Secondary consequences of beta cell inexcitability: identification and prevention in a murine model of K(ATP)-induced neonatal diabetes mellitus. - Wikidata - wikimedia - TriplyDB

Secondary consequences of beta cell inexcitability: identification and prevention in a murine model of K(ATP)-induced neonatal diabetes mellitus.

Secondary consequences of beta cell inexcitability: identification and prevention in a murine model of K(ATP)-induced neonatal diabetes mellitus.

http://www.wikidata.org/entity/Q39035715

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Neonatal diabetes: an expanding list of genes allows for improved diagnosis and treatment Phase transitions in the multi-cellular regulatory behavior of pancreatic islet excitability Neonatal diabetes mellitus: a model for personalized medicine Reversible changes in pancreatic islet structure and function produced by elevated blood glucose.Tamoxifen-Induced Cre-loxP Recombination Is Prolonged in Pancreatic Islets of Adult Mice Glucose stimulation of hypothalamic MCH neurons involves K(ATP) channels, is modulated by UCP2, and regulates peripheral glucose homeostasis.Modeling K,ATP--dependent excitability in pancreatic islets.Peroxisomal lipid synthesis regulates inflammation by sustaining neutrophil membrane phospholipid composition and viability.Muscle KATP channels: recent insights to energy sensing and myoprotection Fatty acid synthase modulates homeostatic responses to myocardial stress.Acute sulfonylurea therapy at disease onset can cause permanent remission of KATP-induced diabetes.Successful sulfonylurea treatment of an insulin-naïve neonate with diabetes mellitus due to a KCNJ11 mutation Hyperinsulinism and diabetes: genetic dissection of beta cell metabolism-excitation coupling in mice Decreases in Gap Junction Coupling Recovers Ca2+ and Insulin Secretion in Neonatal Diabetes Mellitus, Dependent on Beta Cell Heterogeneity and Noise PERK is required in the adult pancreas and is essential for maintenance of glucose homeostasis.Diabetes induced by gain-of-function mutations in the Kir6.1 subunit of the KATP channel.Molecular biology of K(ATP) channels and implications for health and disease.Decreasing cx36 gap junction coupling compensates for overactive KATP channels to restore insulin secretion and prevent hyperglycemia in a mouse model of neonatal diabetes.The role of the KATP channel in glucose homeostasis in health and disease: more than meets the islet.Use of mouse models in studying type 2 diabetes mellitus.Current understanding of K ATP channels in neonatal diseases: focus on insulin secretion disorders.The diabetic β-cell: hyperstimulated vs. hyperexcited.Neonatal diabetes caused by activating mutations in the sulphonylurea receptor K(ATP) channels and islet hormone secretion: new insights and controversies.Sulfonylureas: a new look at old therapy.Intermittent Fasting Preserves Beta-Cell Mass in Obesity-induced Diabetes via the Autophagy-Lysosome Pathway.Glibenclamide treatment blocks metabolic dysfunctions and improves vagal activity in monosodium glutamate-obese male rats.Pancreatic β-cell identity in diabetes.Sulfonylurea challenge test in subjects diagnosed with type 1 diabetes mellitus.Neonatal Diabetes and the KATP Channel: From Mutation to Therapy.All mixed up: defining roles for β-cell subtypes in mature islets.Promoter DNA methylation regulates murine SUR1 (Abcc8) and SUR2 (Abcc9) expression in HL-1 cardiomyocytes.Interaction between mutations in the slide helix of Kir6.2 associated with neonatal diabetes and neurological symptoms.Defects in beta cell Ca²+ signalling, glucose metabolism and insulin secretion in a murine model of K(ATP) channel-induced neonatal diabetes mellitus Pancreatic β cell dedifferentiation in diabetes and redifferentiation following insulin therapy.Fatty acid synthase modulates intestinal barrier function through palmitoylation of mucin 2.ATP and sulfonylurea linkage in the K(ATP) channel solves a diabetes puzzler Inferring gene-to-phenotype and gene-to-disease relationships at Mouse Genome Informatics: challenges and solutions.K(ATP)-channel-dependent regulation of catecholaminergic neurons controls BAT sympathetic nerve activity and energy homeostasis.Preservation of Reduced Numbers of Insulin-Positive Cells in Sulfonylurea-Unresponsive KCNJ11-Related Diabetes.

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Secondary consequences of beta cell inexcitability: identification and prevention in a murine model of K(ATP)-induced neonatal diabetes mellitus.

http://www.wikidata.org/entity/Q39035715

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Secondary consequences of beta ...... vention in a murine model of K

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Secondary consequences of beta ...... vention in a murine model of K

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J.CMET.2008.12.005

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Cell Metabolism

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Secondary consequences of beta ...... ed neonatal diabetes mellitus.

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Ailing Tong

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Alexis Scott

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Andre Kleinridders

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Eva Rother

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Joseph C Koster

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Maria Sara Remedi

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P2860

The G53D mutation in Kir6.2 (KCNJ11) is associated with neonatal diabetes and motor dysfunction in adulthood that is improved with sulfonylurea therapy.

Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes

A heterozygous activating mutation in the sulphonylurea receptor SUR1 (ABCC8) causes neonatal diabetes.

KATP channels as molecular sensors of cellular metabolism

Chronic antidiabetic sulfonylureas in vivo: reversible effects on mouse pancreatic beta-cells

Targeted Overactivity of β Cell KATP Channels Induces Profound Neonatal Diabetes

ATP-sensitive K+ channels and insulin secretion: their role in health and disease.

Beta cell mass and growth after syngeneic islet cell transplantation in normal and streptozocin diabetic C57BL/6 mice.

Minireview: Secondary beta-cell failure in type 2 diabetes--a convergence of glucotoxicity and lipotoxicity.

A gating mutation at the internal mouth of the Kir6.2 pore is associated with DEND syndrome.

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