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The Reprogramming of White Adipose T...

Abdullahi, Abdikarim Said.

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The Reprogramming of White Adipose Tissue to Brown Adipose Tissue Mediates Adverse Metabolic Dysfunction After a Burn Injury.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	The Reprogramming of White Adipose Tissue to Brown Adipose Tissue Mediates Adverse Metabolic Dysfunction After a Burn Injury./
作者:	Abdullahi, Abdikarim Said.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2019,
面頁冊數:	239 p.
附註:	Source: Dissertations Abstracts International, Volume: 81-02, Section: B.
Contained By:	Dissertations Abstracts International81-02B.
標題:	Molecular biology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=13806353
ISBN:	9781085573221

The Reprogramming of White Adipose Tissue to Brown Adipose Tissue Mediates Adverse Metabolic Dysfunction After a Burn Injury.
Abdullahi, Abdikarim Said.

The Reprogramming of White Adipose Tissue to Brown Adipose Tissue Mediates Adverse Metabolic Dysfunction After a Burn Injury. - Ann Arbor : ProQuest Dissertations & Theses, 2019 - 239 p.

Source: Dissertations Abstracts International, Volume: 81-02, Section: B.

Thesis (Ph.D.)--University of Toronto (Canada), 2019.

This item must not be sold to any third party vendors.

A burn injury represents one of the most severe forms of trauma and affects more than two million people in North America annually. Of all cases, nearly 4000 people die of complications related to the injury. A hallmark of severely burned patients is the activation of a hypermetabolic stress response, which is characterized by hyperglycemia, lipolysis, and protein catabolism. Perhaps the most serious gap in our understanding of the hypermetabolic response in burns is the role of the adipose tissue. Humans harbour two distinct adipose depots, white adipose tissue (WAT) and brown adipose tissue (BAT) that carry out essentially opposite functions. WAT is primarily involved in storing excess energy, whereas BAT burns excess energy in the form heat. This fat burning aspect of BAT has emerged as a powerful tool in combating the metabolic syndrome (hyperglycemia, excess body fat, hypertension). Additionally, it has been discovered that our WAT can be reprogrammed to become BAT, however, whether or not such reprogramming (white to brown fat) occurs after a burn injury is unknown. We therefore investigated the adipose tissue, and its role in post-burn hypermetabolism, by using an animal model of burn injury and tissue from clinical burn patients. In our first study, we report the reprogramming of WAT to BAT in both burn patients and post-burn mice indicated by increased expression of the brown adipocyte marker, uncoupling protein 1 (UCP-1). This reprogramming of WAT post-burn injury required both IL-6 and catecholamine secretion from alternatively activated macrophages. In our second study, we demonstrated that WAT browning with its associated lipolysis increased plasma levels of free fatty acids, leading to the accelerated development of hepatic steatosis and dysfunction after a burn injury. The last study of this thesis was geared towards clinical applications, and centered on the inhibition of the WAT to BAT switch via the use of an IL-6R blocker and propranolol to improve post-burn hypermetabolism and organ steatosis. In summary, our findings highlight an essential role of the adipose tissue in contributing to post-burn hypermetabolism and pathology.

ISBN: 9781085573221Subjects--Topical Terms:

517296
Molecular biology.
Subjects--Index Terms:

Adipose

The Reprogramming of White Adipose Tissue to Brown Adipose Tissue Mediates Adverse Metabolic Dysfunction After a Burn Injury.
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520 $a A burn injury represents one of the most severe forms of trauma and affects more than two million people in North America annually. Of all cases, nearly 4000 people die of complications related to the injury. A hallmark of severely burned patients is the activation of a hypermetabolic stress response, which is characterized by hyperglycemia, lipolysis, and protein catabolism. Perhaps the most serious gap in our understanding of the hypermetabolic response in burns is the role of the adipose tissue. Humans harbour two distinct adipose depots, white adipose tissue (WAT) and brown adipose tissue (BAT) that carry out essentially opposite functions. WAT is primarily involved in storing excess energy, whereas BAT burns excess energy in the form heat. This fat burning aspect of BAT has emerged as a powerful tool in combating the metabolic syndrome (hyperglycemia, excess body fat, hypertension). Additionally, it has been discovered that our WAT can be reprogrammed to become BAT, however, whether or not such reprogramming (white to brown fat) occurs after a burn injury is unknown. We therefore investigated the adipose tissue, and its role in post-burn hypermetabolism, by using an animal model of burn injury and tissue from clinical burn patients. In our first study, we report the reprogramming of WAT to BAT in both burn patients and post-burn mice indicated by increased expression of the brown adipocyte marker, uncoupling protein 1 (UCP-1). This reprogramming of WAT post-burn injury required both IL-6 and catecholamine secretion from alternatively activated macrophages. In our second study, we demonstrated that WAT browning with its associated lipolysis increased plasma levels of free fatty acids, leading to the accelerated development of hepatic steatosis and dysfunction after a burn injury. The last study of this thesis was geared towards clinical applications, and centered on the inhibition of the WAT to BAT switch via the use of an IL-6R blocker and propranolol to improve post-burn hypermetabolism and organ steatosis. In summary, our findings highlight an essential role of the adipose tissue in contributing to post-burn hypermetabolism and pathology.
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