指出增加細胞內PC合成或外源性添加PC皆可改善細胞凋亡的情形,因此PC合成是調節β細胞功能以及胰島素釋放重要的機制。本研究假設雞隻胰臟對葡萄糖較不敏感可能是胰臟細胞在營養過剩下的自我保護機制。試驗以白肉種母雞給予任飼與限飼,並於任飼處理7天與21天時取樣,分析在任飼或限飼下對屠體性狀以及生理代謝之影響。結果顯示任飼組體重、絕對腹脂重與相對腹脂比率皆較高,而絕對胰臟重與相對胰臟比率則是限飼組較高,此顯示以任飼處理之白肉種雞已出現肥胖的傾向。在任飼處理21天後,飢餓時血液中葡萄糖濃度任飼組較高,NEFA濃度則是限飼組較高 ; 飽食顯著提高限飼組血液中胰島素濃度,但任飼組則不受影響。任飼處理7天或21天顯著提高胰臟中三酸甘油脂 (TG)、IL-1β與ceramide含量。此結果顯示任飼處理21天的雞隻胰臟已出現肥胖造成脂肪代謝異常與可能脂肪中毒之現象。胰臟中PC含量不論在任飼處理7天或任飼處理21天,皆為任飼組較高,胰臟中CTP1與PEMT這兩個合成PC主要之酵素mRNA表現,只有PEMT mRNA含量在任飼處理7天後,任飼組較限飼組高,然而任飼處理21天時,PEMT mRNA含量為限飼組較高,且餵食後1小時任飼組血液胰島素濃度沒有提高,胰臟中insulin mRNA含量不論在任飼處理7天或任飼處理21天,兩組間皆無差異,此結果顯示胰臟細胞提高PC合成並非用在補充葡萄糖所誘發的磷脂水解與胰島素分泌的損失,而是用來保護細胞對抗脂肪中毒。胰臟中SMase與SPT這兩個ceramide形成主要之酵素mRNA表現,SMase mRNA含量在任飼處理21天時任飼組較低,而SPT mRNA含量不論任飼處理7天或任飼處理21天任飼組皆較高,這兩個基因表現結果與胰臟中神經鞘磷脂 (sphingomyelin)以及ceramide含量在任飼組皆較高的結果一致。同時胰臟中SOD活性在任飼處理7天時任飼組較高,而任飼處理21天無差異 ; 胰臟中GSH含量在任飼處理21天時,任飼組顯著高於限飼組,這些結果顯示長期任飼引發肥胖與可能的脂肪中毒現象,而此現象可藉由提高胰臟中GSH、PC與SPM含量,降低胰島素分泌的敏感性以及活性氧的釋出得到舒緩,推測此現象可能是胰臟細胞自我保護機制來對抗肥胖引起脂肪中毒之傷害。
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.
URI: http://hdl.handle.net/11455/25079
其他識別: U0005-2608201117440400
文章連結: http://www.airitilibrary.com/Publication/alDetailedMesh1?DocID=U0005-2608201117440400
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