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1. Identification and characterization of human GDF15 knockouts

Author

Gurtan, Allan M., Khalid, Shareef, Koch, Christopher, Khan, Maleeha Zaman, Lamarche, Lindsey B., Splawski, Igor, Dolan, Elizabeth, Carrion, Ana M., Zessis, Richard, Clement, Matthew E., Chen, Zhiping, Lindsley, Loren D., Chiu, Yu-Hsin, Streeper, Ryan S., Denning, Daniel P., Goldfine, Allison B., Doyon, Brian, Abbasi, Ali, Harrow, Jennifer L., Tsunoyama, Kazuhisa, Asaumi, Makoto, Kou, Ikuyo, Shuldiner, Alan R., Rodriguez-Flores, Juan L., Rasheed, Asif, Jahanzaib, Muhammad, Mian, Muhammad Rehan, Liaqat, Muhammad Bilal, Raza, Syed Shahzaib, Sultana, Riffat, Jalal, Anjum, Saeed, Muhammad Hamid, Abbas, Shahid, Memon, Fazal Rehman, Ishaq, Mohammad, Dominy, John E., and Saleheen, Danish

Published
2024
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4. Immunogenicity assessment strategy for a chemically modified therapeutic protein in clinical development.

Author

Hagman, Charlotte, Chasseigne, Gaetan, Nelson, Robert, Anlauff, Florian, Kagan, Mark, Goldfine, Allison B., Terszowski, Grzegorz, and Jadhav, Maria

Subjects
GROWTH differentiation factors, THERAPEUTIC use of proteins, IMMUNE response, POLYETHYLENE glycol, HUMAN growth
Abstract

The clinical immunogenicity assessment for complex multidomain biological drugs is challenging due to multiple factors that must be taken into consideration. Here, we describe a strategy to overcome multiple bioanalytical challenges in order to assess anti-drug antibodies (ADA) for a novel and unique chemically modified protein therapeutic. A risk-centered approach was adopted to evaluate the immunogenic response to a modified version of human growth differentiation factor 15 (GDF15) connected to an albumin-binding fatty acid via a polyethylene glycol (PEG) linker. Key steps include monitoring anti-drug antibodies (ADAs), using a standard tiered approach of screening and confirmation. To deepen our understanding of ADA response, as a third tier of immunogenicity assessment, novel extensive characterization using a set of assays was developed, validated, and used routinely in clinical sample analysis. This characterization step included performance of titration, mapping of ADA response including anti-GDF15 and anti-PEG–fatty-acid antibody characterization, and assessment of the neutralizing anti-drug antibodies (NAbs) using cell-based assays for immunogenicity in parallel. The analytical methods were applied during two clinical trials involving both healthy volunteers and overweight or obese patients. We observed low incident rates for ADA and no ADAs against the PEG linker with fatty acid conjugation. In one of the clinical studies, we identified neutralizing ADAs. The proposed novel strategy of extensive characterization proved effective for monitoring the presence of ADAs and NAbs and can be used to support clinical development of a broad range of chemically modified proteins and multidomain biotherapeutics. [ABSTRACT FROM AUTHOR]

Published
2024
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5. Identification and characterization of human GDF15 knockouts

Author

Gurtan, Allan M, primary, Khalid, Shareef, additional, Koch, Christopher, additional, Khan, Maleeha Z, additional, Lamarche, Lindsey B, additional, Dolan, Elizabeth, additional, Carrion, Ana M, additional, Zessis, Richard, additional, Clement, Matthew E, additional, Chen, Zhiping, additional, Lindsley, Loren D, additional, Chiu, Yu-Hsin, additional, Streeper, Ryan S, additional, Denning, Daniel P, additional, Goldfine, Allison B, additional, Doyon, Brian, additional, Abbasi, Ali, additional, Harrow, Jennifer L, additional, Tsunoyama, Kazuhisa, additional, Asaumi, Makoto, additional, Kou, Ikuyo, additional, Shuldiner, Alan R, additional, Rodriguez-Flores, Juan L, additional, Rasheed, Asif, additional, Jahanzaib, Muhammad, additional, Mian, Muhammad Rehan, additional, Liaqat, Muhammad Bilal, additional, Raza, Syed Shahzaib, additional, Sultana, Riffat, additional, Jalal, Anjum, additional, Saeed, Muhammad Hamid, additional, Abbas, Shahid, additional, Memon, Fazal Rehman, additional, Ishaq, Muhammad, additional, Dominy, John E, additional, and Saleheen, Danish, additional

Published
2024
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9. Visceral Adiposity and the Risk of Metabolic Syndrome Across Body Mass Index The MESA Study

Author

Shah, Ravi V, Murthy, Venkatesh L, Abbasi, Siddique A, Blankstein, Ron, Kwong, Raymond Y, Goldfine, Allison B, Jerosch-Herold, Michael, Lima, João AC, Ding, Jingzhong, and Allison, Matthew A

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Aging, Prevention, Clinical Research, Heart Disease, Cardiovascular, Obesity, Biomedical Imaging, Nutrition, 4.1 Discovery and preclinical testing of markers and technologies, Detection, screening and diagnosis, Metabolic and endocrine, Cancer, Adiposity, Aged, Biomarkers, Blood Glucose, Blood Pressure, Body Mass Index, Chi-Square Distribution, Humans, Incidence, Intra-Abdominal Fat, Lipids, Male, Metabolic Syndrome, Middle Aged, Predictive Value of Tests, Prognosis, Proportional Hazards Models, Risk Assessment, Risk Factors, Tomography, X-Ray Computed, United States, cardiometabolic risk, metabolic syndrome, obesity, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences
Abstract

ObjectivesThis study sought to evaluate differential effects of visceral fat (VF) and subcutaneous fat and their effects on metabolic syndrome (MetS) risk across body mass index (BMI) categories.BackgroundThe regional distribution of adipose tissue is an emerging risk factor for cardiometabolic disease, although serial changes in fat distribution have not been extensively investigated. VF and its alterations over time may be a better marker for risk than BMI in normal weight and overweight or obese individuals.MethodsWe studied 1,511 individuals in the MESA (Multi-Ethnic Study of Atherosclerosis) with adiposity assessment by computed tomography (CT). A total of 253 participants without MetS at initial scan underwent repeat CT (median interval 3.3 years). We used discrete Cox regression with net reclassification to investigate whether baseline and changes in VF area are associated with MetS.ResultsHigher VF was associated with cardiometabolic risk and coronary artery calcification, regardless of BMI. After adjustment, VF was more strongly associated with incident MetS than subcutaneous fat regardless of weight, with a 28% greater MetS hazard per 100 cm(2)/m VF area and significant net reclassification (net reclassification index: 0.44, 95% confidence interval [CI]: 0.29 to 0.60) over clinical risk. In individuals with serial imaging, initial VF (hazard ratio: 1.24 per 100 cm(2)/m, 95% CI: 1.08 to 1.44 per 100 cm(2)/m, p = 0.003) and change in VF (hazard ratio: 1.05 per 5% change, 95% CI: 1.01 to 1.08 per 5% change, p = 0.02) were associated with MetS after adjustment. Changes in subcutaneous fat were not associated with incident MetS after adjustment for clinical risk and VF area.ConclusionsVF is modestly associated with BMI. However, across BMI, a single measure of and longitudinal change in VF predict MetS, even accounting for weight changes. Visceral adiposity is essential to assessing cardiometabolic risk, regardless of age, race, or BMI, and may serve as a marker and target of therapy in cardiometabolic disease.

Published
2014

12. The Foxo1-Inducible Transcriptional Repressor Zfp125 Causes Hepatic Steatosis and Hypercholesterolemia

Author

Fernandes, Gustavo W., Bocco, Barbara M.L.C., Fonseca, Tatiana L., McAninch, Elizabeth A., Jo, Sungro, Lartey, Lattoya J., O-Sullivan, InSug, Unterman, Terry G., Preite, Nailliw Z., Voigt, Robin M., Forsyth, Christopher B., Keshavarzian, Ali, Sinkó, Richárd, Goldfine, Allison B., Patti, Mary E., Ribeiro, Miriam O., Gereben, Balázs, and Bianco, Antonio C.

Published
2018
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19. SerpinB1 Promotes Pancreatic β Cell Proliferation

Author

El Ouaamari, Abdelfattah, Dirice, Ercument, Gedeon, Nicholas, Hu, Jiang, Zhou, Jian-Ying, Shirakawa, Jun, Hou, Lifei, Goodman, Jessica, Karampelias, Christos, Qiang, Guifeng, Boucher, Jeremie, Martinez, Rachael, Gritsenko, Marina A., De Jesus, Dario F., Kahraman, Sevim, Bhatt, Shweta, Smith, Richard D., Beer, Hans-Dietmar, Jungtrakoon, Prapaporn, Gong, Yanping, Goldfine, Allison B., Liew, Chong Wee, Doria, Alessandro, Andersson, Olov, Qian, Wei-Jun, Remold-O’Donnell, Eileen, and Kulkarni, Rohit N.

Published
2016
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24. Contributors

Author

Ahmann, Andrew J., Aiello, Lloyd Paul, Akamizu, Takashi, Aleksic, Sandra, Alexander, Erik K., Allen, Rebecca H., Anawalt, Bradley D., Anderson, Mark S., Apovian, Caroline M., Arbeláez, Ana María, Arosemena, Marilyn, Atkinson, Mark A., Auchus, Richard J., Babayev, Elnur, Barker, Jennifer M., Bartalena, Luigi, Bartke, Andrzej, Battelino, Tadej, Berga, Sarah L., Berli, Jens U., Bhadada, Sanjay K., Bhan, Arti, Bhasin, Shalender, Bidlingmaier, Martin, Bilezikian, John P., Binkley, Neil, Black, Dennis M., Boulton, Andrew JM, Brown, Todd T., Brownlee, Michael, Bulun, Serdar E., Bushinsky, David A., Casanueva, Felipe F., Chait, Alan, Chan, Yee-Ming, Christ-Crain, Mirjam, Cohen, Ronald, Dattani, Mehul T., Davis, Susan R., de Herder, Wouter W., de Paula, Francisco J.A., DiVall, Sara A., Dovc, Klemen, El-Khairi, Ranna, Feelders, Richard, Feldman, Eva L., Feldt-Rasmussen, Ulla, Ferrannini, Ele, Ferris, Heather A., Flück Pandey, Christa E., Galderisi, Alfonso, Ghigo, Ezio, Gillard, Pieter, Ginsberg, Henry N., Giustina, Andrea, Goldfine, Allison B., Goltzman, David, Gottlieb, Peter A., Gunst, Jan, Hafida, Samar, Hannema, Sabine E., Hayes, Frances J., Haymart, Megan R., Hickey, Martha, Hirschhorn, Joel, Ho, Ken K.Y., Hofland, Johannes, Hollenberg, Anthony, Huguenin, Annabelle, Jacobs, An, Jee, Youn Hee, Jonklaas, Jacqueline, Kahn, C. Ronald, Kaiser, Ursula, Karsenty, Gerard, Katugampola, Harshini, Kaunitz, Andrew M., Kopp, Peter A., Lamberts, Steven W.J., Lanfranco, Fabio, Lechan, Ronald M., Majithia, Amit R., Mannstadt, Michael, Mari, Andrea, Matsumoto, Alvin M., Matthieu, Chantal, Melmed, Shlomo, Miller, Paul D., Milman, Sofiya, Moeller, Lars C., Naylor, Rochelle N., Newey, Paul J., O’Neill, Brian T., Papadakis, Georgios E., Pattison, David A., Philipson, Louis H., Pitteloud, Nelly, Radovick, Sally, Rao, Ajay D., Rao, Sudhaker D., Rickels, Michael R., Riddle, Matthew C., Rosen, Clifford J., Rosen, Evan D., Rosenthal, Stephen M., Rossing, Peter, Rui, Liangyou, Salama, Mahmoud, Salguero, Maria V., Salvatore, Domenico, Silva, Paolo Sandico, Sattar, Naveed, Schoenmakers, Nadia, Sherr, Jennifer L., Sluss, Patrick M., Stanley, Takara, Strasburger, Christian J., Sun, Jennifer K., Takahashi, Yutaka, Tangpricha, Vin, Thakker, Rajesh V., Thompson, Christopher J., Van den Berghe, Greet, Verbalis, Joseph G., Walch, Abby, Walker, Marcella D., Waters, Thaddeus P., Wiersinga, Wilmar, Wirth, Lori J., Witztum, Joseph L., Woodruff, Teresa K., Young, William F., Jr., and Zeiger, Martha A.

Published
2025
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27. Therapeutic approaches targeting inflammation for diabetes and associated cardiovascular risk

Author

Goldfine, Allison B. and Shoelson, Steven E.

Subjects
Care and treatment, Analysis, Risk factors, Inflammation -- Analysis, Type 2 diabetes -- Risk factors -- Care and treatment, Cardiovascular diseases -- Risk factors -- Care and treatment
Abstract

Introduction The obesity epidemic foreshadowed subsequent increases in incident type 2 diabetes (T2D) and atherosclerotic cardiovascular disease (ASCVD), supporting a role for obesity to promote or accelerate pathophysiologic processes underlying [...], Obesity-related sub-acute chronic inflammation has been associated with incident type 2 diabetes and atherosclerotic cardiovascular disease. Inflammation is increasingly considered to be a pathologic mediator of these commonly co-occurring diseases. A growing number of preclinical and clinical studies support the inflammatory hypothesis, but clinical trials to confirm the therapeutic potential to target inflammation to treat or prevent cardiometabolic conditions are still ongoing. There are multiple inflammatory signaling pathways. Regulation is complex, with substantial crosstalk across these multiple pathways. The activity of select pathways may be differentially regulated in different tissues. Pharmacologic approaches to diabetes management may have direct or indirect antiinflammatory effects, the latter potentially attributable to an improved metabolic state. Conversely, some antiinflammatory approaches may affect glucose metabolism and cardiovascular health. To date, clinical trials suggest that targeting one portion of the inflammatory cascade may differentially affect dysglycemia and atherothrombosis. Understanding the underlying biological processes may contribute to the development of safe and effective therapies, although a single approach may not be sufficient for optimal management of both metabolic and athrothrombotic disease states.

Published
2017
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30. Diabetes primes neutrophils to undergo NETosis, which impairs wound healing

Author

Wong, Siu Ling, Demers, Melanie, Martinod, Kimberly, Gallant, Maureen, Wang, Yanming, Goldfine, Allison B., Kahn, C.Ronald, and Wagner, Denisa D.

Subjects
Physiological aspects, Complications and side effects, Genetic aspects, Research, Diabetes mellitus -- Health aspects -- Complications and side effects -- Genetic aspects -- Research, Wound healing -- Health aspects -- Physiological aspects -- Genetic aspects -- Research, Neutrophils -- Physiological aspects -- Genetic aspects -- Research
Abstract

NETs were originally recognized as a host defense mechanism in which neutrophils release their nuclear and granular contents to contain and kill pathogens (1). Bacterial endotoxins, such as lipopolysaccharides (LPS), [...], Wound healing is impaired in diabetes, resulting in significant morbidity and mortality. Neutrophils are the main leukocytes involved in the early phase of healing. As part of their anti-microbial defense, neutrophils form extracellular traps (NETs) by releasing decondensed chromatin lined with cytotoxic proteins (1). NETs, however, can also induce tissue damage. Here we show that neutrophils isolated from type 1 and type 2 diabetic humans and mice were primed to produce NETs (a process termed NETosis). Expression of peptidylarginine deiminase 4 (PAD4, encoded by Padi4 in mice), an enzyme important in chromatin decondensation, was elevated in neutrophils from individuals with diabetes. When subjected to excisional skin wounds, wild-type (WT) mice produced large quantities of NETs in wounds, but this was not observed in [Padi4.sup.-/-] mice. In diabetic mice, higher levels of citrullinated histone H3 (H3Cit, a NET marker) were found in their wounds than in normoglycemic mice and healing was delayed. Wound healing was accelerated in [Padi4.sup.-/-] mice as compared to WT mice, and it was not compromised by diabetes. DNase 1, which disrupts NETs, accelerated wound healing in diabetic and normoglycemic WT mice. Thus, NETs impair wound healing, particularly in diabetes, in which neutrophils are more susceptible to NETosis. Inhibiting NETosis or cleaving NETs may improve wound healing and reduce NET-driven chronic inflammation in diabetes.

Published
2015

34. Expression of the Splicing Factor Gene SFRS10 Is Reduced in Human Obesity and Contributes to Enhanced Lipogenesis

Author

Pihlajamäki, Jussi, Lerin, Carles, Itkonen, Paula, Boes, Tanner, Floss, Thomas, Schroeder, Joshua, Dearie, Farrell, Crunkhorn, Sarah, Burak, Furkan, Jimenez-Chillaron, Josep C., Kuulasmaa, Tiina, Miettinen, Pekka, Park, Peter J., Nasser, Imad, Zhao, Zhenwen, Zhang, Zhaiyi, Xu, Yan, Wurst, Wolfgang, Ren, Hongmei, Morris, Andrew J., Stamm, Stefan, Goldfine, Allison B., Laakso, Markku, and Patti, Mary Elizabeth

Published
2011
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36. Diabetes Remission in the Alliance of Randomized Trials of Medicine Versus Metabolic Surgery in Type 2 Diabetes (ARMMS-T2D)

Author

Kirwan, John P., primary, Courcoulas, Anita P., primary, Cummings, David E., primary, Goldfine, Allison B., primary, Kashyap, Sangeeta R., primary, Simonson, Donald C., primary, Arterburn, David E., primary, Gourash, William F., primary, Vernon, Ashley H., primary, Jakicic, John M., primary, Patti, Mary Elizabeth, primary, Wolski, Kathy, primary, and Schauer, Philip R., primary

Published
2022
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38. Bariatric Surgery

Author

Ding, Su-Ann, primary, McKenzie, Travis, additional, Vernon, Ashley H., additional, and Goldfine, Allison B., additional

Published
2016
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39. 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
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45. PKCδ regulates hepatic insulin sensitivity and hepatosteatosis in mice and humans

Author

Bezy, Olivier, Tran, Thien T., Pihlajamaki, Jussi, Suzuki, Ryo, Emanuelli, Brice, Winnay, Jonathan, Mori, Marcelo A., Haas, Joel, Biddinger, Sudha B., Leitges, Michael, Goldfine, Allison B., Patti, Mary Elizabeth, King, George L., and Kahn, C. Ronald

Subjects
Glucose, Glucose metabolism, Genes, Insulin resistance, Insulin, Gene expression, Triglycerides, Dextrose
Abstract

C57BL/6J and 129S6/Sv (B6 and 129) mice differ dramatically in their susceptibility to developing diabetes in response to diet- or genetically induced insulin resistance. A major locus contributing to this [...]

Published
2011
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46. Increased SRF transcriptional activity in human and mouse skeletal muscle is a signature of insulin resistance

Author

Jin, Wanzhu, Goldfine, Allison B., Boes, Tanner, Henry, Robert R., Ciaraldi, Theodore P., Kim, Eun-Young, Emecan, Merve, Fitzpatrick, Connor, Sen, Anish, Shah, Ankit, Mun, Edward, Vokes, Martha, Schroeder, Joshua, Tatro, Elizabeth, Jimenez-Chillaron, Jose, and Patti, Mary-Elizabeth

Subjects
Physiological aspects, Genetic aspects, Research, Skeletal muscle -- Physiological aspects -- Genetic aspects -- Research, Transcription (Genetics) -- Research, Insulin resistance -- Genetic aspects -- Analysis -- Health aspects -- Research, Genetic transcription -- Research, Muscles -- Physiological aspects -- Genetic aspects -- Research
Abstract

Introduction Type 2 diabetes (T2D) is increasing at an alarming rate worldwide, affecting a projected 366 million individuals by the year 2030 (1). Despite genome-wide association studies confirming genetic links [...], Insulin resistance in skeletal muscle is a key phenotype associated with type 2 diabetes (T2D) for which the molecular mediators remain unclear. We therefore conducted an expression analysis of human muscle biopsies from patients with T2D; normoglycemic but insulin-resistant subjects with a parental family history ([FH.sup.+]) of T2D; and family history-negative control individuals ([FH.sup.-]). Actin cytoskeleton genes regulated by serum response factor (SRF) and its coactivator megakaryoblastic leukemia 1 (MKL1) had increased expression in T2D and [FH.sup.+] groups. Furthermore, striated muscle activator of Rho signaling (STARS), an activator of SRF, was upregulated in T2D and [FH.sup.+] and was inversely correlated with insulin sensitivity. Skeletal muscle from insulin-resistant mice recapitulated this gene expression pattern and showed reduced G-actin and increased nuclear localization of MKL1, each of which regulates SRF activity. Overexpression of MKL1 or reduction in G-actin decreased insulin-stimulated Akt phosphorylation, whereas reduction of STARS expression increased insulin signaling and glucose uptake. Pharmacological SRF inhibition by CCG-1423 reduced nuclear MKL1 and improved glucose uptake and tolerance in insulin-resistant mice in vivo. Thus, SRF pathway alterations are linked to insulin resistance, may contribute to T2D pathogenesis, and could represent therapeutic targets.

Published
2011
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47. The impact of salsalate treatment on serum levels of advanced glycation end products in type 2 diabetes

Author

Barzilay, Joshua I., Jablonski, Kathleen A., Fonseca, Vivian, Shoelson, Steven E., Goldfine, Allison B., Strauch, Christopher, and Monnier, Vincent M.

Subjects
Usage, Research, Measurement, Advanced glycation end products -- Research -- Measurement, Type 2 diabetes -- Research, Salsalate -- Research -- Usage
Abstract

OBJECTIVE Salsalate is a nonacetylated salicylate that lowers glucose levels in people with type 2 diabetes (T2D). Here we examined whether salsalate also lowered serum-protein-bound levels of early and advanced [...]

Published
2014
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