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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Purification and characterization of a peptide from amyloid-rich pancreases of type 2 diabetic patients
TL;DR: A peptide, of calculated molecular mass 3905 Da, that was a major protein component of amyloid-rich pancreatic extracts of three type 2 diabetic patients is described, indicating that these peptides are related in evolution.
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The fat-derived hormone adiponectin alleviates alcoholic and nonalcoholic fatty liver diseases in mice
TL;DR: Adiponectin was effective in ameliorating hepatomegaly, steatosis, and alanine aminotransferase abnormality associated with nonalcoholic obese, ob/ob mice and could suppress the hepatic production of TNF-alpha and plasma concentrations of this proinflammatory cytokine.
Journal Article
Islet amyloid, increased A-cells, reduced B-cells and exocrine fibrosis: quantitative changes in the pancreas in type 2 diabetes.
A Clark,C. A. Wells,I. D. Buley,J. K. Cruickshank,R. I. Vanhegan,David R Matthews,Garth J. S. Cooper,Rury R. Holman,R. C. Turner +8 more
TL;DR: The impaired insulin secretion in Type 2 diabetes may be due to a decrease in B-cells and to disruption of the islet structure by amyloid, and the increase in A-cells may contribute to the hyperglucagonaemia and hyperglycaemia of Type 2 Diabetes.
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Pancreatic amylin and calcitonin gene-related peptide cause resistance to insulin in skeletal muscle in vitro
TL;DR: It is reported that human pancreatic amylin and rat CGRP-1 are potent inhibitors of both basal and insulin-stimulated rates of glycogen synthesis in stripped rat soleus muscle in vitro, which may provide a basis for a new understanding of the molecular mechanisms that cause insulin resistance in skeletal muscle.
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Testosterone selectively reduces the high molecular weight form of adiponectin by inhibiting its secretion from adipocytes
Aimin Xu,Aimin Xu,Kok Weng Chan,Ruby L. C. Hoo,Yu Wang,Yu Wang,Kathryn C.B. Tan,Jialiang Zhang,Baoying Chen,Michael C. Lam,Cynthia A. Tse,Garth J. S. Cooper,Karen S.L. Lam +12 more
TL;DR: The selective inhibition of HMW adip onectin by testosterone might contribute to the sex dimorphism of adiponectin in terms of its oligomeric complex distribution and could partly explain why men have higher risk to insulin resistance and atherosclerosis than women.