Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

References
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and, recently, there have been reports of mitochondrial muscle
disorders in animals ( Breitschwerdt et al. , 1992 ; Houlton
and Herrtage, 1980 ; Paciello et al. , 2003 ; Valberg et al. ,
1994 ; Vijayasarathy et al. , 1994 ). When the utilization of
oxygen is reduced, lactate formation is favored and results
in elevated blood lactate even with low-intensity exercise.
Disorders of the respiratory chain often result in increased
numbers of abnormal mitochondria and aggregates of mitochondria
under the sarcolemma. In sections, these mitochondrial
aggregates impart a “ ragged-red ” appearance to
the periphery of myofibers when stained with the modified
trichrome stain. The presence of ragged red myofibers and
elevated lactate concentrations with exercise warrant investigation
of metabolic abnormalities involving mitochondria.
1 . Respiratory Chain Complex I (NADH Ubiquinone
Oxidoreductase) Defi ciency
A deficiency of complex I was observed in an Arabian
mare with severe limitations to even mild exercise in which
there was an elevated venous pO 2 , low oxygen consumption
and lactic acidosis ( Valberg et al. , 1994 ). Complex I
of the respiratory chain is one of four complexes involved
in oxidative phosphorylation and transfers electrons from
NADH to CoQ in the conversion of oxygen to water.
2 . Cytochrome c Oxidase Defi ciency
An episodic weakness reported in Old English sheepdog
littermates is accompanied by elevated serum enzymes,
lactic acidosis, and increased pO 2 ( Breitschwerdt et al. ,
1992 ). This disorder may involve a reduction in cytochrome
c oxidase ( Vijayasarathy et al. , 1994 ).
3 . Lipid Storage Disorders
Abnormal accumulation of lipid droplets has been observed
in type 1 fibers of dogs with generalized myalgia, weakness,
and muscle atrophy ( Platt et al. , 1999 ; Shelton et al. , 1998 ). In
human beings, lipid storage myopathies have been attributed
to several different deficiencies of enzymes involved with
lipid transport into mitochondria (carnitine palmityl transferase
deficiency) or beta oxidation of free fatty acids. Clinical
features include muscle necrosis and myoglobinuria without
painful contractures. A specific enzyme deficiency remains
to be defined for the lipid storage myopathies in dogs.
F . Endocrine Myopathies
Signs referable to muscle weakness are frequently observed
as part of the clinical presentations of endocrine disorders.
1 . Corticosteroid Myopathy
Hyperadrenocorticism causes muscle wasting (atrophy)
and weakness in dogs and horses with Cushing’s disease
and following corticosteroid administration ( Braund et al. ,
1980a, 1980b ; Duncan et al. , 1977 ); ( Aleman et al. , 2006 ).
The muscle wasting is due to a rather selective anguloid to
angular atrophy of type 2 myofibers; however, quantitative
studies reveal atrophy of type 1 fibers as well. Myotonia
is a variable accompanying sign of this disorder ( Duncan
et al. , 1977 ). Muscle wasting appears to be due to catabolism
with decreased protein synthesis and increased protein
degradation mediated by altered transcription in protein
metabolism.
2 . Hypothyroid Myopathy
Thyroid status has a profound affect on skeletal muscle, and
hypothyroid states are often accompanied by manifestations
of neuromuscular disease. However, descriptions of muscle
disorders in clinical veterinary medicine are limited ( Braund
et al. , 1981 ). Selective type 2 myofiber atrophy and type 1
myofiber predominance (or type 2 myofiber paucity) are
common findings in canine hypothyroidism. Experimental
studies reveal that the proportion of myofiber types is influenced
by thyroid status in which thyroidectomy results in
type 1 myofiber predominance and thyroid excess results
in type 2 myofiber predominance ( Li et al. , 1996 ; Li and
Larsson, 1997 ).
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