Date of Award

2009

Degree Type

Thesis

Degree Name

Master of Science (MS)

Department

Biology

Supervisor

Grant B. McClelland

Language

English

Abstract

Surviving at high-altitudes requires organisms to endure the combined
stresses of cold temperature and low atmospheric oxygen. Maintaining a stable
body temperature (Tb) is a constant battle that endotherms must defend when they
are subjected to temperatures beyond their thermal neutral zones (TNZ). Once
outside their TNZ, they elicit mechanisms of adaptive thermogenesis which
stimulate heat production via non-shivering (NST) and shivering thermogenesis
(ST). These processes are carried out in brown adipose tissue (BAT) and skeletal
muscle, respectively. Uncoupling proteins (UCP) carry out mechanisms of NST
by uncoupling substrate oxidation from ATP synthesis to generate heat. Many
studies have examined responses in endotherms to cold temperature acclimations
as well as episodes of acute hypoxia. However very few studies have looked at
the chronic effects of hypoxia and even less have investigated the combined
. effects of cold and hypoxia acclimations. Therefore, to address this issue we
examined the chronic effect of four weeks of exposure to hypobaric hypoxia (H,
480mmHg), cold (C, SOC) and the combination of the two stressors (HC)
compared to normoxic thermoneutral controls (N, 28°C) in CD-l mice. Overall
we found that HC mice had significantly lower Tb after periods of acclimation
while still residing in hypoxia compared to all other treatment groups. However,
experiments during acute temperature exposures in normoxia revealed that HC
mice were able to increase Tb as well as they demonstrated higher rates of thermal
conductance at high ambient temperatures. Investigations into BAT and UCP
regulation revealed that HC had a greater amount of BAT mass compared to controls and lower UCPl mRNA expression in BAT but no differences in UCPl
protein content. However, HC had lower mitochondrial density indicated by
lower activity of citrate synthase in BAT as well as UCP3 mRNA expression.
Together results from cold mice suggest that they exhibit an enhanced NST
capacity through the up-regulation of BAT mass and UCPl mRNA expression
whereas hypoxia inhibits NST response by down-regulation of UCPl and
mitochondrial density. Moreover the acclimation to both hypoxia and cold may
create barriers on an animal's ability to up-regulate NST in hypoxia by decreasing
mitochondrial density, UCPl and 3 mRNA expressions but still allows BAT
mechanisms to generate heat through UCPl protein that regulates Tbin normoxia.

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