Search Results - "REMEDI, Maria S"

Pancreatic β Cell Dedifferentiation in Diabetes and Redifferentiation following Insulin Therapy by Wang, Zhiyu, York, Nathaniel W., Nichols, Colin G., Remedi, Maria S.

“…Diabetes is characterized by “glucotoxic” loss of pancreatic β cell function and insulin content, but underlying mechanisms remain unclear. A mouse model of…”
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ATP-Sensitive Potassium Channels in Hyperinsulinism and Type 2 Diabetes: Inconvenient Paradox or New Paradigm? by Nichols, Colin G, York, Nathaniel W, Remedi, Maria S

“…Secretion of insulin from pancreatic β-cells is complex, but physiological glucose-dependent secretion is dominated by electrical activity, in turn controlled…”
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Glibenclamide reverses cardiovascular abnormalities of Cantu syndrome driven by KATP channel overactivity by McClenaghan, Conor, Huang, Yan, Yan, Zihan, Harter, Theresa M, Halabi, Carmen M, Chalk, Rod, Kovacs, Attila, van Haaften, Gijs, Remedi, Maria S, Nichols, Colin G

“…Cantu syndrome (CS) is a complex disorder caused by gain-of-function (GoF) mutations in ABCC9 and KCNJ8, which encode the SUR2 and Kir6.1 subunits,…”
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Loss of β-cell identity and dedifferentiation, not an irreversible process? by Patel, Sumit, Remedi, Maria S

“…Type 2 diabetes (T2D) is a polygenic metabolic disorder characterized by insulin resistance in peripheral tissues and impaired insulin secretion by the…”
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SGLT2 inhibitors therapy protects glucotoxicity-induced β-cell failure in a mouse model of human KATP-induced diabetes through mitigation of oxidative and ER stress by Shyr, Zeenat A, Yan, Zihan, Ustione, Alessandro, Egan, Erin M, Remedi, Maria S

“…Progressive loss of pancreatic β-cell functional mass and anti-diabetic drug responsivity are classic findings in diabetes, frequently attributed to…”
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Preferential Gq signaling in diabetes: an electrical switch in incretin action and in diabetes progression? by Nichols, Colin G, York, Nathaniel W, Remedi, Maria S

“…Patients with type 2 diabetes (T2D) fail to secrete insulin in response to increased glucose levels that occur with eating. Glucagon-like peptide-1 (GLP-1) and…”
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ABCC9-related Intellectual disability Myopathy Syndrome is a KATP channelopathy with loss-of-function mutations in ABCC9 by Smeland, Marie F., McClenaghan, Conor, Roessler, Helen I., Savelberg, Sanne, Hansen, Geir Åsmund Myge, Hjellnes, Helene, Arntzen, Kjell Arne, Müller, Kai Ivar, Dybesland, Andreas Rosenberger, Harter, Theresa, Sala-Rabanal, Monica, Emfinger, Chris H., Huang, Yan, Singareddy, Soma S., Gunn, Jamie, Wozniak, David F., Kovacs, Attila, Massink, Maarten, Tessadori, Federico, Kamel, Sarah M., Bakkers, Jeroen, Remedi, Maria S., Van Ghelue, Marijke, Nichols, Colin G., van Haaften, Gijs

“…Mutations in genes encoding K ATP channel subunits have been reported for pancreatic disorders and Cantú syndrome. Here, we report a syndrome in six patients…”
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Mitochondrial Pyruvate Carrier 2 Hypomorphism in Mice Leads to Defects in Glucose-Stimulated Insulin Secretion by Vigueira, Patrick A., McCommis, Kyle S., Schweitzer, George G., Remedi, Maria S., Chambers, Kari T., Fu, Xiaorong, McDonald, William G., Cole, Serena L., Colca, Jerry R., Kletzien, Rolf F., Burgess, Shawn C., Finck, Brian N.

“…Carrier-facilitated pyruvate transport across the inner mitochondrial membrane plays an essential role in anabolic and catabolic intermediary metabolism…”
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Diabetes induced by gain-of-function mutations in the Kir6.1 subunit of the KATP channel by Remedi, Maria S, Friedman, Jonathan B, Nichols, Colin G

“…Gain-of-function (GOF) mutations in the pore-forming (Kir6.2) and regulatory (SUR1) subunits of K channels have been identified as the most common cause of…”
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A Unique High-Output Cardiac Hypertrophy Phenotype Arising From Low Systemic Vascular Resistance in Cantu Syndrome by Singh, Gautam K, McClenaghan, Conor, Aggarwal, Manish, Gu, Hongjie, Remedi, Maria S, Grange, Dorothy K, Nichols, Colin G

“…Background Cardiomegaly caused by left ventricular hypertrophy is a risk factor for development of congestive heart failure, classically associated with…”
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Glycogen Synthase Kinase-3 and Mammalian Target of Rapamycin Pathways Contribute to DNA Synthesis, Cell Cycle Progression, and Proliferation in Human Islets by Liu, Hui, Remedi, Maria S, Pappan, Kirk L, Kwon, Guim, Rohatgi, Nidhi, Marshall, Connie A, McDaniel, Michael L

“…Glycogen Synthase Kinase-3 and Mammalian Target of Rapamycin Pathways Contribute to DNA Synthesis, Cell Cycle Progression, and Proliferation in Human Islets…”
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Intermittent fasting protects β-cell identity and function in a type-2 diabetes model by Patel, Sumit, Yan, Zihan, Remedi, Maria S.

“…Type 2 diabetes (T2DM) is caused by the interaction of multiple genes and environmental factors. T2DM is characterized by hyperglycemia, insulin secretion…”
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Signaling Elements Involved in the Metabolic Regulation of mTOR by Nutrients, Incretins, and Growth Factors in Islets by KWON, Guim, MARSHALL, Connie A, PAPPAN, Kirk L, REMEDI, Maria S, MCDANIEL, Michael L

“…Signaling Elements Involved in the Metabolic Regulation of mTOR by Nutrients, Incretins, and Growth Factors in Islets Guim Kwon 1 , Connie A. Marshall 1 , Kirk…”
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KATP channels are necessary for glucose-dependent increases in amyloid-β and Alzheimer's disease-related pathology by Grizzanti, John, Moritz, William R, Pait, Morgan C, Stanley, Molly, Kaye, Sarah D, Carroll, Caitlin M, Constantino, Nicholas J, Deitelzweig, Lily J, Snipes, James A, Kellar, Derek, Caesar, Emily E, Pettit-Mee, Ryan J, Day, Stephen M, Sens, Jonathon P, Nicol, Noelle I, Dhillon, Jasmeen, Remedi, Maria S, Kiraly, Drew D, Karch, Celeste M, Nichols, Colin G, Holtzman, David M, Macauley, Shannon L

“…Elevated blood glucose levels, or hyperglycemia, can increase brain excitability and amyloid-β (Aβ) release, offering a mechanistic link between type 2…”
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An ancestral role for the mitochondrial pyruvate carrier in glucose-stimulated insulin secretion by McCommis, Kyle S, Hodges, Wesley T, Bricker, Daniel K, Wisidagama, Dona R, Compan, Vincent, Remedi, Maria S, Thummel, Carl S, Finck, Brian N

“…Abstract Objective Transport of pyruvate into the mitochondrial matrix by the Mitochondrial Pyruvate Carrier (MPC) is an important and rate-limiting step in…”
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Critical role of gap junction coupled KATP channel activity for regulated insulin secretion by Rocheleau, Jonathan V, Remedi, Maria S, Granada, Butch, Head, W Steven, Koster, Joseph C, Nichols, Colin G, Piston, David W

“…Pancreatic beta-cells secrete insulin in response to closure of ATP-sensitive K+ (KATP) channels, which causes membrane depolarization and a concomitant rise…”
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1354-P: Alternate-Day Intermittent Fasting Improves Diabetes and Protects Beta-Cell Function in Polygenic Mouse Models of T2DM by PATEL, SUMIT, YAN, ZIHAN, REMEDI, MARIA S.

“…Type 2 diabetes (T2DM) , caused by the interaction of multiple genes and environmental factors, is characterized by hyperglycemia, insulin secretion deficiency…”
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Complex consequences of Cantu syndrome SUR2 variant R1154Q in genetically modified mice by Zhang, Haixia, Hanson, Alex, de Almeida, Tobias Scherf, Emfinger, Christopher, McClenaghan, Conor, Harter, Theresa, Yan, Zihan, Cooper, Paige E, Brown, G Schuyler, Arakel, Eric C, Mecham, Robert P, Kovacs, Atilla, Halabi, Carmen M, Schwappach, Blanche, Remedi, Maria S, Nichols, Colin G

“…Cantu syndrome (CS) is caused by gain-of-function (GOF) mutations in pore-forming (Kir6.1, KCNJ8) and accessory (SUR2, ABCC9) ATP-sensitive potassium (KATP)…”
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Beta‐cell excitability and excitability‐driven diabetes in adult Zebrafish islets by Emfinger, Christopher H., Lőrincz, Réka, Wang, Yixi, York, Nathaniel W., Singareddy, Soma S., Ikle, Jennifer M., Tryon, Robert C., McClenaghan, Conor, Shyr, Zeenat A., Huang, Yan, Reissaus, Christopher A., Meyer, Dirk, Piston, David W., Hyrc, Krzysztof, Remedi, Maria S., Nichols, Colin G.

“…Islet β‐cell membrane excitability is a well‐established regulator of mammalian insulin secretion, and defects in β‐cell excitability are linked to multiple…”
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Glucokinase Inhibition: A Novel Treatment for Diabetes? by Remedi, Maria S, Nichols, Colin G

“…Chronic hyperglycemia increases pancreatic β-cell metabolic activity, contributing to glucotoxicity-induced β-cell failure and loss of functional β-cell mass,…”
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