Search

Your search keyword '"WHITE, MORRIS F"' showing total 818 results
Start Over Author "WHITE, MORRIS F"
818 results on '"WHITE, MORRIS F"'

1. Impairment of insulin-stimulated glucose utilization is associated with burn-induced insulin resistance in mouse muscle by hyperinsulinemic-isoglycemic clamp

Author

Yamagiwa, Takeshi, Yu, Yong-Ming, Inoue, Yoshitaka, Belov, Vasily V., Papisov, Mikhail I., Inokuchi, Sadaki, Kaneki, Masao, White, Morris F., Fischman, Alan J., and Tompkins, Ronald G.

Subjects
Quantitative Biology - Tissues and Organs
Abstract

Burn-induced insulin resistance is associated with increased morbidity and mortality; however, the impact of burn injury on tissue-specific insulin sensitivity and its molecular mechanisms with consideration of insulin state remains unknown in rodent models. This study was designed to characterize a burn mouse model with tissue-specific insulin resistance under insulin clamp conditions. C57BL6/J mice were subjected to 30% full-thickness burn injury and underwent the combination of hyperinsulinemic isoglycemicclamp (HIC) and positron emission tomography (PET). Hepatic glucose production (HGP) and peripheral glucose disappearance rate (Rd) were measured at different time points up to 7 days post injury. Burned mice showed a significant fasting hypoglycemia and hypoinsulinemia (P < 0.01) on post-burn day (PBD) 3 and 7 along with significantly higher energy expenditure (P < 0.01). HICon PBD 3 demonstrated that burn injury induced systemic insulin resistance, resulting from a significant decrease in insulin-stimulated Rd (33.0 +/- 10.2 vs 68.3 +/- 5.9 mg/kg/min; P < 0.05). In contrast, HGP of burned and sham mice was comparable both in the basal and clamp period. PET on PBD 3 showed a lower insulin-stimulated 18F-labeled 2-fluoro-2-deoxy-D-glucose uptake in the quadriceps of burned mice compared with sham-burned mice. Gastrocnemius muscle harvested from burned mice on PBD 3 showed decreased insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 to 34.7% of that in sham-burn mice by immunoblotting analysis (P < 0.05). These findings suggest that impaired insulin-stimulated Rd in skeletal muscle, not elevated HGP, plays a role in the development of burn-induced insulin resistance in a mouse model.

Published
2020

2. Insulin receptor substrates differentially exacerbate insulin-mediated left ventricular remodeling

Author

Riehle, Christian, Weatherford, Eric T, Wende, Adam R, Jaishy, Bharat P, Seei, Alec W, McCarty, Nicholas S, Rech, Monika, Shi, Qian, Reddy, Gopireddy R, Kutschke, William J, Oliveira, Karen, Pires, Karla Maria, Anderson, Joshua C, Diakos, Nikolaos A, Weiss, Robert M, White, Morris F, Drakos, Stavros G, Xiang, Yang K, and Abel, E Dale

Subjects
Genetics, Heart Disease, Cardiovascular, Aetiology, 2.1 Biological and endogenous factors, Animals, Cardiomegaly, Humans, Hyperinsulinism, Insulin, Insulin Receptor Substrate Proteins, Insulin Resistance, Mice, Mice, Knockout, Proto-Oncogene Proteins c-akt, Ventricular Remodeling, Cardiology, Heart failure, Insulin signaling
Abstract

Pressure overload (PO) cardiac hypertrophy and heart failure are associated with generalized insulin resistance and hyperinsulinemia, which may exacerbate left ventricular (LV) remodeling. While PO activates insulin receptor tyrosine kinase activity that is transduced by insulin receptor substrate 1 (IRS1), the present study tested the hypothesis that IRS1 and IRS2 have divergent effects on PO-induced LV remodeling. We therefore subjected mice with cardiomyocyte-restricted deficiency of IRS1 (CIRS1KO) or IRS2 (CIRS2KO) to PO induced by transverse aortic constriction (TAC). In WT mice, TAC-induced LV hypertrophy was associated with hyperactivation of IRS1 and Akt1, but not IRS2 and Akt2. CIRS1KO hearts were resistant to cardiac hypertrophy and heart failure in concert with attenuated Akt1 activation. In contrast, CIRS2KO hearts following TAC developed more severe LV dysfunction than WT controls, and this was prevented by haploinsufficiency of Akt1. Failing human hearts exhibited isoform-specific IRS1 and Akt1 activation, while IRS2 and Akt2 activation were unchanged. Kinomic profiling identified IRS1 as a potential regulator of cardioprotective protein kinase G-mediated signaling. In addition, gene expression profiling revealed that IRS1 signaling may promote a proinflammatory response following PO. Together, these data identify IRS1 and Akt1 as critical signaling nodes that mediate LV remodeling in both mice and humans.

Published
2020

7. Elevated circulating follistatin associates with an increased risk of type 2 diabetes

Author

Wu, Chuanyan, Borné, Yan, Gao, Rui, López Rodriguez, Maykel, Roell, William C., Wilson, Jonathan M., Regmi, Ajit, Luan, Cheng, Aly, Dina Mansour, Peter, Andreas, Machann, Jürgen, Staiger, Harald, Fritsche, Andreas, Birkenfeld, Andreas L., Tao, Rongya, Wagner, Robert, Canouil, Mickaël, Hong, Mun-Gwan, Schwenk, Jochen M., Ahlqvist, Emma, Kaikkonen, Minna U., Nilsson, Peter, Shore, Angela C., Khan, Faisel, Natali, Andrea, Melander, Olle, Orho-Melander, Marju, Nilsson, Jan, Häring, Hans-Ulrich, Renström, Erik, Wollheim, Claes B., Engström, Gunnar, Weng, Jianping, Pearson, Ewan R., Franks, Paul W., White, Morris F., Duffin, Kevin L., Vaag, Allan Arthur, Laakso, Markku, Stefan, Norbert, Groop, Leif, and De Marinis, Yang

Published
2021
Full Text
View/download PDF

10. Insulin receptor substrate signaling suppresses neonatal autophagy in the heart

Author

Riehle, Christian, Wende, Adam R, Sena, Sandra, Pires, Karla Maria, Pereira, Renata Oliveira, Zhu, Yi, Bugger, Heiko, Frank, Deborah, Bevins, Jack, Chen, Dong, Perry, Cynthia N, Dong, Xiaocheng C, Valdez, Steven, Rech, Monika, Sheng, Xiaoming, Weimer, Bart C, Gottlieb, Roberta A, White, Morris F, and Abel, E Dale

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Heart Disease, Prevention, Cardiovascular, Genetics, Nutrition, Pediatric, Good Health and Well Being, Amino Acids, Animals, Apoptosis, Apoptosis Regulatory Proteins, Autophagy, Beclin-1, Cardiomyopathy, Dilated, Fetal Heart, Heart, Heart Failure, Insulin, Insulin Receptor Substrate Proteins, Insulin-Like Growth Factor I, Mice, Mitochondria, Heart, Myocytes, Cardiac, Oxidative Phosphorylation, Phosphorylation, Protein Processing, Post-Translational, Receptor, IGF Type 1, Signal Transduction, TOR Serine-Threonine Kinases, Medical and Health Sciences, Immunology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

The induction of autophagy in the mammalian heart during the perinatal period is an essential adaptation required to survive early neonatal starvation; however, the mechanisms that mediate autophagy suppression once feeding is established are not known. Insulin signaling in the heart is transduced via insulin and IGF-1 receptors (IGF-1Rs). We disrupted insulin and IGF-1R signaling by generating mice with combined cardiomyocyte-specific deletion of Irs1 and Irs2. Here we show that loss of IRS signaling prevented the physiological suppression of autophagy that normally parallels the postnatal increase in circulating insulin. This resulted in unrestrained autophagy in cardiomyocytes, which contributed to myocyte loss, heart failure, and premature death. This process was ameliorated either by activation of mTOR with aa supplementation or by genetic suppression of autophagic activation. Loss of IRS1 and IRS2 signaling also increased apoptosis and precipitated mitochondrial dysfunction, which were not reduced when autophagic flux was normalized. Together, these data indicate that in addition to prosurvival signaling, insulin action in early life mediates the physiological postnatal suppression of autophagy, thereby linking nutrient sensing to postnatal cardiac development.

Published
2013

11. Pulsatile Portal Vein Insulin Delivery Enhances Hepatic Insulin Action and Signaling

Author

Matveyenko, Aleksey V, Liuwantara, David, Gurlo, Tatyana, Kirakossian, David, Man, Chiara Dalla, Cobelli, Claudio, White, Morris F, Copps, Kyle D, Volpi, Elena, Fujita, Satoshi, and Butler, Peter C

Subjects
Biomedical and Clinical Sciences, Diabetes, Digestive Diseases, Liver Disease, Metabolic and endocrine, Animals, Blood Glucose, Diabetes Mellitus, Experimental, Diabetes Mellitus, Type 2, Dogs, Forkhead Transcription Factors, Glucokinase, Insulin, Insulin Receptor Substrate Proteins, Insulin Resistance, Insulin Secretion, Liver, Male, Nerve Tissue Proteins, Portal Vein, Proto-Oncogene Proteins c-akt, Rats, Rats, Sprague-Dawley, Signal Transduction, Medical and Health Sciences, Endocrinology & Metabolism, Biomedical and clinical sciences
Abstract

Insulin is secreted as discrete insulin secretory bursts at ~5-min intervals into the hepatic portal vein, these pulses being attenuated early in the development of type 1 and type 2 diabetes mellitus (T2DM). Intraportal insulin infusions (pulsatile, constant, or reproducing that in T2DM) indicated that the pattern of pulsatile insulin secretion delivered via the portal vein is important for hepatic insulin action and, therefore, presumably for hepatic insulin signaling. To test this, we examined hepatic insulin signaling in rat livers exposed to the same three patterns of portal vein insulin delivery by use of sequential liver biopsies in anesthetized rats. Intraportal delivery of insulin in a constant versus pulsatile pattern led to delayed and impaired activation of hepatic insulin receptor substrate (IRS)-1 and IRS-2 signaling, impaired activation of downstream insulin signaling effector molecules AKT and Foxo1, and decreased expression of glucokinase (Gck). We further established that hepatic Gck expression is decreased in the HIP rat model of T2DM, a defect that correlated with a progressive defect of pulsatile insulin secretion. We conclude that the physiological pulsatile pattern of insulin delivery is important in hepatic insulin signaling and glycemic control. Hepatic insulin resistance in diabetes is likely in part due to impaired pulsatile insulin secretion.

Published
2012

16. Lower Hepatic Fat is Associated with Improved Insulin Secretion in a High-Risk Prediabetes Subphenotype During Lifestyle Intervention

Author

Wagner, Robert, Heni, Martin, Kantartzis, Konstantinos, Sandforth, Arvid, Machann, Jürgen, Schick, Fritz, Peter, Andreas, Fritsche, Louise, Szendrödi, Julia, Pfeiffer, Andreas Fh, Schürmann, Annette, Blüher, Matthias, Hauner, Hans, Seissler, Jochen, Bornstein, Stefan, Roden, Michael, Stefan, Norbert, Birkenfeld, Andreas L, White, Morris F, Häring, Hans-Ulrich, Fritsche, Andreas, Wagner, Robert, Heni, Martin, Kantartzis, Konstantinos, Sandforth, Arvid, Machann, Jürgen, Schick, Fritz, Peter, Andreas, Fritsche, Louise, Szendrödi, Julia, Pfeiffer, Andreas Fh, Schürmann, Annette, Blüher, Matthias, Hauner, Hans, Seissler, Jochen, Bornstein, Stefan, Roden, Michael, Stefan, Norbert, Birkenfeld, Andreas L, White, Morris F, Häring, Hans-Ulrich, and Fritsche, Andreas

Abstract

The objective of this work was to investigate whether impaired insulin secretion can be restored by lifestyle intervention in specific subphenotypes of prediabetes. One thousand forty-five participants from the Prediabetes Lifestyle Intervention Study (PLIS) were assigned to 6 recently established prediabetes clusters. Insulin secretion was assessed by a C-peptide-based index derived from oral glucose tolerance tests and modeled from three time-points during a 1-yr intervention. We also analyzed the change of glycemia, insulin sensitivity and liver fat. All pre-diabetes high-risk clusters (cluster 3, 5 and 6) had improved glycemic traits during lifestyle intervention, whereas insulin secretion only increased in clusters 3 and 5 (p<0.001); however, high liver fat in cluster 5 was associated with a failure to improve insulin secretion (pinteraction<0.001). Thus, interventions to reduce liver fat have the potential to improve insulin secretion in a defined subgroup of prediabetes. Prediabetes is a heterogenous condition comprising subphenotypes with different risks of diabetes and its complications (1). From its two key features, insulin resistance and impaired insulin secretion, insulin resistance can be clearly improved by lifestyle intervention (LI); however, it is not known, if LI can improve insulin secretion in specific subphenotypes of reduced insulin secretion (2). Recently, we described 6 clusters of prediabetic metabolism (1). Two of these clusters (cluster 3 and 5) have high risk of progression to diabetes. Another group (cluster 6) has an intermediate risk of diabetes as these persons are capable of compensating insulin resistance via hyperinsulinemia over years. In this study, we retrospectively stratified participants of a large multi-center study into these novel clusters of prediabetic metabolism (1) and investigated whether LI improved their insulin secretion and other glycemic traits.

Published
2023

22. BRD7 improves glucose homeostasis independent of IRS proteins.

Author

Yoo Kim, Lee, Junsik M., Youngah Han, Rongya Tao, White, Morris F., Renyan Liu, and Sang Won Park

Subjects
HOMEOSTASIS, METABOLIC regulation, BROMODOMAIN-containing proteins, INSULIN receptors, GLUCOSE
Abstract

Bromodomain-containing protein 7 (BRD7) has emerged as a player in the regulation of glucose homeostasis. Hepatic BRD7 levels are decreased in obese mice, and the reinstatement of hepatic BRD7 in obese mice has been shown to establish euglycemia and improve glucose homeostasis. Of note, the upregulation of hepatic BRD7 levels activates the AKT cascade in response to insulin without enhancing the sensitivity of the insulin receptor (InsR)–insulin receptor substrate (IRS) axis. In this report, we provide evidence for the existence of an alternative insulin signaling pathway that operates independently of IRS proteins and demonstrate the involvement of BRD7 in this pathway. To investigate the involvement of BRD7 as a downstream component of InsR, we utilized liver-specific InsR knockout mice. Additionally, we employed liver-specific IRS1/2 knockout mice to examine the requirement of IRS1/2 for the action of BRD7. Our investigation of glucose metabolism parameters and insulin signaling unveiled the significance of InsR activation in mediating BRD7’s effect on glucose homeostasis in the liver. Moreover, we identified an interaction between BRD7 and InsR. Notably, our findings indicate that IRS1/2 is not necessary for BRD7's regulation of glucose metabolism, particularly in the context of obesity. The upregulation of hepatic BRD7 significantly reduces blood glucose levels and restores glucose homeostasis in high-fat diet-challenged liver-specific IRS1/2 knockout mice. These findings highlight the presence of an alternative insulin signaling pathway that operates independently of IRS1/2 and offer novel insights into the mechanisms of a previously unknown insulin signaling in obesity. [ABSTRACT FROM AUTHOR]

Published
2023
Full Text
View/download PDF

23. Lower hepatic fat is associated with improved insulin secretion in a high-risk prediabetes subphenotype during lifestyle intervention

Author

Wagner, Robert, primary, Heni, Martin, primary, Kantartzis, Konstantinos, primary, Sandforth, Arvid, primary, Machann, Jurgen, primary, Schick, Fritz, primary, Peter, Andreas, primary, Fritsche, Louise, primary, Szendrodi, Julia, primary, Pfeiffer, Andreas FH, primary, Schurmann, Annette, primary, Bluher, Matthias, primary, Hauner, Hans, primary, Seissler, Johchen, primary, Bornstein, Stefan, primary, Roden, Michael, primary, Stefan, Norbert, primary, Birkenfeld, Andreas L, primary, White, Morris F., primary, Haring, Hans-Ulrich, primary, and Fritsche, Andreas, primary

Published
2022
Full Text
View/download PDF

25. Downregulation of hepatic ceruloplasmin ameliorates NAFLD via SCO1-AMPK-LKB1 complex

Author

Xie, Liping, primary, Yuan, Yanmei, additional, Xu, Simiao, additional, Lu, Sijia, additional, Gu, Jinyang, additional, Wang, Yanping, additional, Wang, Yibing, additional, Zhang, Xianjing, additional, Chen, Suzhen, additional, Li, Jian, additional, Lu, Junxi, additional, Sun, Honglin, additional, Hu, Ruixiang, additional, Piao, Hailong, additional, Wang, Wen, additional, Wang, Cunchuan, additional, Wang, Jing, additional, Li, Na, additional, White, Morris F., additional, Han, Liu, additional, Jia, Weiping, additional, Miao, Ji, additional, and Liu, Junli, additional

Published
2022
Full Text
View/download PDF

32. Regulation of Protein Synthesis by Insulin Through IRS-1

Author

Mendez, Raul, Welsh, Gavin, Kleijn, Miranda, Myers, Martin G., White, Morris F., Proud, Christopher G., Rhoads, Robert E., Müller, W. E. G., editor, Jeanteur, Ph., editor, Kostovic, I., editor, Kuchino, Y., editor, Macieira-Coelho, A., editor, and Rhoads, Robert E., editor

Published
2001
Full Text
View/download PDF

34. The P300 acetyltransferase inhibitor C646 promotes membrane translocation of insulin receptor protein substrate and interaction with the insulin receptor

Author

Peng, Jinghua, primary, Ramatchandirin, Balamurugan, additional, Wang, Yu, additional, Pearah, Alexia, additional, Namachivayam, Kopperuncholan, additional, Wolf, Risa M., additional, Steele, Kimberley, additional, MohanKumar, Krishnan, additional, Yu, Liqing, additional, Guo, Shaodong, additional, White, Morris F., additional, Maheshwari, Akhil, additional, and He, Ling, additional

Published
2022
Full Text
View/download PDF

35. Contributors

Author

Aiello, Lloyd Paul, primary, Alatzoglou, Kyriaki S., additional, Alexander, Erik K., additional, Allan, Carolyn A., additional, Allolio, Bruno, additional, Amino, Nobuyuki, additional, Anawalt, Bradley D., additional, Angelos, Peter, additional, Arboleda, Valerie A., additional, Auchus, Richard J., additional, Axelrod, Lloyd, additional, Bahn, Rebecca S., additional, Baker, MD, PhD, FRACP, H.W. Gordon, additional, Barak, Shlomi, additional, Barnes, Randall B., additional, Barthel, Andreas, additional, Bastepe, Murat, additional, Beardsley, Emma K., additional, Beck-Peccoz, Paolo, additional, Bell, Graeme I., additional, Bi, Wenya Linda, additional, Bilezikian, John P., additional, Blum, Manfred, additional, Bonnema, Steen J., additional, Bornstein, Stefan R., additional, Bouillon, Roger, additional, Boulton, Andrew J.M., additional, Braunstein, Glenn D., additional, Bringhurst, F. Richard, additional, Broekmans, Frank J., additional, Bronstein, Marcello D., additional, Brown, Edward M., additional, Brown, Wendy A., additional, Bulun, Serdar E., additional, Burch, Henry B., additional, Burger, Henry G., additional, Burney, Richard O., additional, Burt, Morton G., additional, Cagliero, Enrico, additional, Callender, Glenda G., additional, Avancini Caramori, Maria Luiza, additional, Carey, Robert M., additional, Carling, Tobias, additional, Cavagnini, Francesco, additional, Cavallerano, Jerry D., additional, Challet, Etienne, additional, Chan, Shu Jin, additional, Chang, R. Jeffrey, additional, Chapurlat, Roland D., additional, Chatterjee, V. Krishna, additional, Chiofalo, Francesco, additional, Chiovato, Luca, additional, Cho, Kyung J., additional, Christison-Lagay, Emily, additional, Christophe, Daniel, additional, Chrousos, George P., additional, Cidlowski, John A., additional, Clemmons, David R., additional, Considine, Robert V., additional, Conti, Marco, additional, Copinschi, Georges, additional, Copps, Kyle D., additional, Cowley, Michael A., additional, Cuttler, Leona, additional, Dattani, Mehul T., additional, Davis, Stephen N., additional, De Felice, Mario, additional, De Groot, Leslie J., additional, de Kretser, David M., additional, DeFronzo, Ralph A., additional, Delli, Ahmed J., additional, Demay, Marie B., additional, Dennedy, Michael C., additional, Di Lauro, Roberto, additional, Dineen, Rosemary, additional, Ding, Su Ann, additional, Dinneen, Sean F., additional, Drucker, Daniel J., additional, Dumont, Jacques E., additional, Dungan, Kathleen M., additional, Dunn, Ian F., additional, Econs, Michael J., additional, Ehrmann, David A., additional, Eisenhofer, Graeme, additional, Ergun-Longmire, Berrin, additional, Eugster, Erica A., additional, Farooqi, Sadaf I., additional, Fassnacht, Martin, additional, Fauser, Bart C.J.M., additional, Fenzi, Gianfranco, additional, Ferrannini, Ele, additional, Findlay, David M., additional, Finlayson, Courtney Anne, additional, Fisher, Delbert A., additional, Francis, Isaac R., additional, Freeman, Mason W., additional, Frohman, Lawrence A., additional, Frydenberg, Mark, additional, Fuller, Peter J., additional, Gaglia, Jason L., additional, Galizia, Gianluigi, additional, Gardella, Thomas J., additional, Garvey, Katharine C., additional, Genant, Harry K., additional, German, Michael S., additional, Gevers, Evelien F., additional, Giraldi, Francesca Pecori, additional, Giudice, Linda C., additional, Giustina, Andrea, additional, Glasier, Anna, additional, Glorieux, Francis H., additional, Goldfine, Allison B., additional, Gooren, Louis J., additional, Gordon, David F., additional, Gregerson, Karen A., additional, Grogan, Raymon H., additional, Gross, Milton D., additional, Grossman, Ashley B., additional, Gruber, Matthias, additional, Guimarães, Valeria C., additional, Gurnell, Mark, additional, Haddad, Nadine G., additional, Haisenleder, Daniel J., additional, Handelsman, David J., additional, Hanks, John B., additional, Hannon, Mark J., additional, Harno, Erika, additional, Hebrok, Matthias, additional, Hedger, Mark P., additional, Hegedüs, Laszlo, additional, Heindel, Jerrold J., additional, Hernandez, Arturo, additional, Herndon, Maria K., additional, Ho, Ken K.Y., additional, Horseman, Nelson D., additional, Hughes, Ieuan A., additional, Hupfeld, Christopher J., additional, Hussain, Hero K., additional, Iodice, Valeria, additional, James, Benjamin C., additional, Jameson, J. Larry, additional, Jones, Glenville, additional, Josso, Nathalie, additional, Jüppner, Harald, additional, Juszczak, Agata, additional, Kalish, Jeffrey, additional, Kaplan, Edwin L., additional, Karavitaki, Niki, additional, Karczewska-Kupczewska, Monika, additional, Khattab, Ahmed, additional, Klein, David C., additional, Klein, Ronald, additional, Kleinau, Gunnar, additional, Koontz, Michaela, additional, Kopchick, John J., additional, Kopp, Peter, additional, Kowalska, Irina, additional, Krane, Stephen M., additional, Krohn, Knut, additional, Kronenberg, Henry M., additional, Lamos, Elizabeth M., additional, Lania, Andrea, additional, Lau, Sue Lynn, additional, Laws, Edward R., additional, Lazarus, John H., additional, Learoyd, Diana L., additional, Lebovitz, Harold E., additional, Lenmark, Åke, additional, List, Edward O., additional, Loveland, Kate, additional, Low, David A., additional, Macchia, Paolo E., additional, Maclaren, Noel K., additional, Madeiros-Neto, Geraldo, additional, Maenhaut, Carine, additional, Maes, Christa, additional, Main, Katharina M., additional, Malchoff, Carl D., additional, Malchoff, Diana M., additional, Malik, Rayaz A., additional, Mandel, Susan J., additional, Mantzoros, Christos S., additional, Maratos-Flier, Eleftheria, additional, Marino, Michele, additional, Marshall, John C., additional, Martin, T. John, additional, Martin, Thomas F.J., additional, Mathias, Christopher J., additional, McGee, Elizabeth A., additional, McKenzie, Travis, additional, McLachlan, Robert I., additional, Meier, Juris J., additional, Melmed, Shlomo, additional, Metzger, Boyd E., additional, Meyer-Bahlburg, Heino F.L., additional, Millar, Robert P., additional, Miller, Walter L., additional, Misra, Madhusmita, additional, Molitch, Mark E., additional, Moravek, Molly B., additional, Morris, Damian G., additional, Nagar, Sapna, additional, Nakamoto, Jon, additional, New, Maria I., additional, Nieman, Lynnette K., additional, Nilson, John H., additional, Ntali, Georgia, additional, O’Bryan, Moira, additional, O’Rahilly, Stephen, additional, Öberg, Kjell, additional, Olefsky, Jerrold M., additional, Olson, Matthew T., additional, Pacak, Karel, additional, Pacini, Furio, additional, Padia, Shetal H., additional, Paschke, Ralf, additional, Pasquel, Francisco J., additional, Perry, Katherine Wesseling, additional, Persani, Luca, additional, Philipson, Louis H., additional, Pina, Christian, additional, Pomposelli, Frank B., additional, Potts, John T., additional, Quigley, Charmian A., additional, Quinkler, Marcus O., additional, Quirk, Christine Campion, additional, Rajpert-De Meyts, Ewa, additional, Ravussin, Eric, additional, Ray, David W., additional, Refetoff, Samuel, additional, Retnakaran, Ravi, additional, Rey, Rodolfo A., additional, Rhodes, Christopher J., additional, Ridgway, E. Chester, additional, Risbridger, Gail P., additional, Rizza, Robert A., additional, Robinson, Bruce G., additional, Roger, Pierre P., additional, Rosenfeld, Michael G., additional, Rosenfield, Robert L., additional, Rossing, Peter, additional, Rubin, Robert T., additional, Rubio, Ileana G.S., additional, Ruderman, Neil B., additional, Russo, Jose, additional, Russo, Irma H., additional, Salusky, Isidro B., additional, Santoro, Nanette, additional, Scully, Kathleen M., additional, Sexton, Patrick M., additional, Shulman, Gerald I., additional, Silva, Paolo S., additional, Silverberg, Shonni J., additional, Singer, Frederick R., additional, Skakkebaek, Niels E., additional, Skaznik-Wikiel, Malgorzata E., additional, Skowronska-Krawczyk, Dorota, additional, Smith, Carolyn L., additional, Smith, Philip W., additional, Smith, Roger, additional, Smith, Steven R., additional, Snyder, Peter J., additional, St. Germain, Donald L., additional, St-Arnaud, René, additional, Steiner, Donald F., additional, Stewart, Paul M., additional, Strączkowski, Marek, additional, Strauss, Jerome F., additional, Styne, Dennis M., additional, Swan, Karena L., additional, Swerdloff, Ronald S., additional, Tacon, Lyndal J., additional, Tello, Javier A., additional, Thakker, Rajesh V., additional, Thompson, Christopher J., additional, Timmers, Henri J.L.M., additional, Toppari, Jorma, additional, Traub, Michael L., additional, Tsoukas, Michael A., additional, Udelsman, Robert, additional, Umpierrez, Guillermo E., additional, Van den Berghe, Greet, additional, Vassart, Gilbert, additional, Vernon, Ashley H., additional, Vilain, Eric, additional, Visser, Theo J., additional, Vitti, Paolo, additional, Walford, Geoffrey A., additional, Wang, Christina, additional, Weetman, Anthony P., additional, Weigel, Nancy L., additional, Weir, Gordon C., additional, Weiss, Roy E., additional, White, Anne, additional, White, Kenneth E., additional, White, Morris F., additional, Whyte, Michael P., additional, Wiersinga, Wilmar M., additional, Willenberg, Holger S., additional, Wolfsdorf, Joseph I., additional, Wondisford, Fredric E., additional, Wong, Ka Kit, additional, Wysolmerski, John J., additional, Yau, Mabel, additional, Young, Morag J., additional, Younk, Lisa M., additional, Yu, Run, additional, Yuen, Tony, additional, Zeiger, Martha A., additional, Zinman, Bernard, additional, and Zoeller, R. Thomas, additional

Published
2016
Full Text
View/download PDF

41. TAZ inhibits glucocorticoid receptor and coordinates hepatic glucose homeostasis in normal physiological states

Author

Xu, Simiao, primary, Liu, Yangyang, primary, Hu, Ruixiang, primary, Wang, Min, additional, Stöhr, Oliver, additional, Xiong, Yibo, additional, Chen, Liang, additional, Kang, Hong, additional, Zheng, Lingyun, additional, Cai, Songjie, additional, He, Li, additional, Wang, Cunchuan, additional, Copps, Kyle D, additional, White, Morris F, additional, and Miao, Ji, additional

Published
2021
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results