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Ap2 clock mutant mice: baseline char...

Birky, Tana L.

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Ap2 clock mutant mice: baseline characteristics and novel responses to a lipopolysaccharide challenge.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Ap2 clock mutant mice: baseline characteristics and novel responses to a lipopolysaccharide challenge./
作者:	Birky, Tana L.
面頁冊數:	99 p.
附註:	Source: Masters Abstracts International, Volume: 52-06.
Contained By:	Masters Abstracts International52-06(E).
標題:	Behavioral sciences. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1555102
ISBN:	9781303867576

Ap2 clock mutant mice: baseline characteristics and novel responses to a lipopolysaccharide challenge.
Birky, Tana L.

Ap2 clock mutant mice: baseline characteristics and novel responses to a lipopolysaccharide challenge. - 99 p.

Source: Masters Abstracts International, Volume: 52-06.

Thesis (M.A.)--The University of Alabama at Birmingham, 2014.

This item is not available from ProQuest Dissertations & Theses.

Circadian rhythms are the daily biological changes present within most organisms that occur in a predictable, approximately 24 hour pattern, even in the absence of external stimuli. These rhythms occur both at a global and cellular level, and although the molecular mechanics are highly conserved, their functions may vary depending on the tissues in which they are expressed. These functions include various aspects of metabolic processes such as satiety signaling and cellular proliferation. In order to explore the specific functions of circadian rhythms within adipocytes, a mouse model with Clock disruption driven by the fatty acid-binding protein 2 (aP2) promoter was created. aP2 has been shown to be expressed in adipocytes as well as macrophages, and clock disruption was verified in adipocytes. This model showcased a phenotype including increased total weight, body fat percentage, and surprisingly, a large increase in early and unexpected death. Since clock disruption likely has occurred within macrophages, immune disruption was identified as a potential cause for these unexpected deaths. To investigate, an immune challenge was presented to both transgenic and wild-type mice, and several behavioral and physiological variables were recorded. Unfortunately, no significant differences were apparent between genotypes. At this point, the cause of higher rates of deaths among the adipocyte and macrophage specific circadian disruption mouse models remains unknown.

ISBN: 9781303867576Subjects--Topical Terms:

529833
Behavioral sciences.

Ap2 clock mutant mice: baseline characteristics and novel responses to a lipopolysaccharide challenge.
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520 $a Circadian rhythms are the daily biological changes present within most organisms that occur in a predictable, approximately 24 hour pattern, even in the absence of external stimuli. These rhythms occur both at a global and cellular level, and although the molecular mechanics are highly conserved, their functions may vary depending on the tissues in which they are expressed. These functions include various aspects of metabolic processes such as satiety signaling and cellular proliferation. In order to explore the specific functions of circadian rhythms within adipocytes, a mouse model with Clock disruption driven by the fatty acid-binding protein 2 (aP2) promoter was created. aP2 has been shown to be expressed in adipocytes as well as macrophages, and clock disruption was verified in adipocytes. This model showcased a phenotype including increased total weight, body fat percentage, and surprisingly, a large increase in early and unexpected death. Since clock disruption likely has occurred within macrophages, immune disruption was identified as a potential cause for these unexpected deaths. To investigate, an immune challenge was presented to both transgenic and wild-type mice, and several behavioral and physiological variables were recorded. Unfortunately, no significant differences were apparent between genotypes. At this point, the cause of higher rates of deaths among the adipocyte and macrophage specific circadian disruption mouse models remains unknown.
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