Manipulating creatine kinase activity in transgenic mice to study control of energy metabolism

1991 ◽  
Vol 19 (4) ◽  
pp. 1010-1014 ◽  
Author(s):  
M. Julia Brosnan ◽  
Jessica M. Halow ◽  
Alan P. Koretsky
Keyword(s):  
Creatine Kinase ◽  
Energy Metabolism ◽  
Transgenic Mice ◽  
Kinase Activity ◽  
Creatine Kinase Activity

Single dose and repeated administrations of liraglutide alter energy metabolism in the brains of young and adult rats

2016 ◽  
Vol 94 (5) ◽  
pp. 451-458 ◽  
Author(s):  
Morgana Prá ◽  
Gabriela Kozuchovski Ferreira ◽  
Aline Haas de Mello ◽  
Rosiane de Bona Schraiber ◽  
Larissa Colonetti Cardoso ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Single Dose ◽  
Energy Metabolism ◽  
Kinase Activity ◽  
Creatine Kinase Activity ◽  
Daily Injection ◽  
Adult Rats ◽  
Posterior Cortex ◽  
Young Rats ◽  
Repeated Administrations

Liraglutide is a human glucagon-like peptide-1 (GLP-1) analogue that was recently approved to treat obesity in some countries. Considering that liraglutide effects on brain energy metabolism are little known, we evaluated the effects of liraglutide on the energy metabolism. Animals received a single or daily injection of saline or liraglutide during 7 days (25, 50, 100, or 300 μg/kg i.p.). Twenty-four hours after the single or last injection, the rats were euthanized and the hypothalamus, prefrontal cortex, cerebellum, hippocampus, striatum, and posterior cortex were isolated. Our results demonstrated that a single dose of liraglutide in young rats increased the activity of complexes and inhibited creatine kinase activity. Repeated administrations of liraglutide in young rats reduced the activity of complexes and activated creatine kinase activity. In adult rats, a single dose of liraglutide reduced the activity of complex I and creatine kinase and increased the activity of complexes II and IV. Repeated administrations of liraglutide in adult rats increased the activity of complexes I and IV and reduced the activity of complex II and creatine kinase. We concluded that liraglutide may interfere in energy metabolism, because analysis of different times of administrations, concentrations, and level of brain development leads to divergent results.

Creatine kinase activity of urinary bladder and skeletal muscle from control and streptozotocin-diabetic rats

1990 ◽  
Vol 97 (2) ◽  
Author(s):  
RobertM. Levin ◽  
PenelopeA. Longhurst ◽  
SheilaS. Levin ◽  
Niels Haugaard ◽  
AlanJ. Wein
Keyword(s):  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Urinary Bladder ◽  
Kinase Activity ◽  
Diabetic Rats ◽  
Creatine Kinase Activity ◽  
Streptozotocin Diabetic Rats

Distribution of serum creatine kinase activity in young healthy persons

1999 ◽  
Vol 279 (1-2) ◽  
pp. 107-115 ◽  
Author(s):  
Eli I. Lev ◽  
Ilan Tur-Kaspa ◽  
Isaac Ashkenazy ◽  
Anat Reiner ◽  
David Faraggi ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Kinase Activity ◽  
Creatine Kinase Activity ◽  
Serum Creatine Kinase ◽  
Healthy Persons

scholarly journals Ability of adenovirus 5 E1A proteins to suppress differentiation of BC3H1 myoblasts correlates with their binding to a 300 kDa cellular protein.

1992 ◽  
Vol 3 (10) ◽  
pp. 1107-1115 ◽  
Author(s):  
J S Mymryk ◽  
R W Lee ◽  
S T Bayley
Keyword(s):  
Creatine Kinase ◽  
Kinase Activity ◽  
Cellular Protein ◽  
Creatine Kinase Activity ◽  
Cellular Proteins ◽  
Deletion Mutants ◽  
Transcriptional Enhancers ◽  
Actin Mrna ◽  
Alpha Actin ◽  
Adenovirus 5

We have used deletion mutants to define the regions in Ad5 E1A proteins necessary to suppress differentiation of mouse BC3H1 myoblasts. We examined the differentiation of cells infected at a low multiplicity with viruses containing the E1A deletions and constructed so as to produce only the smaller of the two major E1A proteins. Only four of the mutant viruses containing deletions within the N-terminal 69 residues failed to suppress differentiation as judged by changes in morphology and in levels of muscle-specific alpha-actin mRNA and creatine kinase activity. The results were confirmed by analyses of lines of cells stably transfected with representative E1A mutants. The mouse cellular proteins to which mutant E1A proteins bound were identified by immunoprecipitating E1A proteins specifically from infected BC3H1 cells and by analyzing the precipitates on denaturing gels. Bands of proteins of 300, 130, 107, 105 (the retinoblastoma product), and 60 kDa (cyclin A) were distinguished. Failure to suppress differentiation correlated with loss of binding to the 300-kDa protein but not to any of the others. The regions of E1A defined in this way have been shown to be required for several other activities, including enhancer repression and transformation. One function of the 300-kDa protein appears to be to facilitate the action of transcriptional enhancers of differentiation-specific genes.

Skeletal muscle collagen content in humans after high-force eccentric contractions

2004 ◽  
Vol 97 (1) ◽  
pp. 197-203 ◽  
Author(s):  
Abigail L. Mackey ◽  
Alan E. Donnelly ◽  
Taina Turpeenniemi-Hujanen ◽  
Helen P. Roper
Keyword(s):  
Creatine Kinase ◽  
Kinase Activity ◽  
Staining Intensity ◽  
Creatine Kinase Activity ◽  
Serum Creatine Kinase ◽  
Muscle Contractions ◽  
Tissue Inhibitors Of Metalloproteinases ◽  
Eccentric Contractions ◽  
Knee Extensors ◽  
Type Iv

The purpose of this study was to investigate the effects of high-force eccentric muscle contractions on collagen remodeling and on circulating levels of matrix metalloproteinases (MMP) and tissue inhibitors of metalloproteinases (TIMP) in humans. Nine volunteers [5 men and 4 women, mean age 23 (SD 4) yr] each performed a bout of 100 maximum voluntary eccentric contractions of the knee extensors. Muscle biopsies were taken before exercise and on days 4 and 22 afterward. Image analysis of stained tissue sections was used to quantify endomysial collagen staining intensity. Maximum voluntary contractile isometric force was recorded preexercise and on days 1, 2, 3, 4, 8, 11, and 14 postexercise. Venipuncture blood samples were also drawn on these days for measurement of serum creatine kinase activity and concentrations of MMP-9, TIMP-1, TIMP-2, and the MMP-2/TIMP-2 complex. Maximum voluntary contractile force declined by 39 ± 23% (mean ± SD) on day 2 postexercise and recovered thereafter. Serum creatine kinase activity peaked on day 4 postexercise ( P < 0.01). Collagen type IV staining intensity increased significantly on day 22 postexercise to 126 ± 29% (mean ± SD) of preexercise values ( P < 0.05). Serum MMP-9 levels increased on day 8 postexercise ( P < 0.01), and serum TIMP-1 was also significantly elevated on days 1, 2, 3, 4, and 14 postexercise ( P < 0.05). These results suggest that a single bout of eccentric muscle contractions results in remodeling of endomysial type IV collagen, possibly via the MMP pathway.

Inhibition of creatine kinase activity by lysine in rat cerebral cortex

2009 ◽  
Vol 24 (2) ◽  
pp. 349-360 ◽  
Author(s):  
Anelise Miotti Tonin ◽  
Gustavo Costa Ferreira ◽  
Patrícia Fernanda Schuck ◽  
Carolina Maso Viegas ◽  
Ângela Zanatta ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Cerebral Cortex ◽  
Kinase Activity ◽  
Creatine Kinase Activity ◽  
Rat Cerebral Cortex

A "Reagentless" Fluorometric Method for Creatine Kinase Activity in Serum

1973 ◽  
Vol 19 (9) ◽  
pp. 1045-1048 ◽  
Author(s):  
Herbert K Y Lau ◽  
George G Guilbault
Keyword(s):  
Creatine Kinase ◽  
Silicone Rubber ◽  
Kinase Activity ◽  
Creatine Kinase Activity ◽  
Serum Creatine Kinase ◽  
Fluorometric Method ◽  
Nadh Fluorescence

Abstract A "reagentless" fluorometric method is described for the analysis of serum creatine kinase (CK) activity. The method is based on the use of silicone rubber pads, upon which are placed all the reagents for assay of CK. The rate of formation of NADH fluorescence at 460 nm is measured and equated to CK activity. The method is simple, rapid, inexpensive, and as little as 3 µl of serum is needed.

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