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New Potential Targets of Glucagon-Like Peptide 1 Receptor Agonists in Pancreatic β-Cells and Hepatocytes
Endocrinology and Metabolism ; : 1-5, 2017.
Artículo en Inglés | WPRIM | ID: wpr-194439
ABSTRACT
It is well known that both insulin resistance and decreased insulin secretory capacity are important factors in the pathogenesis of type 2 diabetes mellitus (T2DM). In addition to genetic factors, obesity and lipotoxicity can increase the risk of T2DM. Glucagon-like peptide 1 (GLP-1) receptor agonists are novel antidiabetic drugs with multiple effects. They can stimulate glucose-dependent insulin secretion, inhibit postprandial glucagon release, delay gastric emptying, and induce pancreatic β-cell proliferation. They can also reduce the weight of patients with T2DM and relieve lipotoxicity at the cellular level. Many intracellular targets of GLP-1 have been found, but more remain to be identified. Elucidating these targets could be a basis for developing new potential drugs. My colleagues and I have investigated new targets of GLP-1, with a particular focus on pancreatic β-cell lines and hepatic cell lines. Herein, I summarize the recent work from my laboratory, with profound gratitude for receiving the prestigious 2016 Namgok Award.
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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Distinciones y Premios / Resistencia a la Insulina / Glucagón / Hepatocitos / Diabetes Mellitus / Diabetes Mellitus Tipo 2 / Péptido 1 Similar al Glucagón / Receptor del Péptido 1 Similar al Glucagón / Vaciamiento Gástrico / Hipoglucemiantes Límite: Humanos Idioma: Inglés Revista: Endocrinology and Metabolism Año: 2017 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Distinciones y Premios / Resistencia a la Insulina / Glucagón / Hepatocitos / Diabetes Mellitus / Diabetes Mellitus Tipo 2 / Péptido 1 Similar al Glucagón / Receptor del Péptido 1 Similar al Glucagón / Vaciamiento Gástrico / Hipoglucemiantes Límite: Humanos Idioma: Inglés Revista: Endocrinology and Metabolism Año: 2017 Tipo del documento: Artículo