G
Garth J. S. Cooper
Researcher at University of Auckland
Publications - 309
Citations - 17579
Garth J. S. Cooper is an academic researcher from University of Auckland. The author has contributed to research in topics: Amylin & Insulin. The author has an hindex of 63, co-authored 299 publications receiving 16490 citations. Previous affiliations of Garth J. S. Cooper include Manchester Academic Health Science Centre & University of Manchester.
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Journal ArticleDOI
Diabetic cardiomyopathy is associated with defective myocellular copper regulation and both defects are rectified by divalent copper chelation.
Shaoping Zhang,Hong Liu,Greeshma Vazhoor Amarsingh,Carlos Chun Ho Cheung,Sebastian Hogl,Umayal Narayanan,Lin Zhang,Selina McHarg,Jingshu Xu,Deming Gong,John Kennedy,B. Barry,Yee Soon Choong,Anthony R. J. Phillips,Garth J. S. Cooper +14 more
TL;DR: Myocardial copper deficiency and defective cellular copper transport/trafficking are revealed as key molecular defects underlying LV impairment in diabetes, and TETA-mediated restoration of copper regulation provides a potential new class of therapeutic molecules for DCM.
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Dissociation of the effects of amylin on osteoblast proliferation and bone resorption
Jillian Cornish,Karen E. Callon,C. Q.-X. Lin,C. L. Xiao,T. B. Mulvey,David H. Coy,Garth J. S. Cooper,Ian R. Reid +7 more
TL;DR: Dissociation of the actions of amylin suggests that it acts through two separate receptors, one on the osteoclast (possibly the calcitonin receptor) and a second on the bones of fetal rat osteoblasts and neonatal mouse calvariae.
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Response to intravenous injections of amylin and glucagon in fasted, fed, and hypoglycemic rats
TL;DR: Compared actions of intravenous glucagon and amylin, a newly discovered hyperglycemic pancreatic islet hormone, have been compared in 20-h fasted and fed, lightly anesthetized rats, and in rats made hypoglycemic with an insulin infusion to show consistency with glucagon's known action to promote hyperglycemia from hepatic glycogenolysis.
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Altered Calcium Homeostasis Does Not Explain the Contractile Deficit of Diabetic Cardiomyopathy
TL;DR: The slower action potential and reduced SERCA2a expression can explain the slower Ca2+ transient kinetics in diabetic rats but not the contractile deficit, and it is suggested that the observed LV remodeling may play a crucial role.
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8–37h-CGRP antagonizes actions of amylin on carbohydrate metabolism in vitro and in vivo
TL;DR: It is reported that 8–37hCGRP antagonizes amylin inhibition of insulin‐stimulated labelled glucose uptake into isolated rat soleus muscle, and inhibits amyl in‐evoked elevation of plasma lactate and glucose in fasted anaesthetized rats.