TY  - JOUR
T1  - Key Proteins at the Interface of Bioenergetics and Mitochondrial Function
AU - Baldassini, W.A. AU - . Branco, R.H AU - Ramsey, J.J. AU - Dauria, B.D. AU - Bonilha, S.F.M AU - Lanna, D.P.D. 
JO  - Journal of Animal and Veterinary Advances
VL  - 17
IS  - 5
SP  - 111
EP  - 121
PY  - 2018
DA  - 2001/08/19
SN  - 1680-5593
DO  - javaa.2018.111.121
UR  - https://makhillpublications.co/view-article.php?doi=javaa.2018.111.121
KW  - oxidative stress
KW  -metabolism
KW  -feed efficiency
KW  -Energy expenditure
KW  -Shc protein
KW  -uncoupling
AB  - The Shc molecules and the mitochondrial Uncoupling Proteins (UCP) have been proposed to play
an important role in Energy Expenditure (EE) and cellular metabolism. We discuss the results of published
studies regarding the influence of Shc proteins and UCP on energy metabolism of mice and beef cattle.
Additionally, we review the possible association between mitochondrial function from animals classified
according to Feed Efficiency (FE). Several studies have been conducted to investigate the role of Shc proteins
play in aging and control of Reactive Oxygen Species (ROS) production. Studies have investigated the impact
of low Shc levels (ShcKO) in preventing oxidative stress, apoptosis and hyperglycemia. In general, ShcKO is
associated with changes in mitochondrial function and EE and protection of tissues against oxidative stress.
However, little is known about the role of Shc proteins on energy metabolism in animals fed a high fat diet. In
mitochondria, UCP activity provides adaptive thermogenesis, carbon flux maintenance and also protection of
cell membranes against oxidative stress caused by ROS. In mitochondrial metabolism, UCP activity (uncoupling)
is a paradigm in the context of FE. It may represent a cellular inefficiency but also a reduction in oxidative stress
by attenuating mitochondrial ROS production. Thus, studies suggest that mitochondria from less FE animals
have greater protein oxidation due to greater basal mitochondrial ROS generation. This increased ROS
production could oxidize proteins, causing impaired protein synthesis. However, additional studies are needed
to understand the physiological significance of these changes in mitochondrial function and energy metabolism
and therefore, the impacts of these molecular mechanisms on animal performance and FE. Changes of very small
magnitude in either mitochondrial function or enzyme activities could greatly alter energy metabolism and cause
the changes in FE observed <i>in vivo</i>. Most of current biochemical studies are unable to detect the magnitude
of the changes.
ER  -