12 results on '"Wright, Lauren E"'
Search Results
2. Leveraging Electronic Health Records Data for Enhanced Colorectal Cancer Screening Efforts
- Author
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Baus, Adam, Wright, Lauren E., Kennedy-Rea, Stephenie, Conn, Mary E, Eason, Susan, Boatman, Dannell, Pollard, Cecil, Calkins, Andrea, and Gadde, Divya
- Published
- 2020
3. Erratum to “Muscle insulin sensitivity and glucose metabolism are controlled by the intrinsic muscle clock” [Mol Metab 3 (2014) 29–41]
- Author
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Dyar, Kenneth A, Ciciliot, Stefano, Wright, Lauren E, Biensø, Rasmus S, Tagliazucchi, Guidantonio Malagoli, Patel, Vishal R, Forcato, Mattia, Peña-Paz, Marcia I, Gudiksen, Anders, Solagna, Francesca, Albiero, Mattia, Moretti, Irene, Eckel-Mahan, Kristin L, Baldi, Pierre, Sassone-Corsi, Paolo, Rizzuto, Rosario, Bicciato, Silvio, Pilegaard, Henriette, Blaauw, Bert, and Schiaffino, Stefano
- Subjects
Biochemistry and Cell Biology ,Biological Sciences ,Physiology ,Biochemistry and cell biology - Abstract
[This corrects the article DOI: 10.1016/j.molmet.2013.10.005.].
- Published
- 2014
4. Muscle insulin sensitivity and glucose metabolism are controlled by the intrinsic muscle clock.
- Author
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Dyar, Kenneth A, Ciciliot, Stefano, Wright, Lauren E, Biensø, Rasmus S, Tagliazucchi, Guidantonio M, Patel, Vishal R, Forcato, Mattia, Paz, Marcia IP, Gudiksen, Anders, Solagna, Francesca, Albiero, Mattia, Moretti, Irene, Eckel-Mahan, Kristin L, Baldi, Pierre, Sassone-Corsi, Paolo, Rizzuto, Rosario, Bicciato, Silvio, Pilegaard, Henriette, Blaauw, Bert, and Schiaffino, Stefano
- Subjects
2-DG ,2-Deoxyglucose ,BSA ,bovine serum albumin ,Bmal1 ,Circadian rhythms ,GSEA ,Gene Set Enrichment Analysis ,Glucose metabolism ,Glucose uptake ,HK2 ,hexokinase 2 ,KHB ,Krebs–Henseleit buffer ,Muscle insulin resistance ,PDH ,pyruvate dehydrogenase ,PDK ,PDH kinase ,PDP ,PDH phosphatase ,SCN ,suprachiasmatic nucleus ,Skeletal muscle ,ZT ,Zeitgeber time ,imKO ,inducible muscle-specific Bmal1 knockout ,mKO ,muscle-specific Bmal1 knockout ,2-DG ,2-Deoxyglucose ,BSA ,bovine serum albumin ,GSEA ,Gene Set Enrichment Analysis ,HK2 ,hexokinase 2 ,KHB ,Krebs–Henseleit buffer ,PDH ,pyruvate dehydrogenase ,PDK ,PDH kinase ,PDP ,PDH phosphatase ,SCN ,suprachiasmatic nucleus ,ZT ,Zeitgeber time ,imKO ,inducible muscle-specific Bmal1 knockout ,mKO ,muscle-specific Bmal1 knockout ,Biochemistry and Cell Biology ,Physiology - Abstract
Circadian rhythms control metabolism and energy homeostasis, but the role of the skeletal muscle clock has never been explored. We generated conditional and inducible mouse lines with muscle-specific ablation of the core clock gene Bmal1. Skeletal muscles from these mice showed impaired insulin-stimulated glucose uptake with reduced protein levels of GLUT4, the insulin-dependent glucose transporter, and TBC1D1, a Rab-GTPase involved in GLUT4 translocation. Pyruvate dehydrogenase (PDH) activity was also reduced due to altered expression of circadian genes Pdk4 and Pdp1, coding for PDH kinase and phosphatase, respectively. PDH inhibition leads to reduced glucose oxidation and diversion of glycolytic intermediates to alternative metabolic pathways, as revealed by metabolome analysis. The impaired glucose metabolism induced by muscle-specific Bmal1 knockout suggests that a major physiological role of the muscle clock is to prepare for the transition from the rest/fasting phase to the active/feeding phase, when glucose becomes the predominant fuel for skeletal muscle.
- Published
- 2014
5. SIRT3 overexpression in rat muscle does not ameliorate peripheral insulin resistance
- Author
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Osborne, Brenna, Wright, Lauren E., Brandon, Amanda E., Stuart, Ella, Small, Lewin, Hoeks, Joris, Schrauwen, Patrick, Sinclair, David A, Montgomery, Magdalene K, Cooney, Gregory J, Turner, Nigel, Osborne, Brenna, Wright, Lauren E., Brandon, Amanda E., Stuart, Ella, Small, Lewin, Hoeks, Joris, Schrauwen, Patrick, Sinclair, David A, Montgomery, Magdalene K, Cooney, Gregory J, and Turner, Nigel
- Abstract
Reduced expression of the NAD+-dependent deacetylase, SIRT3, has been associated with insulin resistance and metabolic dysfunction in humans and rodents. In this study, we investigated whether specific overexpression of SIRT3 in vivo in skeletal muscle could prevent high-fat diet (HFD)-induced muscle insulin resistance. To address this, we used a muscle-specific adeno-associated virus (AAV) to overexpress SIRT3 in rat tibialis and extensor digitorum longus (EDL) muscles. Mitochondrial substrate oxidation, substrate switching and oxidative enzyme activity were assessed in skeletal muscles with and without SIRT3 overexpression. Muscle-specific insulin action was also assessed by hyperinsulinaemic–euglycaemic clamps in rats that underwent a 4-week HFD-feeding protocol. Ex vivo functional assays revealed elevated activity of selected SIRT3-target enzymes including hexokinase, isocitrate dehydrogenase and pyruvate dehydrogenase that was associated with an increase in the ability to switch between fatty acid- and glucose-derived substrates in muscles with SIRT3 overexpression. However, during the clamp, muscles from rats fed an HFD with increased SIRT3 expression displayed equally impaired glucose uptake and insulin-stimulated glycogen synthesis as the contralateral control muscle. Intramuscular triglyceride content was similarly increased in the muscle of high-fat-fed rats, regardless of SIRT3 status. Thus, despite SIRT3 knockout (KO) mouse models indicating many beneficial metabolic roles for SIRT3, our findings show that muscle-specific overexpression of SIRT3 has only minor effects on the acute development of skeletal muscle insulin resistance in high-fat-fed rats., Reduced expression of the NAD+-dependent deacetylase, SIRT3, has been associated with insulin resistance and metabolic dysfunction in humans and rodents. In this study we investigated whether specific overexpression of SIRT3 in vivo in skeletal muscle could prevent HFD-induced muscle insulin resistance. To address this we used a muscle-specific adeno-associated virus (AAV) to overexpress SIRT3 in rat tibialis and EDL muscles. Mitochondrial substrate oxidation, substrate switching and oxidative enzyme activity were assessed in skeletal muscle with and without SIRT3 overexpression. Muscle-specific insulin action was also assessed by hyperinsulinaemic-euglycaemic clamps in rats that underwent a 4-week HFD-feeding protocol. Ex vivo functional assays revealed elevated activity of selected SIRT3-target enzymes including hexokinase, isocitrate dehydrogenase and pyruvate dehydrogenase that was associated with an increase in the ability to switch between fatty acid and glucose-derived substrates in muscle with SIRT3 overexpression. However, during the clamp, muscle from rats fed a HFD with increased SIRT3 expression displayed equally impaired glucose uptake and insulin-stimulated glycogen synthesis as the contralateral control muscle. Intramuscular triglyceride content was similarly increased in muscle of high fat fed rats, regardless of SIRT3 status. Thus, despite SIRT3 KO mouse models indicating many beneficial metabolic roles for SIRT3, our findings show that muscle-specific overexpression of SIRT3 has only minor effects on the acute development of skeletal muscle insulin resistance in high fat fed rats.
- Published
- 2023
6. Case Study of a Comprehensive Team-Based Approach to Increase Colorectal Cancer Screening
- Author
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Wright, Lauren E., Baus, Adam, Calkins, Andrea, Hartman-Adams, Holly, Conn, Mary E., Eason, Susan, and Kennedy-Rea, Stephenie
- Subjects
FOS: Medical and health sciences - Abstract
Introduction: Colorectal cancer is the second leading cause of cancer deaths among men and women in West Virginia. In addition, 51% of all colorectal cancers diagnosed in West Virginia from 2012 to 2016 were detected at either regional (31%) or distant (20%) stages indicating a need for improved early detection. Methods: West Virginia University Cheat Lake Physicians participated in the West Virginia Program to Increase Colorectal Cancer Screening, a program of Cancer Prevention and Control at the WVU Cancer Institute. As a result, Cheat Lake Physicians assembled a team of health care professionals to implement evidence-based interventions and system changes including provider assessment and feedback, patient reminders, accurate data capture, and tracking of CRC screening tests. Results: These efforts resulted in a 15.8% increase in colorectal cancer screening rates within one year of implementation. Additionally, the clinic achieved a 66% return rate for Fecal Immunochemical Test kits, an inexpensive, stool-based colorectal cancer screening test. Implications: The utilization of a team-based approach to patient care yields positive results that can be carried over to other cancer and disease prevention efforts in primary care clinics., Copyright © 2021 Lauren E. Wright, Adam Baus, Andrea Calkins, Holly Hartman-Adams, Mary E. Conn, Susan Eason, and Stephenie Kennedy-Rea
- Published
- 2022
7. Enhancement of Muscle Mitochondrial Oxidative Capacity and Alterations in Insulin Action Are Lipid Species Dependent: Potent Tissue-Specific Effects of Medium-Chain Fatty Acids
- Author
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Turner, Nigel, Hariharan, Krit, TidAng, Jennifer, Frangioudakis, Georgia, Beale, Susan M., Wright, Lauren E., Zeng, Xiao Yi, Leslie, Simon J., Li, Jing-Ya, Kraegen, Edward W., Cooney, Gregory J., and Ye, Ji-Ming
- Published
- 2009
8. Increased mitochondrial calcium uniporter in adipocytes underlies mitochondrial alterations associated with insulin resistance
- Author
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Wright, Lauren E., primary, Vecellio Reane, Denis, additional, Milan, Gabriella, additional, Terrin, Anna, additional, Di Bello, Giorgia, additional, Belligoli, Anna, additional, Sanna, Marta, additional, Foletto, Mirto, additional, Favaretto, Francesca, additional, Raffaello, Anna, additional, Mammucari, Cristina, additional, Nitti, Donato, additional, Vettor, Roberto, additional, and Rizzuto, Rosario, additional
- Published
- 2017
- Full Text
- View/download PDF
9. Overexpression of SIRT1 in Rat Skeletal Muscle Does Not Alter Glucose Induced Insulin Resistance
- Author
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Brandon, Amanda E., primary, Tid-Ang, Jennifer, additional, Wright, Lauren E., additional, Stuart, Ella, additional, Suryana, Eurwin, additional, Bentley, Nicholas, additional, Turner, Nigel, additional, Cooney, Gregory J., additional, Ruderman, Neil B., additional, and Kraegen, Edward W., additional
- Published
- 2015
- Full Text
- View/download PDF
10. Muscle insulin sensitivity and glucose metabolism are controlled by the intrinsic muscle clock
- Author
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Dyar, Kenneth A., Ciciliot, Stefano, Wright, Lauren E., Biensø, Rasmus Sjørup, Tagliazucchi, Guidantonio M., Patel, Vishal R., Forcato, Mattia, Paz, Marcia I.P., Gudiksen, Anders, Solagna, Francesca, Albiero, Mattia, Moretti, Irene, Eckel-Mahan, Kristin L., Baldi, Pierre, Sassone-Corsi, Paolo, Rizzuto, Rosario, Bicciato, Silvio, Pilegaard, Henriette, Blaauw, Bert, Schiaffino, Stefano, Dyar, Kenneth A., Ciciliot, Stefano, Wright, Lauren E., Biensø, Rasmus Sjørup, Tagliazucchi, Guidantonio M., Patel, Vishal R., Forcato, Mattia, Paz, Marcia I.P., Gudiksen, Anders, Solagna, Francesca, Albiero, Mattia, Moretti, Irene, Eckel-Mahan, Kristin L., Baldi, Pierre, Sassone-Corsi, Paolo, Rizzuto, Rosario, Bicciato, Silvio, Pilegaard, Henriette, Blaauw, Bert, and Schiaffino, Stefano
- Abstract
Circadian rhythms control metabolism and energy homeostasis, but the role of the skeletal muscle clock has never been explored. We generated conditional and inducible mouse lines with muscle-specific ablation of the core clock gene Bmal1. Skeletal muscles from these mice showed impaired insulin-stimulated glucose uptake with reduced protein levels of GLUT4, the insulin-dependent glucose transporter, and TBC1D1, a Rab-GTPase involved in GLUT4 translocation. Pyruvate dehydrogenase (PDH) activity was also reduced due to altered expression of circadian genes Pdk4 and Pdp1, coding for PDH kinase and phosphatase, respectively. PDH inhibition leads to reduced glucose oxidation and diversion of glycolytic intermediates to alternative metabolic pathways, as revealed by metabolome analysis. The impaired glucose metabolism induced by muscle-specific Bmal1 knockout suggests that a major physiological role of the muscle clock is to prepare for the transition from the rest/fasting phase to the active/feeding phase, when glucose becomes the predominant fuel for skeletal muscle.
- Published
- 2014
11. Increased mitochondrial calcium uniporter in adipocytes underlies mitochondrial alterations associated with insulin resistance.
- Author
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Wright LE, Vecellio Reane D, Milan G, Terrin A, Di Bello G, Belligoli A, Sanna M, Foletto M, Favaretto F, Raffaello A, Mammucari C, Nitti D, Vettor R, and Rizzuto R
- Subjects
- 3T3-L1 Cells, Adult, Animals, Case-Control Studies, Diabetes Mellitus, Experimental genetics, Diabetes Mellitus, Experimental metabolism, Female, Humans, Intra-Abdominal Fat metabolism, Intra-Abdominal Fat pathology, Male, Mice, Mice, Inbred C57BL, Mice, Obese, Mice, Transgenic, Middle Aged, Mitochondria pathology, Obesity genetics, Obesity metabolism, Obesity pathology, Prediabetic State genetics, Prediabetic State metabolism, Prediabetic State pathology, Subcutaneous Fat metabolism, Subcutaneous Fat pathology, Adipocytes metabolism, Calcium Channels genetics, Calcium Channels metabolism, Insulin Resistance physiology, Mitochondria metabolism
- Abstract
Intracellular calcium influences an array of pathways and affects cellular processes. With the rapidly progressing research investigating the molecular identity and the physiological roles of the mitochondrial calcium uniporter (MCU) complex, we now have the tools to understand the functions of mitochondrial Ca
2+ in the regulation of pathophysiological processes. Herein, we describe the role of key MCU complex components in insulin resistance in mouse and human adipose tissue. Adipose tissue gene expression was analyzed from several models of obese and diabetic rodents and in 72 patients with obesity as well as in vitro insulin-resistant adipocytes. Genetic manipulation of MCU activity in 3T3-L1 adipocytes allowed the investigation of the role of mitochondrial calcium uptake. In insulin-resistant adipocytes, mitochondrial calcium uptake increased and several MCU components were upregulated. Similar results were observed in mouse and human visceral adipose tissue (VAT) during the progression of obesity and diabetes. Intriguingly, subcutaneous adipose tissue (SAT) was spared from overt MCU fluctuations. Furthermore, MCU expression returned to physiological levels in VAT of patients after weight loss by bariatric surgery. Genetic manipulation of mitochondrial calcium uptake in 3T3-L1 adipocytes demonstrated that changes in mitochondrial calcium concentration ([Ca2+ ]mt ) can affect mitochondrial metabolism, including oxidative enzyme activity, mitochondrial respiration, membrane potential, and reactive oxygen species formation. Finally, our data suggest a strong relationship between [Ca2+ ]mt and the release of IL-6 and TNFα in adipocytes. Altered mitochondrial calcium flux in fat cells may play a role in obesity and diabetes and may be associated with the differential metabolic profiles of VAT and SAT., (Copyright © 2017 the American Physiological Society.)- Published
- 2017
- Full Text
- View/download PDF
12. Muscle insulin sensitivity and glucose metabolism are controlled by the intrinsic muscle clock.
- Author
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Dyar KA, Ciciliot S, Wright LE, Biensø RS, Tagliazucchi GM, Patel VR, Forcato M, Paz MI, Gudiksen A, Solagna F, Albiero M, Moretti I, Eckel-Mahan KL, Baldi P, Sassone-Corsi P, Rizzuto R, Bicciato S, Pilegaard H, Blaauw B, and Schiaffino S
- Abstract
Circadian rhythms control metabolism and energy homeostasis, but the role of the skeletal muscle clock has never been explored. We generated conditional and inducible mouse lines with muscle-specific ablation of the core clock gene Bmal1. Skeletal muscles from these mice showed impaired insulin-stimulated glucose uptake with reduced protein levels of GLUT4, the insulin-dependent glucose transporter, and TBC1D1, a Rab-GTPase involved in GLUT4 translocation. Pyruvate dehydrogenase (PDH) activity was also reduced due to altered expression of circadian genes Pdk4 and Pdp1, coding for PDH kinase and phosphatase, respectively. PDH inhibition leads to reduced glucose oxidation and diversion of glycolytic intermediates to alternative metabolic pathways, as revealed by metabolome analysis. The impaired glucose metabolism induced by muscle-specific Bmal1 knockout suggests that a major physiological role of the muscle clock is to prepare for the transition from the rest/fasting phase to the active/feeding phase, when glucose becomes the predominant fuel for skeletal muscle.
- Published
- 2013
- Full Text
- View/download PDF
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