Dissociated insulinotropic sensitivity to glucose and carbachol in high-fat diet—induced insulin resistance in C57BL/6J mice☆
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2021, CytokineCitation Excerpt :We used the HFD obese mouse model introduced by Surwit et al. in 1988 [36]. This model is accompanied by insulin resistance with insufficient islet compensation, and previously used to study the pathophysiology of impaired glucose tolerance and early T2D [37,38]. In agreement with previous studies, we also observed LSF beneficial effects on the metabolic phenotype of this mouse model [26,39,40].
Muscarinic Agonist Ameliorates Insulin Secretion in Wfs1-Deficient Mice
2019, Canadian Journal of DiabetesCitation Excerpt :IP3 binds to IP3 receptors on the surface of the ER, mobilizing intracellular Ca2+ stores, which leads to an increase in cytoplasmic Ca2+ levels, thus potentiating glucose-stimulated insulin secretion (20–22). Previous reports have shown that the muscarinic agonist carbachol can restore insulin secretion in mice fed a high-fat diet (23) and in spontaneously diabetic Goto-Kakizaki rats (24). The aim of the present study was to investigate insulin-release dynamics in Wfs1-deficient mice and to determine whether stimulating muscarinic receptors diminishes deficiency in insulin secretion caused by the Wfs1 defect.
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Supported by the Swedish Medical Research Council (14X-6834 and 12X-4499), Novo Nordic, the Albert Påhlsson, Crafoord, Ernhold Lundström, and Ester Ohlssons Foundations, the Diabetes Association of Malmö with surroundings, the Swedish Diabetes Association, Malmö University Hospital, and the Faculty of Medicine, Lund University.