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1. Islet Autoimmunity is Highly Prevalent and Associated With Diminished β-Cell Function in Patients With Type 2 Diabetes in the Grade Study.

Author

Brooks-Worrell, Barbara, Hampe, Christiane S, Hattery, Erica G, Palomino, Brenda, Zangeneh, Sahar Z, Utzschneider, Kristina, Kahn, Steven E, Larkin, Mary E, Johnson, Mary L, Mather, Kieren J, Younes, Naji, Rasouli, Neda, Desouza, Cyrus, Cohen, Robert M, Park, Jean Y, Florez, Hermes J, Valencia, Willy Marcos, Shojaie, Ali, Palmer, Jerry P, Balasubramanyam, Ashok, Crandall, Jill P, McKee, Melissa Diane, Brown-Friday, Janet, Xhori, Entila, Ballentine-Cargill, Keisha, Duran, Sally, Lukin, Jennifer, Beringher, Stephanie, Gonzalez de la Torre, Susana, Phillips, Lawrence, Burgess, Elizabeth, Olson, Darin, Rhee, Mary, Wilson, Peter, Raines, Tasha Stephanie, Costello, Julie, Gullett, Chona, Maher-Albertelli, Maxine, Morehead, Folayan, Mungara, Radhika, Person, Saranjit, Savoye, Louise, Sibymon, Mabil, Tanukonda, Sridhar, White, Carol Ann, Holloway, Leah, Adams, Cynthia, Ross, April, Gonzalez Hattery, Erica, Gaba, Ruchi, Montes, Graciela, Wright, Charlyne, Hollander, Priscilla, Roe, Erin, Uy, Analyn, Burt, Polly, Estrada, Lorie, Chionh, Kris, Ismail-Beigi, Faramarz, Falck-Ytter, Corinna, Sayyed Kassem, Laure, Sood, Ajay, Tiktin, Margaret, Cramer, Bethany, Iacoboni, Jacalyn, Kononets, Maria V, Kulow, Tanya, Newman, Cynthia, Stancil, Katherine A, Sanders, Cristina, Tucker, Lisa, Werner, Amanda, Krol, Adrienne, McPhee, Gloria, Patel, Christine, Colosimo, Linda, Goland, Robin, Pring, James, Kringas, Patricia, Tejada, Jessica, Hausheer, Camille, Schneier, Harvey, Gumpel, Kelly, Kirpitch, Amanda, Green, Jennifer B, AbouAssi, Hiba, Chatterjee, Ranee, Feinglos, Mark N, English Jones, Jennifer, Khan, Shubi A, Kimpel, Jeanne B, Zimmer, Ronna P, Furst, Mary, Satterwhite, Barbara M, Thacker, Connie, Evans Kreider, Kathryn, Lteif, Amale, and Hamilton, Tonya

Subjects
Biomedical and Clinical Sciences, Immunology, Autoimmune Disease, Clinical Research, Diabetes, 2.1 Biological and endogenous factors, Aetiology, Metabolic and endocrine, GRADE Beta-cell Ancillary Study Network, Medical and Health Sciences, Endocrinology & Metabolism, Biomedical and clinical sciences
Abstract

Islet autoimmunity may contribute to β-cell dysfunction in type 2 diabetes (T2D). Its prevalence and clinical significance have not been rigorously determined. In this ancillary study to the Glycemia Reduction Approaches in Diabetes-A Comparative Effectiveness (GRADE) Study, we investigated the prevalence of cellular and humoral islet autoimmunity in patients with T2D duration 4·0±3·0 y, HbA1c 7·5±0·5% on metformin alone. We measured T cell autoreactivity against islet proteins, islet autoantibodies against GAD65, IA2, ZnT8, and β-cell function. Cellular islet autoimmunity was present in 41·3%, humoral islet autoimmunity in 13·5%, and both in 5·3%. β-cell function calculated as iAUC-CG and ΔC-peptide(0- 30)/Δglucose(0-30) from an oral glucose tolerance test was lower among T cell-positives (T+) than T cell-negatives (T-) using two different adjustments for insulin sensitivity (iAUC-CG: 13·2% [95% CI 0·3, 24·4%] or 11·4% [95% CI 0·4, 21·2%] lower; ΔC-peptide(0-30)/Δglucose(0-30)) 19% [95% CI 3·1, 32·3%] or 17·7% [95% CI 2·6, 30·5%] lower). T+ patients had 17% higher HbA1c (95% CI 0·07, 0·28) and 7·7 mg/dL higher fasting plasma glucose levels (95% CI 0·2,15·3) than T- patients. We conclude that islet autoimmunity is much more prevalent in T2D patients than previously reported. T cell-mediated autoimmunity is associated with diminished β-cell function and worse glycemic control.

Published
2022

2. Low-Dose Anti-Thymocyte Globulin Preserves C-Peptide, Reduces HbA1c, and Increases Regulatory to Conventional T-Cell Ratios in New-Onset Type 1 Diabetes: Two-Year Clinical Trial Data

Author

Haller, Michael J, Long, S Alice, Blanchfield, J Lori, Schatz, Desmond A, Skyler, Jay S, Krischer, Jeffrey P, Bundy, Brian N, Geyer, Susan M, Warnock, Megan V, Miller, Jessica L, Atkinson, Mark A, Becker, Dorothy J, Baidal, David A, DiMeglio, Linda A, Gitelman, Stephen E, Goland, Robin, Gottlieb, Peter A, Herold, Kevan C, Marks, Jennifer B, Moran, Antoinette, Rodriguez, Henry, Russell, William E, Wilson, Darrell M, Greenbaum, Carla J, Battaglia, Manuela, Becker, Dorothy, Bingley, Penelope, Bosi, Emanuele, Buckner, Jane, Clements, Mark, Colman, Peter G, DiMeglio, Linda, Evans-Molina, Carmella, Gottlieb, Peter, Herold, Kevan, Knip, Mikael, Lernmark, Ake, Moore, Wayne, Muir, Andrew, Palmer, Jerry, Peakman, Mark, Philipson, Louis, Raskin, Philip, Redondo, Maria, Russell, William, Sosenko, Jay M, Spain, Lisa, Wentworth, John, Wherrett, Diane, Winter, William, Ziegler, Anette, Anderson, Mark, Antinozzi, Peter, Insel, Richard, Kay, Thomas, Pugliese, Alberto, Roep, Bart, Toppari, Jorma, Leschek, Ellen, Bourcier, Katarzyna, Ridge, John, Rafkin, Lisa, Santiago, Irene, Bundy, Brian, Abbondondolo, Michael, Adams, Timothy, Asif, Ilma, Bjellquist, Jenna, Boonstra, Matthew, Burroughs, Cristina, Cleves, Mario, Cuthbertson, David, DeSalvatore, Meagan, Eberhard, Christopher, Fiske, Steve, Ford, Julie, Garmeson, Jennifer, Geyer, Susan, and Hays, Brian

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Immunology, Clinical Trials and Supportive Activities, Clinical Research, Diabetes, 6.1 Pharmaceuticals, Metabolic and endocrine, Adolescent, Adult, Antilymphocyte Serum, C-Peptide, CD4-CD8 Ratio, Child, Diabetes Mellitus, Type 1, Double-Blind Method, Female, Flow Cytometry, Glycated Hemoglobin, Granulocyte Colony-Stimulating Factor, Humans, Immunologic Factors, Male, T-Lymphocytes, Regulatory, Young Adult, Type 1 Diabetes TrialNet ATG-GCSF Study Group, Medical and Health Sciences, Endocrinology & Metabolism, Biomedical and clinical sciences
Abstract

A three-arm, randomized, double-masked, placebo-controlled phase 2b trial performed by the Type 1 Diabetes TrialNet Study Group previously demonstrated that low-dose anti-thymocyte globulin (ATG) (2.5 mg/kg) preserved β-cell function and reduced HbA1c for 1 year in new-onset type 1 diabetes. Subjects (N = 89) were randomized to 1) ATG and pegylated granulocyte colony-stimulating factor (GCSF), 2) ATG alone, or 3) placebo. Herein, we report 2-year area under the curve (AUC) C-peptide and HbA1c, prespecified secondary end points, and potential immunologic correlates. The 2-year mean mixed-meal tolerance test-stimulated AUC C-peptide, analyzed by ANCOVA adjusting for baseline C-peptide, age, and sex (n = 82) with significance defined as one-sided P < 0.025, was significantly higher in subjects treated with ATG versus placebo (P = 0.00005) but not ATG/GCSF versus placebo (P = 0.032). HbA1c was significantly reduced at 2 years in subjects treated with ATG (P = 0.011) and ATG/GCSF (P = 0.022) versus placebo. Flow cytometry analyses demonstrated reduced circulating CD4:CD8 ratio, increased regulatory T-cell:conventional CD4 T-cell ratios, and increased PD-1+CD4+ T cells following low-dose ATG and ATG/GCSF. Low-dose ATG partially preserved β-cell function and reduced HbA1c 2 years after therapy in new-onset type 1 diabetes. Future studies should determine whether low-dose ATG might prevent or delay the onset of type 1 diabetes.

Published
2019

4. GAD65Abs Are Not Associated With Beta-Cell Dysfunction in Patients With T2D in the GRADE Study

Author

Hampe, Christiane S, primary, Shojaie, Ali, additional, Brooks-Worrell, Barbara, additional, Dibay, Sepideh, additional, Utzschneider, Kristina, additional, Kahn, Steven E, additional, Larkin, Mary E, additional, Johnson, Mary L, additional, Younes, Naji, additional, Rasouli, Neda, additional, Desouza, Cyrus, additional, Cohen, Robert M, additional, Park, Jean Y, additional, Florez, Hermes J, additional, Valencia, Willy Marcos, additional, Palmer, Jerry P, additional, and Balasubramanyam, Ashok, additional

Published
2024
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5. Recommendations for the Definition of Clinical Responder in Insulin Preservation Studies

Author

Beam, Craig A, Gitelman, Stephen E, Palmer, Jerry P, and Group, the Type 1 Diabetes TrialNet Study

Subjects
Medical Biotechnology, Biomedical and Clinical Sciences, Diabetes, Clinical Trials and Supportive Activities, Clinical Research, Metabolic and endocrine, Adolescent, Bias, C-Peptide, Clinical Trials as Topic, Diabetes Mellitus, Type 1, Female, Humans, Hypoglycemic Agents, Insulin, Insulin-Secreting Cells, Male, Reproducibility of Results, Treatment Outcome, Type 1 Diabetes TrialNet Study Group, Medical and Health Sciences, Endocrinology & Metabolism, Biomedical and clinical sciences
Abstract

Clinical responder studies should contribute to the translation of effective treatments and interventions to the clinic. Since ultimately this translation will involve regulatory approval, we recommend that clinical trials prespecify a responder definition that can be assessed against the requirements and suggestions of regulatory agencies. In this article, we propose a clinical responder definition to specifically assist researchers and regulatory agencies in interpreting the clinical importance of statistically significant findings for studies of interventions intended to preserve β-cell function in newly diagnosed type 1 diabetes. We focus on studies of 6-month β-cell preservation in type 1 diabetes as measured by 2-h-stimulated C-peptide. We introduce criteria (bias, reliability, and external validity) for the assessment of responder definitions to ensure they meet U.S. Food and Drug Administration and European Medicines Agency guidelines. Using data from several published TrialNet studies, we evaluate our definition (no decrease in C-peptide) against published alternatives and determine that our definition has minimum bias with external validity. We observe that reliability could be improved by using changes in C-peptide later than 6 months beyond baseline. In sum, to support efficacy claims of β-cell preservation therapies in type 1 diabetes submitted to U.S. and European regulatory agencies, we recommend use of our definition.

Published
2014

6. Residual [beta] cell function in long-term type 1 diabetes associates with reduced incidence of hypoglycemia

Author

Gubitosi-Klug, Rose A., Braffett, Barbara H., Hitt, Susan, Arends, Valerie, Uschner, Diane, Jones, Kimberly, Diminick, Lisa, Karger, Amy B., Paterson, Andrew D., Roshandel, Delnaz, Marcovina, Santica, Lachin, John M., Steffes, Michael, and Palmer, Jerry P.

Subjects
Polypeptides -- Measurement -- Health aspects, Type 1 diabetes -- Complications and side effects -- Physiological aspects, Pancreatic beta cells -- Physiological aspects -- Health aspects, Hypoglycemia -- Risk factors -- Prevention, Health care industry
Abstract

BACKGROUND. We investigated residual [beta] cell function in Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) study participants with an average 35-year duration of type 1 diabetes mellitus (T1DM). METHODS. Serum C-peptide was measured during a 4-hour mixed-meal tolerance test. Associations with metabolic outcomes and complications were explored among nonresponders (all C-peptide values after meal 0.2), intermediate (>0.03 to RESULTS. Of the 944 participants, 117 (12.4%) were classified as responders. Residual C-peptide concentrations were associated with higher DCCT baseline concentrations of stimulated C-peptide (P value for trend = 0.0001). Residual C- peptide secretion was not associated with current or mean HbA1c, HLA high-risk haplotypes for T1DM, or the current presence of T1DM autoantibodies. The proportion of subjects with a history of severe hypoglycemia was lower with high (27%) and intermediate (48%) residual C-peptide concentrations than with low (74%) and no (70%) residual C-peptide concentrations (P value for trend = 0.0001). Responders and nonresponders demonstrated similar rates of advanced microvascular complications. CONCLUSION. [beta] Cell function can persist in long-duration T1DM. With a peak C-peptide concentration of >0.03 nmol/L, we observed clinically meaningful reductions in the prevalence of severe hypoglycemia. TRIAL REGISTRATION. ClinicalTrials.gov NCT00360815 and NCT00360893. FUNDING. Division of Diabetes Endocrinology and Metabolic Diseases of the National Institute of Diabetes and Digestive and Kidney Diseases (DP3-DK104438, U01 DK094176, and U01 DK094157)., Introduction Insulin secretion declines in most individuals with type 1 diabetes mellitus (T1DM) as duration of diabetes increases, yet residual insulin secretion, as detected by circulating C-peptide after a meal [...]

Published
2021
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11. Effect of Hydrolyzed Infant Formula vs Conventional Formula on Risk of Type 1 Diabetes: The TRIGR Randomized Clinical Trial

Author

Knip, Mikael, Åkerblom, Hans K., Al Taji, Eva, Becker, Dorothy, Bruining, Jan, Castano, Luis, Danne, Thomas, de Beaufort, Carine, Dosch, Hans-Michael, Dupre, John, Fraser, William D., Howard, Neville, Ilonen, Jorma, Konrad, Daniel, Kordonouri, Olga, Krischer, Jeffrey P., Lawson, Margaret L., Ludvigsson, Johnny, Madacsy, Laszlo, Mahon, Jeffrey L., Ormisson, Anne, Palmer, Jerry P., Pozzilli, Paolo, Savilahti, Erkki, Serrano-Rios, Manuel, Songini, Marco, Taback, Shayne, Vaarala, Outi, White, Neil H., Virtanen, Suvi M., and Wasikowa, Renata

Published
2018
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14. β Cell death and dysfunction during type 1 diabetes development in at-risk individuals

Author

Herold, Kevan C., Usmani-Brown, Sahar, Ghazi, Tara, Lebastchi, Jasmin, Beam, Craig A., Bellin, Melena D., Ledizet, Michel, Sosenko, Jay M., Krischer, Jeffrey P., and Palmer, Jerry P.

Subjects
Cell death -- Usage -- Government finance -- Research, Medical research, Medicine, Experimental, Autoimmunity -- Usage -- Government finance -- Research, Type 1 diabetes -- Usage -- Government finance -- Development and progression, Pancreatic beta cells -- Physiological aspects, Health care industry
Abstract

Role of the funding source: Funding from the NIH was used for support of the participating clinical centers and the coordinating center. The funding source did not participate in the collection or the analysis of the data. BACKGROUND. The β cell killing that characterizes type 1 diabetes (T1D) is thought to begin years before patients present clinically with metabolic decompensation; however, this primary pathologic process of the disease has not been measured. METHODS. Here, we measured β cell death with an assay that detects p cell-derived unmethylated insulin (INS) DNA. Using this assay, we performed an observational study of 50 participants from 2 cohorts at risk for developing T1D from the TrialNet Pathway to Prevention study and of 4 subjects who received islet autotransplants. RESULTS. In at-risk subjects, those who progressed to T1D had average levels of unmethylated INS DNA that were elevated modestly compared with those of healthy control subjects. In at-risk individuals that progressed to T1D, the observed increases in unmethylated INS DNA were associated with decreases in insulin secretion, indicating that the changes in unmethylated INS DNA are indicative of β cell killing. Subjects at high risk for T1D had levels of unmethylated INS DNA that were higher than those of healthy controls and higher than the levels of unmethylated INS DNA in the at- risk progressor and at-risk nonprogressor groups followed for 4 years. Evaluation of insulin secretory kinetics also distinguished high-risk subjects who progressed to overt disease from those who did not. CONCLUSION. We conclude that a blood test that measures unmethylated INS DNA serves as a marker of active p cell killing as the result of T1D-associated autoimmunity. Together, the data support the concept that p cell killing occurs sporadically during the years prior to diagnosis of T1D and is more intense in the peridiagnosis period. TRIAL REGISTRATION. Clinicaltrials.gov NCT00097292. FUNDING. Funding was from the NIH, the Juvenile Diabetes Research Foundation, and the American Diabetes Association., Introduction Type 1 diabetes (T1D) begins years before clinical presentation with hyperglycemia (1, 2). Following the initial breech of immune tolerance, the autoimmune response against β cells is thought to [...]

Published
2015
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17. Factor Structure and Construct Validity of the Interaction with Disabled Persons Scale.

Author

Thomas, Adrian, Palmer, Jerry K., Coker-Juneau, Carla J., and Williams, David J.

Abstract

Investigated the psychometric properties of the Interaction with Disabled Persons Scale (IDP; L. Gething, 1991). Exploratory factor analysis with 358 undergraduates and confirmatory factor analysis with a sample of 272 undergraduates suggest that the IDP may provide a reasonable measurement of multidimensional attitudes toward individuals with disabilities. (SLD)

Published
2002

19. Antigen-based therapy with glutamic acid decarboxylase (GAD) vaccine in patients with recent-onset type 1 diabetes: a randomised double-blind trial

Author

Wherrett, Diane K, Bundy, Brian, Becker, Dorothy J, DiMeglio, Linda A, Gitelman, Stephen E, Goland, Robin, Gottlieb, Peter A, Greenbaum, Carla J, Herold, Kevan C, Marks, Jennifer B, Monzavi, Roshanak, Moran, Antoinette, Orban, Tihamer, Palmer, Jerry P, Raskin, Philip, Rodriguez, Henry, Schatz, Desmond, Wilson, Darrell M, Krischer, Jeffrey P, and Skyler, Jay S

Published
2011
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20. Islet Autoimmunity is Highly Prevalent and Associated With Diminished β-Cell Function in Patients With Type 2 Diabetes in the Grade Study

Author

Brooks-Worrell, Barbara, Hampe, Christiane S., Hattery, Erica G., Palomino, Brenda, Zangeneh, Sahar Z., Utzschneider, Kristina, Kahn, Steven E., Larkin, Mary E., Johnson, Mary L., Mather, Kieren J., Younes, Naji, Rasouli, Neda, Desouza, Cyrus, Cohen, Robert M., Park, Jean Y., Florez, Hermes J., Valencia, Willy Marcos, Shojaie, Ali, Palmer, Jerry P., Balasubramanyam, Ashok, Crandall, Jill P., McKee, Melissa Diane, Brown-Friday, Janet, Xhori, Entila, Ballentine-Cargill, Keisha, Duran, Sally, Lukin, Jennifer, Beringher, Stephanie, Gonzalez de la Torre, Susana, Phillips, Lawrence, Burgess, Elizabeth, Olson, Darin, Rhee, Mary, Wilson, Peter, Raines, Tasha Stephanie, Costello, Julie, Gullett, Chona, Maher-Albertelli, Maxine, Morehead, Folayan, Mungara, Radhika, Person, Saranjit, Savoye, Louise, Sibymon, Mabil, Tanukonda, Sridhar, White, Carol Ann, Holloway, Leah, Adams, Cynthia, Ross, April, Gonzalez Hattery, Erica, Gaba, Ruchi, Montes, Graciela, Wright, Charlyne, Hollander, Priscilla, Roe, Erin, Uy, Analyn, Burt, Polly, Estrada, Lorie, Chionh, Kris, Ismail-Beigi, Faramarz, Falck-Ytter, Corinna, Sayyed Kassem, Laure, Sood, Ajay, Tiktin, Margaret, Cramer, Bethany, Iacoboni, Jacalyn, Kononets, Maria V., Kulow, Tanya, Newman, Cynthia, Stancil, Katherine A., Sanders, Cristina, Tucker, Lisa, Werner, Amanda, Krol, Adrienne, McPhee, Gloria, Patel, Christine, Colosimo, Linda, Goland, Robin, Pring, James, Kringas, Patricia, Tejada, Jessica, Hausheer, Camille, Schneier, Harvey, Gumpel, Kelly, Kirpitch, Amanda, Green, Jennifer B., AbouAssi, Hiba, Chatterjee, Ranee, Feinglos, Mark N., English Jones, Jennifer, Khan, Shubi A., Kimpel, Jeanne B., Zimmer, Ronna P., Furst, Mary, Satterwhite, Barbara M., Thacker, Connie, Evans Kreider, Kathryn, Lteif, Amale, Hamilton, Tonya, Patel, Nick, Riera, Gabriela, Jackson, Marcia, Pirics, Vivian, Howard, Devin, Aguillar, Danielle, Hurt, Sloan, Bergenstal, Richard, Carlson, Anders, Martens, Thomas, Johnson, Mary, Hill, Renae, Hyatt, Jamie, Jensen, Connie, Madden, Marcia, Martin, Dianna, Willis, Holly, Konerza, Wanda, Passi, Rebecca, Kleeberger, Kathleen, Fortmann, Stephen, Herson, Michael, Mularski, Karen, Glauber, Harry, Prihoda, James, Ash, Britt, Carlson, Christina, Ramey, Phyllis Anne, Schield, Emily, Torgrimson-Ojerio, Britta, Arnold, Kathy, Kauffman, Bryan, Panos, Elease, Sahnow, Samantha, Bays, Kristi, Cook, Jennifer, Gluth, Jennifer, Sasaki, Debra, Schell, Katrina, Criscola, Jennifer, Friason, Camille, Jones, Suzi, Nazarov, Sergey, Barzilay, Joshua, Rassouli, Negah, Puttnam, Rachel, Curtis, Michelle, Stokes, Kia, Hollis, Bonita, Sanders-Jones, Cynthia, Nelson, Roslin, El-Haqq, Zakiah, Kolli, Abby, Tran, Tu, Wexler, Deborah, Larkin, Mary, Meigs, James, Dushkin, Amy, Rocchio, Gianna, Chambers, Brittany, Yepes, Mike, Steiner, Barbara, Dulin, Hilary, Cayford, Melody, DeManbey, Andrea, Gurry, Lindsey, Hillard, Mallory, Martin, Kimberly, Stevens, Christine, Thangthaeng, Nopporn, Kochis, Raquel, Raymond, Elyse, Ripley, Valerie, Park, Jean, Aroda, Vanita, Ghazi, Adline, Loveland, Amy, Hurtado, Maria, Kuhn, Alexander, Mofor, Florence, Marks, Jennifer, Oropesa-Gonzalez, Lisset, Riccio Veliz, Ana K., Nieto-Martinez, Ramfis, Gutt, Miriam, Ahmann, Andrew, Aby-Daniel, Diana, Joarder, Farahnaz, Morimoto, Victoria, Sprague, Carol, Yamashita, Daisuke, Cady, Nancy, Kirchhoff, Patricia, Rivera-Eschright, Nadia, Adducci, Joseph, Morales Gomez, Brianna, Goncharova, Alina, Hox, Sophia H., Petrovitch, Helen, Matwichyna, Michael, Jenkins, Victoria, Bermudez, Nina O., Ishii, Renée R., Hsia, Daniel S., Cefalu, William T., Greenway, Frank L., Waguespack, Celeste, King, Erin, Haynes, Natalie, Thomassie, Amy, Bourgeois, Brandi, Hazlett, Claire, Henry, Robert, Mudaliar, Sunder, Boeder, Schafer, Pettus, Jeremy, Diaz, Elsa, DeLue, Catherine, Castro, Erick, Hernandez, Sylvia, Krakoff, Jonathan, Curtis, Jeffrey M., Killean, Tina, Joshevama, Erica, Diaz, Enrique, Martin, Denelle, Karshner, Tracey, Albu, Jeanine, Pi-Sunyer, F. Xavier, Frances, Sylvaine, Maggio, Carol, Ellis, Emily, Bastawrose, Joseph, Gong, Xiuqun, Banerji, Mary Ann, August, Phyllis, Lorber, Daniel, Brown, Necole M., Josephson, Debra H., Thomas, Lorraine L., Tsovian, Mari, Cherian, Ajini, Jacobson, Marlo H., Mishko, Motria M., Kirkman, M. Sue, Bergamo, Katherine, Buse, John B., Dostou, Jean, Young, Laura, Goley, April, Kerr, Jeffrey, Largay, Joseph F., Guarda, Sonia, Cuffee, Juanita, Culmer, Dawn, Fraser, Rachael, Almeida, Hope, Coffer, Samantha, Debnam, Elizabeth, Kiker, Lauren, Morton, Sarah, Josey, Kim, Fuller, Gail, Garvey, W. Timothy, Cherrington, Andrea, Golson, Dana, Griffith, Olivia, Robertson, Mary Catherine, Agne, April, McCullars, Steve, Craig, Jacqueline, Kersey, Kimberly, Rogge, M. Colleen, Wilson, Carla, Burton, Kathryn, Lipp, Sonia, Vonder Meulen, Mary Beth, Schroeder, Emily, Steiner, Stephanie, Baker, Chelsea, Underkofler, Chantal, Douglass, Sara, Sivitz, William, Cline, Erin, Knosp, Laura, McConnell, Jennifer, Lowe, Tamara, Herman, William H., Pop-Busui, Rodica, Tan, Meng H., Martin, Catherine, Waltje, Andrea, Goodhall, Lynn, Eggleston, Rebecca, Kuo, Shihchen, Bule, Stephanie, Kessler, Nancy, LaSalle, Elizabeth, Seaquist, Elizabeth R., Bantle, Anne, Kumar, Anjali, Redmon, Bruce, Bantle, John, Harindhanavudhi, Tasma, Coe, Mary, Mech, Michael, Taddese, Abdisa, Lesne, Lesia, Smith, Shannon, Kuechenmeister, Lisa, Shivaswamy, Vijay, Morales, Ana Laura, Rodriguez, Maria Grace, Seipel, Kris, Alfred, Alissa, Eggert, Jenna, Lord, Grace, Taylor, William, Tillson, Renee, Schade, David S., Adolphe, Allen, Burge, Mark, Duran-Valdez, Elizabeth, Martinez, Janae, Hernandez McGinnis, Doris, Pucchetti, Benjamin, Scripsick, Elizabeth, DeFronzo, Ralph A., Cersosimo, Eugenio, Abdul-Ghani, Muhammad, Triplitt, Curtis, Verastiqui, Hector, Garza, Rosa Irene, Wright, Kathryn, Puckett, Curtiss, Raskin, Philip, Rhee, Chanhaeng, Abraham, Soma, Jordan, Lin Fan, Sao, Serey, Morton, Luisa, Smith, Oralenda, Osornio Walker, Laura, Schnurr-Breen, Laura, Ayala, Rosa, Kraymer, Robert, Sturgess, Daytheon, Utzschneider, Kristina M., Alarcon-Casas Wright, Lorena, Boyko, Edward, Tsai, Elaine C., Trence, Dace L., Fattaleh, Basma N., Montgomery, Brenda K., Atkinson, Karen M., Concepcion, Tessa, Kozedub, Alexandra, Moak, Cameron, Rhothisen, Samantha, Elasy, Tom A., Martin, Stephanie, Shackelford, Laura, Goidel, Rita, Hinkle, Nina, Lipps Hogan, Janie, Lovell, Cynthia, Myers, Janet, McGill, Janet B., Salam, Maamoun, Kissel, Sarah, Schweiger, Toni, Recklein, Carol, Tamborlane, William, Gatcomb, Patricia, Camp, Anne, Gulanski, Barbara, Inzucchi, Silvio, Pham, Kim, Alguard, Michele, Lessard, Katarzyna, Perez, Magalys, Magenheimer, Elizabeth, Montoza, Abmaridel, Nathan, David M., Lachin, John, Krause-Steinrauf, Heidi, Burch, Henry, Linder, Barbara, Bremer, Andrew, Backman, Michael, Bebu, Ionut, Buys, C.J., Fagan Murphy, Anna, Gao, Yuping, Gramzinski, Michaela, Hall, Stephanie, Legowski, Elizabeth, Arey, Alyssa, Bethepu, Joel, Lund, Claire, Mangat Dhaliwal, Pam, McGee, Paula, Mesimer, Emily, Ngo, Lisa, Steffes, Michael, Seegmiller, Jesse, Saenger, Amy, Arends, Valerie, Gabrielson, Deanna, Conner, Todd, Stuart, Warren, Day, Jolene, Scrymgeour, Alexandra, Soliman, Elsayed Z., Zhang, Zhu-Ming, Campbell, Charles, Hu, Julie, Keasler, Lisa, Hensley, Susan, Li, Yabing, Herman, William, Mihalcea, Rada, Perez-Rosas, Veronica, Prosser, Lisa, Resnicow, Kenneth, Ye, Wen, Shao, Hui, Zhang, Ping, Luchsinger, Jose, Sanchez, Danurys, Burch, Henry B., Fradkin, Judith, Groessl, Erik, Chong, Helen, Hillery, Naomi, Abdouch, Ivan, Brantley, Paula, Broyles, Frances E., Canaris, Gay, Copeland, Paul, Craine, Jeri J., Fein, Warren L., Lee, Melissa S., Meiners, Rebecca, Meiners, Vaughn, O’Neal, Hollis, Park, James E., Sledge, Edward, Steppel-Resnick, Jeanne, Turchin, Alexander, Higgins, John, Fischer, Lawrence, Golden, Sherita, Gonzalez, Jeffrey, Naik, Aanand, Walker, Elizabeth, Doner Lotenberg, Lynne, Gallivan, Joanne M., Lim, Joanne, Tuncer, Diane M., and Behringer-Massera, Stephanie

Subjects
endocrine system diseases, Diabetes Mellitus, Type 2, Endocrinology, Diabetes and Metabolism, Smoke, T-Lymphocytes, Internal Medicine, Humans, Pathophysiology, Fires
Abstract

Islet autoimmunity may contribute to β-cell dysfunction in type 2 diabetes (T2D). Its prevalence and clinical significance have not been rigorously determined. In this ancillary study to the Glycemia Reduction Approaches in Diabetes: A Comparative Effectiveness Study (GRADE), we investigated the prevalence of cellular and humoral islet autoimmunity in patients with T2D duration of 4.0 ± 3.0 years (HbA1c 7.5 ± 0.5% on metformin alone). We measured T-cell autoreactivity against islet proteins, islet autoantibodies against 65-kDa GAD antigen, IA-2, and zinc transporter-8, and β-cell function. Cellular islet autoimmunity was present in 41.3%, humoral islet autoimmunity in 13.5%, and both in 5.3%. β-Cell function calculated as incremental area under the curve of glucose from 0–120 min (iAUC-CG) and ΔC-peptide(0–30)/Δglucose(0–30) from an oral glucose tolerance test was lower among T-cell–positive (T+) than T-cell–negative (T−) individuals using two different adjustments for insulin sensitivity (iAUC-CG: 13.2% [95% CI 0.3, 24.4] or 11.4% [95% CI 0.4, 21.2] lower; ΔC-peptide[0–30]/Δglucose[0–30]: 19% [95% CI 3.1, 32.3] or 17.7% [95% CI 2.6, 30.5%] lower). T+ patients had 17% higher HbA1c (95% CI 0.07, 0.28) and 7.7 mg/dL higher fasting plasma glucose levels (95% CI 0.2, 15.3) than T− patients. We conclude that islet autoimmunity is much more prevalent in patients with T2D than previously reported. T-cell–mediated autoimmunity is associated with diminished β-cell function and worse glycemic control.

Published
2021

23. Islet Autoimmunity is Highly Prevalent and Associated With Diminished β-Cell Function in Patients With Type 2 Diabetes in the Grade Study

Author

Brooks-Worrell, Barbara, primary, Hampe, Christiane S., primary, Hattery, Erica G., primary, Palomino, Brenda, primary, Zangeneh, Sahar Z., primary, Utzschneider, Kristina, primary, Kahn, Steven E., primary, Larkin, Mary E., primary, Johnson, Mary L., primary, Mather, Kieren J., primary, Younes, Naji, primary, Rasouli, Neda, primary, Desouza, Cyrus, primary, Cohen, Robert M., primary, Park, Jean Y., primary, Florez, Hermes J., primary, Valencia, Willy Marcos, primary, Network, GRADE Beta-cell Ancillary Study, primary, Shojaie, Ali, primary, Palmer, Jerry P., primary, Balasubramanyam, Ashok, primary, and Group, GRADE Research, primary

Published
2022
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24. Insulin Autoantibodies

Author

Palmer, Jerry P., Cohen, Margo Panush, editor, Foà, Piero P., editor, Ginsberg-Fellner, Fredda, editor, and McEvoy, Robert C., editor

Published
1990
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31. Time to Peak Glucose and Peak C-Peptide During the Progression to Type 1 Diabetes in the Diabetes Prevention Trial and TrialNet Cohorts

Author

Voss, Michael G, primary, Cuthbertson, David D, primary, Cleves, Mario M, primary, Xu, Ping, primary, Evans-Molina, Carmella, primary, Palmer, Jerry P, primary, Redondo, Maria J., primary, Steck, Andrea K., primary, Lundgren, Markus, primary, Larsson, Helena, primary, Moore, Wayne V, primary, Atkinson, Mark A., primary, Sosenko, Jay, primary, and Ismail, Heba M, primary

Published
2021
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32. Corrigendum to 'Randomized phase 2 trial and open-label extension of domagrozumab in Duchenne muscular dystrophy' [Neuromuscular Disorders, Vol. 30 (6) 2020, 492-502] (Neuromuscular Disorders (2020) 30(6) (492–502), (S0960896620301188), (10.1016/j.nmd.2020.05.002))

Author

Wagner, Kathryn R., Abdel-Hamid, Hoda Z., Mah, Jean K., Campbell, Craig, Guglieri, Michela, Muntoni, Francesco, Takeshima, Yasuhiro, McDonald, Craig M., Kahn, Anna, Atkinson, Karen M., Palmer, Jerry P., Utzschneider, Kristina M., Gebremedhin, Tsige, Kernan-Schloss, Abigail, Kozedub, Alexandra, Montgomery, Brenda K., Morse, Emily J., Mather, Kieren J., Garrett, Tammy, Hannon, Tamara S., Lteif, Amale, Patel, Aniket, Chisholm, Robin, Moore, Karen, Pirics, Vivian, and Pratt, Linda

Abstract

This article reported on the results from a phase 2 trial of domagrozumab and its open-label extension in patients with Duchenne muscular dystrophy (Clinicaltrials.gov identifiers: NCT02310763 and NCT02907619). The manuscript also provided results on two secondary endpoints for magnetic resonance imaging (MRI), muscle volume and muscle volume index. The authors regret that, following publication of the results and in preparation for a separate publication on MRI results from this trial, the MRI images were reviewed and segmentation errors were identified. As a result, the team worked to (1) Perform a rigorous quality inspection of all analysed data; (2) Identify cases where there were incorrect segmentations; (3) correct segmentation errors; (4) Re-analyse all data with correct segmentation. Using the updated MRI data, the MMRM analysis showed there was a change in the significance of secondary endpoints evaluating Thigh Muscle Volume and Muscle Volume Index. No significant differences between treatment groups in muscle volume measures were found in the original analysis. These results have not altered the overall interpretation of the study results but do necessitate revisions to the article. These data confirm that the trial design and execution adequately tested the hypothesis that myostatin inhibition would slow or delay the loss of function in patients with Duchenne muscular dystrophy (DMD). The increase in muscle volume observed by MRI in patients with DMD treated with domagrozumab is in accordance with mechanism of action for domagrozumab, which targets myostatin, a negative regulator of muscle growth. The increase in muscle volume did not lead to a clinical benefit in patients with DMD. The primary endpoint (4 stair climb) did not meet statistical significance, nor did the other functional tests. The study was terminated due to lack of efficacy. Full details of the needed revisions are as follows: 1. In the results section 3.6 (page 8, second paragraph), we reported no significant differences in mean percent change from baseline between domagrozumab and placebo for both muscle volume and muscle volume index. This paragraph was replaced with the following text: “There was a significant difference between domagrozumab and placebo in the mean percent change from baseline in thigh muscle volume at Week 17 (difference 2.945%, P=0.0087) and Week 49 (differences 4.087%, P=0.0298), and in muscle volume index at Week 33 (difference 2.612%, P=0.0376) and Week 49 (differences3.208%, P=0.0411).” 2. In the discussion (page 9), the following sentence, “Although neither muscle volume nor muscle volume index measures were statistically significant in this study, they are both consistent with a potential anabolic effect.” was replaced with, “The increase in muscle volume observed on MRI in patients with DMD treated with domagrozumab, is in accordance with mechanism of action for this compound which targets myostatin, a negative regulator of muscle growth. However, the increase in muscle volume did not lead to a clinical benefit (improved function) in patients with DMD.” 3. In view of the correction to the Results section, this is now reflected in the abstract which has changed to read: “There were no significant between-group differences in secondary clinical endpoints, except for the thigh muscle volume and muscle volume index measures (P

Published
2021

33. Use of the Diabetes Prevention Trial-Type 1 Risk Score (DPTRS) for improving the accuracy of the risk classification of type 1 diabetes

Author

Sosenko, Jay M., Skyler, Jay S., Mahon, Jeffrey, Krischer, Jeffrey P., Greenbaum, Carla J., Rafkin, Lisa E., Beam, Craig A., Boulware, David C., Matheson, Della, Cuthbertson, David, Herold, Kevan C., Eisenbarth, George, and Palmer, Jerry P.

Subjects
Autoimmunity -- Usage, Autoantibodies -- Usage, Type 1 diabetes -- Prevention -- Usage, Clinical trials -- Usage, Health
Abstract

OBJECTIVE We studied the utility of the Diabetes Prevention Trial-Type 1 Risk Score (DPTRS) for improving the accuracy of type 1 diabetes (T1D) risk classification in TrialNet Natural History Study [...]

Published
2014
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34. Impact of C-peptide preservation on metabolic and clinical outcomes in the diabetes control and complications trial

Author

Lachin, John M., McGee, Paula, and Palmer, Jerry P.

Subjects
Diabetes -- Care and treatment, Peptides -- Identification and classification, Health
Abstract

The Diabetes Control and Complications Trial established that a stimulated C-peptide concentration ≥0.2 nmol/L at study entry among subjects with up to a 5-year diabetes duration is associated with favorable metabolic and clinical outcomes over the subsequent 7 years of follow-up. Herein we further examine the association of both fasting and stimulated C-peptide numerical values with outcomes. In the intensive treatment group, for a 50% higher stimulated C-peptide on entry, such as from 0.10 to 0.15 nmol/L, Hb[A.sub.1c] decreased by 0.07% (0.8 mmol/mol; P = 0.0003), insulin dose decreased by 0.0276 units/kg/day (P < 0.0001), hypoglycemia risk decreased by 8.2% (P < 0.0001), and the risk of sustained retinopathy was reduced by 25% (P = 0.0010), all in unadjusted analyses. Other than Hb[A.sub.1c], these effects remained significant after adjusting for the Hb[A.sub.1c] on entry. While C-peptide was not significantly associated with the incidence of nephropathy, it was strongly associated with the albumin excretion rate. The fasting C-peptide had weaker associations with outcomes. As C-peptide decreased to nonmeasurable concentrations, the outcomes changed in a nearly linear manner, with no threshold or breakpoint. While preservation of stimulated C-peptide at ≥0.2 nmol/L has clinically beneficial outcomes, so also does an increase in the concentration of C-peptide across the range of values. Diabetes 2014;63:739-748 | DOI: 10.2337/db13-0881, The concentration of C-peptide in response to a stimulus (mixed-meal or glucagon injection) has been established as a valid and reliable measure of residual β-cell function (1,2). C-peptide is cosecreted [...]

Published
2014
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40. Residual β cell function in long-term type 1 diabetes associates with reduced incidence of hypoglycemia

Author

Gubitosi-Klug, Rose A., primary, Braffett, Barbara H., additional, Hitt, Susan, additional, Arends, Valerie, additional, Uschner, Diane, additional, Jones, Kimberly, additional, Diminick, Lisa, additional, Karger, Amy B., additional, Paterson, Andrew D., additional, Roshandel, Delnaz, additional, Marcovina, Santica, additional, Lachin, John M., additional, Steffes, Michael, additional, and Palmer, Jerry P., additional

Published
2021
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