東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁

切換: 標籤 | MARC模式 | ISBD

Mechanism of Adipose Tissue Specific...

Qu, Huan.

FindBook

Google Book

Amazon

博客來

Mechanism of Adipose Tissue Specific Response to Heat Stress in Pigs.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Mechanism of Adipose Tissue Specific Response to Heat Stress in Pigs./
作者:	Qu, Huan.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2018,
面頁冊數:	228 p.
附註:	Source: Dissertation Abstracts International, Volume: 79-12(E), Section: B.
Contained By:	Dissertation Abstracts International79-12B(E).
標題:	Animal sciences. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10810217
ISBN:	9780438154544

Mechanism of Adipose Tissue Specific Response to Heat Stress in Pigs.
Qu, Huan.

Mechanism of Adipose Tissue Specific Response to Heat Stress in Pigs. - Ann Arbor : ProQuest Dissertations & Theses, 2018 - 228 p.

Source: Dissertation Abstracts International, Volume: 79-12(E), Section: B.

Thesis (Ph.D.)--Purdue University, 2018.

Heat stress (HS) is a major problem facing the swine industry all over the world, especially during the hot summer months. The two major reasons pigs are highly susceptible to elevated ambient temperature are that they have substantial subcutaneous fat layer that serves as a barrier against effective heat dissipation and their lack of functional sweat glands on their skin surface for evaporative heat loss. Paradoxically, HS results in increased fat deposition in pigs. However, the fundamental causes of the increased adiposity during HS are unknown. Therefore, we conducted several in vivo and in vitro experiments to elucidate the precise mechanisms of HS response in pig adipose tissue. In the first study, we used an in vitro adipocyte differentiation model to characterize cellular responses that occur during differentiation of pig adipocytes in HS. We found the existence of cell autonomous response to HS in pig adipocytes that results in increased adipocyte lipid storage. In the second study, we wanted to elucidate the mechanisms of HS management and their relationship to adipose tissue metabolism. Thirty cross-bred (Ossabaw x Duroc x Landrace) pigs (boars n=15, gilts n=15) were assigned to three treatments for 1 week: 1) control and libitum fed (CON) with environment temperature 20 °C +/- 1 °C and ad libitum access to feed, 2) pair-fed (PF) with environment temperature 20 °C +/- 1 °C and fed the amount same as HS pigs, 3) HS with environment temperature 35 °C +/- 1 °C and ad libitum access to feed. Heat stress led to increased glyceroneogenesis accompanied by induction of phosphoenolpyruvate carboxykinase (PCK1) in adipose tissue without alteration of serum glucose, insulin, FFA and triglyceride concentrations and this revealed that glyceroneogenesis, perhaps through PCK1, plays an important role in increased adipose lipid storage under HS. In the third experiment, we used a commercial-type pig genotype, a Duroc x Yorkshire x Landrace terminal cross, to evaluate effects of both acute (24 h) and chronic (7 d) HS on gene expression responses in adipose and other peripheral tissues. The HS induced a robust adipose tissue response in favor of increased lipid storage. This indicates that adipose tissue might play an important role in HS adaptation, irrespective of the genotype of the pig. In the fourth study, the effect of PCK1 inhibition with 3 mercaptopicolinic acid (3MPA) on lipid storage and adipocyte response during HS was investigated. Inhibition of PCK1 during HS, adipocytes were less able to induce adaptive responses such as upregulation of HSP70 and triglycerides, and this exacerbated endoplasmic reticulum (ER) stress during HS. Therefore, PCK1 may function to alleviate ER stress that occurs during HS. In the fifth study, we wanted to determine global changes in adipose tissue and adipocyte metabolites and lipids species to see if they could serve as useful biomarkers that could be associated with HS adaptation response. Using metabolomics, lipidomics, and fatty acid profile analysis with gas chromatography, we found that HS induced distinct metabolite profiles. This may have implications for the explanation of the regulation of lipogenesis, fatty acid oxidation and membrane fluidity in adipose tissue during HS. Overall, these studies indicate a potential major role for PCK1 in the increased lipid storage during HS and in the suppression of ER stress that may occur in adipose tissue during HS. Thus, the increased lipid storage in adipose tissue during HS might be a protective mechanism against excessive ER stress and adipocyte death in this tissue.

ISBN: 9780438154544Subjects--Topical Terms:

3174829
Animal sciences.

Mechanism of Adipose Tissue Specific Response to Heat Stress in Pigs.
LDR:04535nmm a2200289 4500 001 2200234
005 20181214130636.5
008 201008s2018 ||||||||||||||||| ||eng d
020 $a 9780438154544
035 $a (MiAaPQ)AAI10810217
035 $a (MiAaPQ)purdue:22798
035 $a AAI10810217
040 $a MiAaPQ $c MiAaPQ
100 1 $a Qu, Huan. $3 3426982
245 1 0 $a Mechanism of Adipose Tissue Specific Response to Heat Stress in Pigs.
260 1 $a Ann Arbor : $b ProQuest Dissertations & Theses, $c 2018
300 $a 228 p.
500 $a Source: Dissertation Abstracts International, Volume: 79-12(E), Section: B.
500 $a Adviser: Kola Ajuwon.
502 $a Thesis (Ph.D.)--Purdue University, 2018.
520 $a Heat stress (HS) is a major problem facing the swine industry all over the world, especially during the hot summer months. The two major reasons pigs are highly susceptible to elevated ambient temperature are that they have substantial subcutaneous fat layer that serves as a barrier against effective heat dissipation and their lack of functional sweat glands on their skin surface for evaporative heat loss. Paradoxically, HS results in increased fat deposition in pigs. However, the fundamental causes of the increased adiposity during HS are unknown. Therefore, we conducted several in vivo and in vitro experiments to elucidate the precise mechanisms of HS response in pig adipose tissue. In the first study, we used an in vitro adipocyte differentiation model to characterize cellular responses that occur during differentiation of pig adipocytes in HS. We found the existence of cell autonomous response to HS in pig adipocytes that results in increased adipocyte lipid storage. In the second study, we wanted to elucidate the mechanisms of HS management and their relationship to adipose tissue metabolism. Thirty cross-bred (Ossabaw x Duroc x Landrace) pigs (boars n=15, gilts n=15) were assigned to three treatments for 1 week: 1) control and libitum fed (CON) with environment temperature 20 °C +/- 1 °C and ad libitum access to feed, 2) pair-fed (PF) with environment temperature 20 °C +/- 1 °C and fed the amount same as HS pigs, 3) HS with environment temperature 35 °C +/- 1 °C and ad libitum access to feed. Heat stress led to increased glyceroneogenesis accompanied by induction of phosphoenolpyruvate carboxykinase (PCK1) in adipose tissue without alteration of serum glucose, insulin, FFA and triglyceride concentrations and this revealed that glyceroneogenesis, perhaps through PCK1, plays an important role in increased adipose lipid storage under HS. In the third experiment, we used a commercial-type pig genotype, a Duroc x Yorkshire x Landrace terminal cross, to evaluate effects of both acute (24 h) and chronic (7 d) HS on gene expression responses in adipose and other peripheral tissues. The HS induced a robust adipose tissue response in favor of increased lipid storage. This indicates that adipose tissue might play an important role in HS adaptation, irrespective of the genotype of the pig. In the fourth study, the effect of PCK1 inhibition with 3 mercaptopicolinic acid (3MPA) on lipid storage and adipocyte response during HS was investigated. Inhibition of PCK1 during HS, adipocytes were less able to induce adaptive responses such as upregulation of HSP70 and triglycerides, and this exacerbated endoplasmic reticulum (ER) stress during HS. Therefore, PCK1 may function to alleviate ER stress that occurs during HS. In the fifth study, we wanted to determine global changes in adipose tissue and adipocyte metabolites and lipids species to see if they could serve as useful biomarkers that could be associated with HS adaptation response. Using metabolomics, lipidomics, and fatty acid profile analysis with gas chromatography, we found that HS induced distinct metabolite profiles. This may have implications for the explanation of the regulation of lipogenesis, fatty acid oxidation and membrane fluidity in adipose tissue during HS. Overall, these studies indicate a potential major role for PCK1 in the increased lipid storage during HS and in the suppression of ER stress that may occur in adipose tissue during HS. Thus, the increased lipid storage in adipose tissue during HS might be a protective mechanism against excessive ER stress and adipocyte death in this tissue.
590 $a School code: 0183.
650 4 $a Animal sciences. $3 3174829
690 $a 0475
710 2 $a Purdue University. $b Animal Sciences. $3 1031160
773 0 $t Dissertation Abstracts International $g 79-12B(E).
790 $a 0183
791 $a Ph.D.
792 $a 2018
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10810217