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Neprilysin impedes islet amyloid formation by inhibition of fibril formation rather than peptide degradation.Differential effect of inbred mouse strain (C57BL/6, DBA/2, 129T2) on insulin secretory function in response to a high fat diet.β-cell loss and β-cell apoptosis in human type 2 diabetes are related to islet amyloid deposition.Exendin-4 increases islet amyloid deposition but offsets the resultant beta cell toxicity in human islet amyloid polypeptide transgenic mouse islets.cJUN N-terminal kinase (JNK) activation mediates islet amyloid-induced beta cell apoptosis in cultured human islet amyloid polypeptide transgenic mouse islets.Investigational agents that protect pancreatic islet beta-cells from failure.Matrix metalloproteinase-9 reduces islet amyloid formation by degrading islet amyloid polypeptideFructose-1,6-bisphosphatase overexpression in pancreatic beta-cells results in reduced insulin secretion: a new mechanism for fat-induced impairment of beta-cell functionAdipocytokines as features of the metabolic syndrome determined using confirmatory factor analysisOxidative stress is induced by islet amyloid formation and time-dependently mediates amyloid-induced beta cell apoptosis.Amyloid formation in human IAPP transgenic mouse islets and pancreas, and human pancreas, is not associated with endoplasmic reticulum stressOne year of sitagliptin treatment protects against islet amyloid-associated β-cell loss and does not induce pancreatitis or pancreatic neoplasia in mice.Scriptaid enhances skeletal muscle insulin action and cardiac function in obese mice.Amyloid formation results in recurrence of hyperglycaemia following transplantation of human IAPP transgenic mouse islets.High glucose-induced impairment in insulin secretion is associated with reduction in islet glucokinase in a mouse model of susceptibility to islet dysfunction.Rosiglitazone treatment does not decrease amyloid deposition in transplanted islets from transgenic mice expressing human islet amyloid polypeptide.Too much of a good thing: why it is bad to stimulate the beta cell to secrete insulin.Increased nicotinamide nucleotide transhydrogenase levels predispose to insulin hypersecretion in a mouse strain susceptible to diabetes.The influence of genetic background on the induction of oxidative stress and impaired insulin secretion in mouse islets.Class IIa HDACs do not influence beta-cell function under normal or high glucose conditions
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P50
description
researcher ORCID ID = 0000-0003-1412-6715
@en
wetenschapper
@nl
name
Kathryn Aston-Mourney
@ast
Kathryn Aston-Mourney
@en
Kathryn Aston-Mourney
@es
Kathryn Aston-Mourney
@nl
type
label
Kathryn Aston-Mourney
@ast
Kathryn Aston-Mourney
@en
Kathryn Aston-Mourney
@es
Kathryn Aston-Mourney
@nl
prefLabel
Kathryn Aston-Mourney
@ast
Kathryn Aston-Mourney
@en
Kathryn Aston-Mourney
@es
Kathryn Aston-Mourney
@nl
P106
P21
P31
P496
0000-0003-1412-6715