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Fig. 11.1 General scheme of cellular metabolism. Catabolic reactions generating ATP ( top ),
through coupling to anabolic reactions (biosynthesis, bottom ) using ATP, maintain cell structural
organization as an expression of the decrease of internal entropy (
Δ
S in
0) and are also the source
<
of energy for cellular work ( W c ). Abbreviations:
Δ
S ex external entropy,
Δ
S in internal entropy,
Δ
S t
total entropy,
G ex variatuion of Gibbs free energy. For further details, see text. Adapted from
(Saks 2007 ) with permission
Δ
and organ levels, giving rise to biological function. As such, systems biology
provides basic mechanistic insights about the principles that govern metabolic
behavior in living systems. According to Schr ¨ dinger, the metabolic activity of
living systems needs a continuous exchange of metabolites with the surroundings as
a form of extracting free energy from the medium. This process enables cells and
organisms to increase their internal organization such that they are able to perform
biological work from anabolic reactions (Schr¨dinger 1944 ). An increase of inter-
nal order implies a decrease of entropy that should be compensated by an entropy
increase in the environment. Catabolic and anabolic reactions are coupled to
mediate biological work (e.g., muscle contraction) through processes of free energy
conversion involving synthesis and utilization of ATP (Fig. 11.1 ). Coupling
between cellular work, anabolism, and catabolism is achieved by cyclic processes
involving mechanisms of feedback regulation. Herein, we introduce the theory of
integrated metabolic cycles. Cycles of substrate supply (Randle cycle), intracellular
energy conversion (Krebs cycle and mitochondrial oxidative phosphorylation), and
phosphotransfer reactions (kinase cycles) constitute conspicuous examples of both
substrate and energy provision and feedback regulation (Fig. 11.2 ). These cycles
closely interact with calcium (Ca 2+ ) cycling (Fig. 11.2 ). Among the kinase cycles, a
key role is played by the Cr/CK system, adenylate kinase, and AMPK in skeletal
muscle, heart, brain, and other cell types (Wallimann et al. 1992 , 2011 ; Schlattner
et al. 2006a , b ; Schlattner and Wallimann 2004 ; Wallimann 1996 , 2007 ; Saks
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