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Creatine kinase is also sometimes referred to as creatine phosphokinase, creatine phosphotransferase, CPK, or just CK. Along with CKMB, significant levels of CKMM activity are found in cardiac muscle and therefore a large increase in total CK was once used as a tool in the diagnosis of AMI3. The techniques used to measure serum CKMB in the clinical laboratory have changed significantly over the years.
Anyone can submit a comment any time after publication, but only those submitted within 4 weeks of an article’s publication will be considered for print publication. CK-2: MB isoenzyme, highest concentration in cardiac muscle, with lesser amounts in skeletal muscle. In one study, CK isoenzymes were measured in normal dogs (n=20) and cats (n=14) by electrophoresis. The routinely used enzymatic assay takes advantage of the normal ability of CK to catalyze the conversion of phosphocreatine to creatine, releasing ATP in the process. Nicotinamide adenine dinucleotide phosphate (NADPH) and ATP are produced in equal quantities at the same rate.
According to the reagent manufacturer, stability of CK in human serum and plasma samples is as follows: 2 days at room temperature, 7 days refrigerated, or 4 weeks frozen at around -20°C. Increases in serum or plasma CK is most commonly used as a marker of skeletal muscle injury (by sheer mass, it is unlikely to see increases in total CK activity in serum or plasma after cardiac injury, however increases in CK-MB or CK-2 may be seen if electrophoretic separation is done).
Artifact: Hemolysis will increase CK activity as constituents within red blood cells (ADP or glucose-6-phosphate) or in their membranes (adenylate kinase) contribute to the enzymatic reaction for CK, falsely increasing activity.
Physiologic: CK activity in young puppies is higher than in adults, although this is apparently without explanation. Muscle disease: Detection of increased activity in serum is useful as an indicator of muscle injury.
Neurologic disease: Creatine kinase activity has been measured in the cerebrospinal fluid of animals as a marker of neurologic injury. There are two common gene products, one coding for the subunit (so named because of its predominance in muscle) and the other for the B subunit (so named because of its predominance in brain tissue). Once the CK isoenzymes were elucidated and isoenzyme tests became available, CKMB quickly became the marker of choice for AMI4-7, and remained so for many years, only to be eventually surpassed by the cardiac troponins.
One of the earliest tests for measuring CKMB was ion-exchange chromatography, a very time consuming and laborious technique.
One month after publication, editors review all posted comments and select some for publication in the Letters section of the print version of Annals. In muscles, CK functions by making ATP available for contraction by phosphorylating ADP from phosphocreatinine. Injury to brain tissue may increase CK-1 activity in CSF, but rarely results in raised total serum CK activity. In horses, intravenous infusion of a muscle homogenate revealed a terminal half life of 123 minutes (mean) (Volfinger et al 1994). Inadvertant penetration of muscle during venipuncture can cause 3- to 4-fold increases in CK activity in the sample and is a common cause of mildly increased CK values in healthy (or sick) animals. Moderate increases (2-3x) are possible in exercising horses, with the post-exercise increase being less in well-conditioned animals.
The exact mechanism is uncertain, but it is thought to be due to increased muscle catabolism or membrane permeability (blood was withdrawn through an indwelling catheter in these cats, arguing against a muscle puncture during collection) (). Studies in horses have shown that high CK activity is seen in various neurologic conditions, including equine protozoal neuritis (Sarcocystis neurona) but that high values are neither sensitive or specific for the latter disease. Grahame Hardie3, 4 1 Division of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215 2 Cellular Stress Group, MRC Clinical Sciences Centre, Imperial College, Hammersmith Hospital, London W12 0NN, United Kingdom 3 Division of Molecular Physiology, Wellcome Trust Biocentre, University of Dundee, Dundee DD1 4HN, Scotland 4 These authors contributed equally to this work. When electrophoretic methods became more practical this became a common technique, using a chromogenic CK activity stain. In dogs, both macroCK-2 and CK-BB (CK-1) were the next most frequent forms of CK, whereas in cats both macroenzymes were the second most frequent form.
Intramuscular injections will increase CK activity to various degrees depending on the irritant or toxic effects of the drug or if the drug impedes local blood flow.


High CK activity are observed in inherited muscular dystrophies, exercise-induced rhabdomyolysis, polymyositis, vitamin E-selenium deficiency, snake bite poisoning, etc. In another study, anorectic cats with a nasopharyngeal tube had a higher CK activity than non-anorectic cats.
Furthermore, contamination with epidural fat is a major confounding variable that falsely increases CK activity (Jackson et al 1996).
Phosphocreatine is used as an energy storage system in muscle tissue with CK serving to catalyze the reverse reaction; The rapid formation of ATP from phosphocreatine and ADP when ATP is needed by the tissue1.
Subsequently immunoinhibition methods became popular for their speed and their ability to be automated. Determination of Creatine Kinase Isoenzyme MB (CK-MB): Comparison of Methods and Clinical Evaluation. National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical Characteristics and Utilization of Biochemical Markers in Acute Coronary Syndromes. Evaluation and Comparison of Immunoinhibition and Immunoprecipitation Methods for differentiating MB and BB from macro forms of Creatine Kinase in Patients and Healthy Individuals. Direct Measurement of Creatine Kinase-MB Activity in Serum After Extraction with a Monoclonal Antibody Specific to the MB Isoenzyme.
Creatine kinase is a dimeric molecule composed of two types of monomers, the M and B subunits. Increases of CK-BB were seen in 3 dogs with central neurologic disease (Paltrinieri et al 2010). Activity increases quickly (increases at 5 hours and peaks within 12 hours) and returns to normal within 24-48 hours after acute, transient muscle injury in horses.
In one study, increased CK activity was seen in 60% of sick cats with various diseases, with marked increases (>30x upper reference limit) only being seen in 7% of cats. The high CK values were associated with other evidence of muscle injury in these cats, including high AST and lactate dehydrogenase (Fascetti et al 1997). In this technique an anti-M subunit antibody is used to inhibit any CKMM present along with the M subunit of any CKMB that might be present. Various combinations of these monomers make up different CK isoenzymes which are found in specific locations in brains and cells (see below). It is possible that the muscle was secondary to the primary disease process versus anorexia per se.
In contrast, aspartate aminotransferase (AST) (which has a longer half-life) will increase more gradually after muscle injury and stays increased for a longer period of time than CK (see image). The specificity of CKMB for cardiac tissue is what has made it such a powerful diagnostic tool for the diagnosis of acute myocardial infarction (AMI). The disadvantage of this technique is that it would not distinguish CKMB from CKBB, and although the presence of CKBB is rare in practice, it has always been a concern9,10. A traditional immunoassay that could distinguish CKMB from CKBB and CKMM was a little longer in coming due to the fact that CKMB has no unique subunits compared to these other forms.
This is most commonly used in humans with ischemic cardiac events (heart attack) but has been supplanted by measurement of cardiac troponin in many hospitals. When CKMB-specific antibodies directed against regions of the M-B subunit interface were finally developed11, commercial CKMB immunoassays quickly became popular.
Due to the difficulties in identifying CK isoenzymes in animals and the perceived scarcity of cardiac injury, we do not quantitate the different isoenzymes. They are the preferred and most common assays used to measure CKMB to this day, though immunoinhibition and electrophoresis are still performed. In modern society, this genetic constellation has become maladaptive owing to the fact that industrialization has made food supply more abundant and reduced the need to be physically active. Hence, the prevalence of obesity and its associated morbidities (including type 2 diabetes, hypertension, cardiovascular disease, and the metabolic syndrome) continues to climb. Understanding the fundamental biology of energy balance is essential to developing new approaches to ?°stay the tide?± of these metabolic diseases. Historically, the AMP-activated protein kinase (AMPK) pathway was viewed primarily as a sensor and regulator of energy balance at the cellular level.


Indeed, the fact that orthologs of AMPK are found in single celled eukaryotes such as the yeast Saccharomyces cerevisiae and the primitive protist Giardia lamblia ([Carling, 2004] and [Hardie et al., 2003]) is consistent with this being the function for which it originally evolved.
However, during the last three years, it has become apparent that in mammals, AMPK is also involved in the fundamental regulation of energy balance at the whole body level by responding to hormonal and nutrient signals in the central nervous system and peripheral tissues that modulate food intake and energy expenditure. These occur in a number of proteins in archaea, bacteria, and eukaryotes, and since the functional unit is a dimer, Kemp (Kemp, 2004) has suggested the term ?°Bateman domain?± to describe the structure formed by two tandem CBS motifs. Unusually, the ¦A subunits of AMPK contain four repeats, forming two tandem Bateman domains. Each of these domains binds one molecule of AMP or ATP in a mutually exclusive manner (Scott et al., 2004), consistent with the findings that high concentrations of ATP antagonize activation of AMPK by AMP. Constructs containing both Bateman domains bind two molecules of AMP or ATP with strong positive cooperativity, which may be a further mechanism to increase the sensitivity of the AMPK system to small changes in nucleotide levels.
AMPK is also activated by pathological stresses such as glucose deprivation, ischemia, hypoxia, oxidative stress, and hyperosmotic stress. Thiazolidinediones also increase plasma adiponectin and decrease plasma resistin levels, which could contribute to the indirect effects on AMPK activity (see below). Most of the actions of thiazolidinediones are thought to be explained by another target, the PPAR-¦A, a nuclear receptor. While there is currently no other known target for metformin, more studies are needed to clarify how critical the activation of AMPK is for the therapeutic effects of these drugs. Role of AMP-activated protein kinase (AMPK) in the control of whole-body energy homeostasisActivation of AMPK in many tissues switches off ATP-consuming processes while switching on catabolic processes that generate ATP. The adipocyte-derived hormones leptin and adiponectin, as well as exercise, activate AMPK in skeletal muscle, stimulating fatty acid oxidation.
Leptin??s activation of AMPK in skeletal muscle involves the hypothalamic-sympathetic nervous system (SNS) axis. Adiponectin also activates AMPK in liver, increasing fatty acid oxidation and reducing gluconeogenesis, and in adipocytes, where the downstream biologic pathway has not been studied.
AMPK inhibits insulin secretion from pancreatic ¦A cells.*Insulin inhibits AMPK activation in ischemic heart and hypothalamus, whereas it has no effect on AMPK in skeletal muscle or adipocytes. In hypothalamus, AMPK activity plays a role in regulation of food intake and body weight (see Figure 3). This phosphorylation inhibits the activity of ACC, which results in decreased malonyl CoA levels. A fall in malonyl CoA levels disinhibits CPT1, resulting in increased fatty acid oxidation. This pathway is thought to be central to the effects of AMPK to reduce lipid stores in muscle and liver and hence to its insulin-sensitizing effects.
These molecules have been termed adipokines and many of their metabolic actions are mediated by AMPK. Adiponectin stimulates AMPK phosphorylation and activity in muscle and liver in vivo and in vitro (Yamauchi et al., 2002). In muscle, the activation of AMPK is necessary for adiponectin??s effects on fatty acid oxidation and glucose transport and is associated with increased AMP levels. In liver, AMPK activation is necessary for the effects on inhibition of PEPCK and glucose 6 phosphatase expression and hepatic glucose production (Yamauchi et al., 2002). Furthermore, blocking the effect of adiponectin to activate AMPK in liver using a dominant-negative AMPK abrogates the glucose lowering effect of adiponectin (Yamauchi et al., 2002).
Adiponectin also activates AMPK in isolated adipocytes, although the biologic effect is unknown (Wu et al., 2003). Thus, the AMPK pathway is critical for the metabolic- and insulin-sensitizing actions of adiponectin as well as leptin.



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