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

Macrophage alternative activation in...

Odegaard, Justin Iver.

FindBook

Google Book

Amazon

博客來

Macrophage alternative activation in obesity and metabolic syndrome.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Macrophage alternative activation in obesity and metabolic syndrome./
作者:	Odegaard, Justin Iver.
面頁冊數:	161 p.
附註:	Adviser: Ajay Chawla.
Contained By:	Dissertation Abstracts International68-12B.
標題:	Biology, Physiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3292398
ISBN:	9780549355717

Macrophage alternative activation in obesity and metabolic syndrome.
Odegaard, Justin Iver.

Macrophage alternative activation in obesity and metabolic syndrome. - 161 p.

Adviser: Ajay Chawla.

Thesis (Ph.D.)--Stanford University, 2008.

Complex interplay between T helper (Th) cells and macrophages contributes to the formation and progression of chronic inflammatory diseases. While Th1 cytokines promote inflammatory activation of macrophages, Th2 cytokines attenuate macrophage-mediated inflammation and enhance reparative functions. In spite of its biologic importance, the biochemical and molecular basis of how Th2 cytokines promote maturation of anti-inflammatory macrophages is not understood. Using both gain- and loss-of-function approaches, we demonstrate that in response to interleukin-4 (IL-4), signal transducer and activator of transcription 6 (STAT6) and PPARgamma-coactivator-1beta (PGC-1beta) induce macrophage programs for oxidative metabolism and mitochondrial biogenesis necessary for expression of the alternative phenotype.

ISBN: 9780549355717Subjects--Topical Terms:

1017816
Biology, Physiology.

Macrophage alternative activation in obesity and metabolic syndrome.
LDR:03744nam 2200325 a 45 001 962807
005 20110830
008 110831s2008 ||||||||||||||||| ||eng d
020 $a 9780549355717
035 $a (UMI)AAI3292398
035 $a AAI3292398
040 $a UMI $c UMI
100 1 $a Odegaard, Justin Iver. $3 1285868
245 1 0 $a Macrophage alternative activation in obesity and metabolic syndrome.
300 $a 161 p.
500 $a Adviser: Ajay Chawla.
500 $a Source: Dissertation Abstracts International, Volume: 68-12, Section: B, page: 7916.
502 $a Thesis (Ph.D.)--Stanford University, 2008.
520 $a Complex interplay between T helper (Th) cells and macrophages contributes to the formation and progression of chronic inflammatory diseases. While Th1 cytokines promote inflammatory activation of macrophages, Th2 cytokines attenuate macrophage-mediated inflammation and enhance reparative functions. In spite of its biologic importance, the biochemical and molecular basis of how Th2 cytokines promote maturation of anti-inflammatory macrophages is not understood. Using both gain- and loss-of-function approaches, we demonstrate that in response to interleukin-4 (IL-4), signal transducer and activator of transcription 6 (STAT6) and PPARgamma-coactivator-1beta (PGC-1beta) induce macrophage programs for oxidative metabolism and mitochondrial biogenesis necessary for expression of the alternative phenotype.
520 $a Obesity and insulin resistance, cardinal features of metabolic syndrome, are driven by low-grade inflammation. In adipose tissue, chronic overnutrition leads to macrophage infiltration and activation, resulting in local inflammation that potentiates insulin resistance. Because macrophages actively participate in the resolution of inflammation, we postulated that macrophage activation programs that attenuate inflammation might ameliorate obesity-induced insulin resistance. Using mice with macrophage-specific deletion of peroxisome proliferator activated receptor (PPAR)-gamma, we show here that PPARgamma is required for maturation of alternatively activated macrophages. Disruption of PPARgamma in myeloid cells impairs alternative macrophage activation, thereby predisposing these animals to development of diet-induced obesity, insulin resistance, and glucose intolerance.
520 $a While inflammatory activation of resident hepatic macrophages potentiates insulin resistance, the functions of alternatively activated Kupffer cells in metabolic disease remain unknown. In response to IL-4, PPARdelta directs expression of the alternative phenotype in Kupffer cells of lean and obese mice. Importantly, adoptive transfer of PPARdelta-/- bone marrow into wild type mice diminishes alternative activation of hepatic macrophages, causing hepatic dysfunction and insulin resistance. Suppression of hepatic oxidative metabolism is recapitulated by co-culturing hepatocytes with PPARdelta -/- macrophages, indicating direct involvement of Kupffer cells in controlling liver lipid metabolism.
520 $a Together, these findings demonstrate coordinate metabolic and immunologic control of macrophage alternative activation and that macrophages resident in WAT and liver thus activated have beneficial roles in regulating nutrient homeostasis. These findings suggest that macrophage polarization towards the alternative state might be a useful strategy for treating metabolic syndrome and other chronic inflammatory diseases.
590 $a School code: 0212.
650 4 $a Biology, Physiology. $3 1017816
650 4 $a Health Sciences, Immunology. $3 1017716
650 4 $a Health Sciences, Medicine and Surgery. $3 1017756
690 $a 0564
690 $a 0719
690 $a 0982
710 2 $a Stanford University. $3 754827
773 0 $t Dissertation Abstracts International $g 68-12B.
790 $a 0212
790 1 0 $a Chawla, Ajay, $e advisor
791 $a Ph.D.
792 $a 2008
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3292398