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1. Novel Zn2+ Modulated GPR39 Receptor Agonists Do Not Drive Acute Insulin Secretion in Rodents.

Author

Ola Fjellström, Niklas Larsson, Shin-Ichiro Yasuda, Takuma Tsuchida, Takahiro Oguma, Anna Marley, Charlotte Wennberg-Huldt, Daniel Hovdal, Hajime Fukuda, Yukimi Yoneyama, Kazuyo Sasaki, Anders Johansson, Sara Lundqvist, Johan Brengdahl, Richard J Isaacs, Daniel Brown, Stefan Geschwindner, Lambertus Benthem, Claire Priest, and Andrew Turnbull

Subjects
Medicine, Science
Abstract

Type 2 diabetes (T2D) occurs when there is insufficient insulin release to control blood glucose, due to insulin resistance and impaired β-cell function. The GPR39 receptor is expressed in metabolic tissues including pancreatic β-cells and has been proposed as a T2D target. Specifically, GPR39 agonists might improve β-cell function leading to more adequate and sustained insulin release and glucose control. The present study aimed to test the hypothesis that GPR39 agonism would improve glucose stimulated insulin secretion in vivo. A high throughput screen, followed by a medicinal chemistry program, identified three novel potent Zn2+ modulated GPR39 agonists. These agonists were evaluated in acute rodent glucose tolerance tests. The results showed a lack of glucose lowering and insulinotropic effects not only in lean mice, but also in diet-induced obese (DIO) mice and Zucker fatty rats. It is concluded that Zn2+ modulated GPR39 agonists do not acutely stimulate insulin release in rodents.

Published
2015
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2. Novel Zn2+ Modulated GPR39 Receptor Agonists Do Not Drive Acute Insulin Secretion in Rodents

Author

Stefan Geschwindner, Andrew V. Turnbull, Sara Lundqvist, Anna Marley, Kazuyo Sasaki, Niklas Larsson, Ola Fjellström, Charlotte Wennberg-Huldt, Richard J. Isaacs, Anders Johansson, Claire Priest, Lambertus Benthem, Yukimi Yoneyama, Johan Brengdahl, Daniel Hovdal, Shin-ichiro Yasuda, Hajime Fukuda, Takuma Tsuchida, Daniel G. Brown, and Takahiro Oguma

Subjects
Blood Glucose, Male, medicine.medical_specialty, medicine.medical_treatment, lcsh:Medicine, Type 2 diabetes, Biology, Receptors, G-Protein-Coupled, Small Molecule Libraries, Islets of Langerhans, Mice, Insulin resistance, In vivo, Internal medicine, Insulin receptor substrate, Drug Discovery, Insulin Secretion, Blood plasma, medicine, Animals, Humans, Insulin, Receptor, lcsh:Science, Glucose tolerance test, Multidisciplinary, Dose-Response Relationship, Drug, medicine.diagnostic_test, lcsh:R, Glucose Tolerance Test, medicine.disease, High-Throughput Screening Assays, Rats, Rats, Zucker, Zinc, Endocrinology, lcsh:Q, Research Article
Abstract

Type 2 diabetes (T2D) occurs when there is insufficient insulin release to control blood glucose, due to insulin resistance and impaired β-cell function. The GPR39 receptor is expressed in metabolic tissues including pancreatic β-cells and has been proposed as a T2D target. Specifically, GPR39 agonists might improve β-cell function leading to more adequate and sustained insulin release and glucose control. The present study aimed to test the hypothesis that GPR39 agonism would improve glucose stimulated insulin secretion in vivo. A high throughput screen, followed by a medicinal chemistry program, identified three novel potent Zn2+ modulated GPR39 agonists. These agonists were evaluated in acute rodent glucose tolerance tests. The results showed a lack of glucose lowering and insulinotropic effects not only in lean mice, but also in diet-induced obese (DIO) mice and Zucker fatty rats. It is concluded that Zn2+ modulated GPR39 agonists do not acutely stimulate insulin release in rodents.

Published
2015

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