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3. Oxidative Stress and Cardiovascular Risk in Type 1 Diabetes Mellitus: Insights From the DCCT/EDIC Study

Author

W.H. Wilson Tang, Paula McGee, John M. Lachin, Daniel Y. Li, Byron Hoogwerf, Stanley L. Hazen, D.M. Nathan, B. Zinman, O. Crofford, S. Genuth, J. Brown‐Friday, J. Crandall, H. Engel, S. Engel, H. Martinez, M. Phillips, M. Reid, H. Shamoon, J. Sheindlin, R. Gubitosi‐Klug, L. Mayer, S. Pendegast, H. Zegarra, D. Miller, L. Singerman, S. Smith‐Brewer, M. Novak, J. Quin, Saul Genuth, M. Palmert, E. Brown, J. McConnell, P. Pugsley, P. Crawford, W. Dahms, N.S. Gregory, M.E. Lackaye, S. Kiss, R. Chan, A. Orlin, M. Rubin, D. Brillon, V. Reppucci, T. Lee, M. Heinemann, S. Chang, B. Levy, L. Jovanovic, M. Richardson, B. Bosco, A. Dwoskin, R. Hanna, S. Barron, R. Campbell, A. Bhan, D. Kruger, J.K. Jones, P.A. Edwards, J.D. Carey, E. Angus, A. Thomas, A. Galprin, M. McLellan, F. Whitehouse, R. Bergenstal, M. Johnson, K. Gunyou, L. Thomas, J. Laechelt, P. Hollander, M. Spencer, D. Kendall, R. Cuddihy, P. Callahan, S. List, J. Gott, N. Rude, B. Olson, M. Franz, G. Castle, R. Birk, J. Nelson, D. Freking, L. Gill, W. Mestrezat, D. Etzwiler, K. Morgan, L.P. Aiello, E. Golden, P. Arrigg, V. Asuquo, R. Beaser, L. Bestourous, J. Cavallerano, R. Cavicchi, O. Ganda, O. Hamdy, R. Kirby, T. Murtha, D Schlossman, S. Shah, G. Sharuk, P. Silva, P. Silver, M. Stockman, J. Sun, E. Weimann, H. Wolpert, L.M. Aiello, A. Jacobson, L. Rand, J. Rosenzwieg, M.E. Larkin, M. Christofi, K. Folino, J. Godine, P. Lou, C. Stevens, E. Anderson, H. Bode, S. Brink, C. Cornish, D. Cros, L. Delahanty, eManbey, C. Haggan, J. Lynch, C. McKitrick, D. Norman, D. Moore, M. Ong, C. Taylor, D. Zimbler, S. Crowell, S. Fritz, K. Hansen, C. Gauthier‐Kelly, F.J. Service, G. Ziegler, A. Barkmeier, L. Schmidt, B. French, R. Woodwick, R. Rizza, W.F. Schwenk, M. Haymond, J. Pach, J. Mortenson, B. Zimmerman, A. Lucas, R. Colligan, L. Luttrell, M. Lopes‐Virella, S. Caulder, C. Pittman, N. Patel, K. Lee, M. Nutaitis, J. Fernandes, K. Hermayer, S. Kwon, A Blevins, J. Parker, J. Colwell, D. Lee, J. Soule, P. Lindsey, M. Bracey, A. Farr, S. Elsing, T. Thompson, J. Selby, T. Lyons, S. Yacoub‐Wasef, M. Szpiech, D. Wood, R. Mayfield, M. Molitch, D. Adelman, S. Colson, L. Jampol, A. Lyon, M. Gill, Z. Strugula, L. Kaminski, R. Mirza, E. Simjanoski, D. Ryan, C. Johnson, A. Wallia, S. Ajroud‐Driss, P. Astelford, N. Leloudes, A. Degillio, B. Schaefer, S. Mudaliar, G Lorenzi, M. Goldbaum, K. Jones, M. Prince, M. Swenson, I. Grant, R. Reed, R. Lyon, O. Kolterman, M. Giotta, T. Clark, G. Friedenberg, W.I. Sivitz, B. Vittetoe, J. Kramer, M. Bayless, R. Zeitler, H. Schrott, N. Olson, L. Snetselaar, R. Hoffman, J. MacIndoe, T. Weingeist, C. Fountain, R. Miller, S. Johnsonbaugh, M. Patronas, M. Carney, S. Mendley, P. Salemi, R. Liss, M. Hebdon, D. Counts, T. Donner, J. Gordon, R. Hemady, A. Kowarski, D. Ostrowski, S. Steidl, B. Jones, W.H. Herman, C.L. Martin, R. Pop‐Busui, D.A. Greene, M.J. Stevens, N. Burkhart, T. Sandford, J. Floyd, J. Bantle, N. Flaherty, J. Terry, D. Koozekanani, S. Montezuma, N. Wimmergren, B. Rogness, M. Mech, T. Strand, J. Olson, L. McKenzie, C. Kwong, F. Goetz, R. Warhol, D. Hainsworth, D. Goldstein, S. Hitt, J. Giangiacomo, D.S Schade, J.L. Canady, M.R. Burge, A. Das, R.B. Avery, L.H. Ketai, J.E. Chapin, M.L. Schluter, J. Rich, C. Johannes, D. Hornbeck, M. Schutta, P.A. Bourne, A. Brucker, S. Braunstein, S. Schwartz, B.J. Maschak‐Carey, L. Baker, T. Orchard, L. Cimino, T. Songer, B. Doft, S. Olson, D. Becker, D. Rubinstein, R.L. Bergren, J. Fruit, R. Hyre, C. Palmer, N. Silvers, L. Lobes, P. Paczan Rath, P.W. Conrad, S. Yalamanchi, J. Wesche, M. Bratkowksi, S. Arslanian, J. Rinkoff, J. Warnicki, D. Curtin, D. Steinberg, G. Vagstad, R. Harris, L. Steranchak, J. Arch, K. Kelly, P. Ostrosaka, M. Guiliani, M. Good, T. Williams, K. Olsen, A. Campbell, C. Shipe, R. Conwit, D. Finegold, M. Zaucha, A. Drash, A. Morrison, J.I. Malone, M.L. Bernal, P.R. Pavan, N. Grove, E.A. Tanaka, D. McMillan, J. Vaccaro‐Kish, L. Babbione, H. Solc, T.J. DeClue, S. Dagogo‐Jack, C. Wigley, H. Ricks, A. Kitabchi, E. Chaum, M.B. Murphy, S. Moser, D. Meyer, A. Iannacone, S. Yoser, M. Bryer‐Ash, S. Schussler, H. Lambeth, P. Raskin, S. Strowig, M. Basco, S. Cercone, A. Barnie, R. Devenyi, M. Mandelcorn, M. Brent, S. Rogers, A. Gordon, N. Bakshi, B. Perkins, L. Tuason, F. Perdikaris, R. Ehrlich, D. Daneman, K. Perlman, S Ferguson, J. Palmer, R. Fahlstrom, I.H. de Boer, J. Kinyoun, L. Van Ottingham, S. Catton, J. Ginsberg, C. McDonald, J. Harth, M. Driscoll, T. Sheidow, J. Mahon, C. Canny, D. Nicolle, P. Colby, J. Dupre, I. Hramiak, N.W. Rodger, M. Jenner, T. Smith, W. Brown, M. May, J. Lipps Hagan, A. Agarwal, T. Adkins, R. Lorenz, S. Feman, L. Survant, N.H. White, L. Levandoski, G. Grand, M. Thomas, D. Joseph, K. Blinder, G. Shah, D. Burgess, I. Boniuk, J. Santiago, W. Tamborlane, P. Gatcomb, K. Stoessel, P. Ramos, K. Fong, P. Ossorio, J. Ahern, L. Meadema‐Mayer, C. Beck, K. Farrell, J Quin, P. Gaston, R. Trail, J. Lachin, J. Backlund, I. Bebu, B. Braffett, L. Diminick, X. Gao, W. Hsu, K. Klumpp, H. Pan, V. Trapani, P. Cleary, P. McGee, W. Sun, S. Villavicencio, K. Anderson, L. Dews, Naji Younes, B. Rutledge, K. Chan, D. Rosenberg, B. Petty, A. Determan, D. Kenny, C. Williams, C. Cowie, C. Siebert, M. Steffes, V. Arends, J. Bucksa, M. Nowicki, B. Chavers, D. O'Leary, J. Polak, A. Harrington, L. Funk, R Crow, B. Gloeb, S. Thomas, C. O'Donnell, E.Z. Soliman, Z.M. Zhang, Y. Li, C. Campbell, L. Keasler, S. Hensley, J. Hu, M. Barr, T. Taylor, R. Prineas, E.L. Feldman, J.W. Albers, P. Low, C. Sommer, K. Nickander, T. Speigelberg, M. Pfiefer, M. Schumer, M. Moran, J. Farquhar, C. Ryan, D. Sandstrom, M. Geckle, E. Cupelli, F. Thoma, B. Burzuk, T. Woodfill, R. Danis, B. Blodi, D. Lawrence, H. Wabers, S. Gangaputra, S. Neill, M. Burger, J. Dingledine, V. Gama, R. Sussman, M. Davis, L. Hubbard, M. Budoff, S. Darabian, P. Rezaeian, N. Wong, M. Fox, R. Oudiz, L Kim, R. Detrano, K. Cruickshanks, D. Dalton, K. Bainbridge, J. Lima, D. Bluemke, E. Turkbey, der Geest, C. Liu, A. Malayeri, A. Jain, C. Miao, H. Chahal, R. Jarboe, V. Monnier, D. Sell, C. Strauch, S. Hazen, A. Pratt, W. Tang, J. Brunzell, J. Purnell, R. Natarajan, F. Miao, L. Zhang, Z. Chen, A. Paterson, A. Boright, S. Bull, L. Sun, S. Scherer, T.J. Lyons, A. Jenkins, R. Klein, G. Virella, A. Jaffa, R. Carter, J. Stoner, W.T. Garvey, D. Lackland, M. Brabham, D. McGee, D. Zheng, R.K. Mayfield, J. Maynard, H. Wessells, A Sarma, R. Dunn, S. Holt, J. Hotaling, C. Kim, Q. Clemens, J. Brown, and K. McVary

Subjects
medicine.medical_specialty, endocrine system diseases, 030209 endocrinology & metabolism, Disease, 030204 cardiovascular system & hematology, Lower risk, medicine.disease_cause, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Diabetes mellitus, medicine, Diseases of the circulatory (Cardiovascular) system, Coronary Heart Disease, Glycemic, Original Research, free radical, Inflammation, Type 1 diabetes, biology, business.industry, Paraoxonase, medicine.disease, paraoxonase, 3. Good health, RC666-701, Cohort, diabetes mellitus, biology.protein, Cardiology and Cardiovascular Medicine, business, Oxidant Stress, Oxidative stress, F2Isoprostane, Biomarkers
Abstract

Background Hyperglycemia leading to increased oxidative stress is implicated in the increased risk for the development of macrovascular and microvascular complications in patients with type 1 diabetes mellitus. Methods and Results A random subcohort of 349 participants was selected from the DCCT / EDIC (Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications) cohort. This included 320 controls and 29 cardiovascular disease cases that were augmented with 98 additional known cases to yield a case cohort of 447 participants (320 controls, 127 cases). Biosamples from DCCT baseline, year 1, and closeout of DCCT , and 1 to 2 years post‐ DCCT ( EDIC years 1 and 2) were measured for markers of oxidative stress, including plasma myeloperoxidase, paraoxonase activity, urinary F 2α isoprostanes, and its metabolite, 2,3 dinor‐8 iso prostaglandin F 2α . Following adjustment for glycated hemoblobin and weighting the observations inversely proportional to the sampling selection probabilities, higher paraoxonase activity, reflective of antioxidant activity, and 2,3 dinor‐8 iso prostaglandin F 2α , an oxidative marker, were significantly associated with lower risk of cardiovascular disease (−4.5% risk for 10% higher paraoxonase, P iso prostaglandin F 2α , P =0.0092). In contrast, the oxidative markers myeloperoxidase and F 2α isoprostanes were not significantly associated with cardiovascular disease after adjustment for glycated hemoblobin. There were no significant differences between DCCT intensive and conventional treatment groups in the change in all biomarkers across time segments. Conclusions Heightened antioxidant activity (rather than diminished oxidative stress markers) is associated with lower cardiovascular disease risk in type 1 diabetes mellitus, but these biomarkers did not change over time with intensification of glycemic control. Clinical Trial Registration URL : https://www.clinicaltrials.gov . Unique identifiers: NCT 00360815 and NCT 00360893.

Published
2018

4. Effects of canagliflozin versus glimepiride on adipokines, inflammatory biomarkers, and chemokines in patients with type 2 diabetes mellitus

Author

L.V. Gaal, Michael J. Davies, James List, Jimmy Ren, Lawrence A. Leiter, W.T. Garvey, Robert Cuddihy, M. Fegade, and Ujjwala Vijapurkar

Subjects
Canagliflozin, medicine.medical_specialty, Chemokine, biology, RD1-811, business.industry, Type 2 Diabetes Mellitus, Adipokine, Gastroenterology, Inflammatory biomarkers, 03 medical and health sciences, Glimepiride, 0302 clinical medicine, 030220 oncology & carcinogenesis, Internal medicine, RC666-701, medicine, biology.protein, Diseases of the circulatory (Cardiovascular) system, In patient, Surgery, Cardiology and Cardiovascular Medicine, business, 030217 neurology & neurosurgery, medicine.drug
Published
2017

5. Noggin Is Novel Inducer of Mesenchymal Stem Cell Adipogenesis

Author

George Tsuladze, Diptiman Chanda, W.T. Garvey, Selvarangan Ponnazhagan, Anandi Sawant, and Tatyana Isayeva

Subjects
chemistry.chemical_classification, medicine.medical_specialty, animal structures, Ccaat-enhancer-binding proteins, Mesenchymal stem cell, CCAAT-Enhancer-Binding Protein-delta, Peroxisome proliferator-activated receptor, Cell Biology, Biology, Bone morphogenetic protein, Biochemistry, Cell biology, Endocrinology, chemistry, Adipogenesis, Internal medicine, embryonic structures, Gene expression, medicine, Noggin, Molecular Biology
Abstract

Noggin is a glycosylated-secreted protein known so far for its inhibitory effects on bone morphogenetic protein (BMP) signaling by sequestering the BMP ligand. We report here for the first time a novel mechanism by which noggin directly induces adipogenesis of mesenchymal stem cells independently of major human adipogenic signals through C/EBPδ, C/EBPα and peroxisome proliferator-activated receptor-γ. Evaluation of a possible mechanism for noggin-induced adipogenesis of mesenchymal stem cells identified the role of Pax-1 in mediating such differentiation. The relevance of elevated noggin levels in obesity was confirmed in a preclinical, immunocompetent mouse model of spontaneous obesity and in human patients with higher body mass index. These data clearly provide a novel role for noggin in inducing adipogenesis and possibly obesity and further indicates the potential of noggin as a therapeutic target to control obesity.

Published
2012
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6. Études SUSTAIN 1-5 : perte de poids sous semaglutide selon la catégorie d’IMC initial

Author

W.T. Garvey, Julie Derving Karsbøl, Lawrence A. Leiter, L. Masmiquel, L. Chaykin, ML Warren, D. Thielke, A. Bouzidi, and G. Charpentier

Subjects
Endocrinology, Endocrinology, Diabetes and Metabolism, General Medicine
Abstract

Objectifs Cette analyse post-hoc s’est interessee a l’efficacite du semaglutide sur le poids en fonction des categories d’IMC initial dans les etudes cliniques SUSTAIN 1-5. Patients et methodes Analyse des donnees des etudes SUSTAIN 1-5 evaluant l’effet du semaglutide (0,5 mg ; 1,0 mg) versus comparateurs (placebo, sitagliptine, exenatide LP, insuline glargine) en fonction des sous-groupes d’IMC ( Resultats Le semaglutide a permis une perte de poids versus comparateurs pour tous les sous-groupes d’IMC avec des diminutions de 2,5 a 5,7 kg pour le semaglutide 0,5 mg et de 2,0 a 7,9 kg avec le semaglutide 1,0 mg (versus une prise de poids allant jusqu’a 1,5 kg–une diminution allant jusqu’a 3,7 kg pour les comparateurs). Pour l’ensemble des patients inclus dans SUSTAIN 1-5, la perte de poids sous semaglutide est significative (p Discussion L’efficacite du semaglutide sur la perte de poids est constante versus comparateurs et ce, quel que soit l’IMC initial.

Published
2017
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7. AdR1-TG/TALLYHO mice have improved lipid accumulation and insulin sensitivity

Author

Yuchang Fu, W.T. Garvey, Nanlan Luo, Wei Zhang, and Xiangdong Wang

Subjects
Male, medicine.medical_treatment, Apoptosis, Fatty Acids, Nonesterified, Biochemistry, chemistry.chemical_compound, Mice, Sirtuin 1, Insulin Secretion, Insulin, Adiponectin receptor 1, Glucose tolerance test, medicine.diagnostic_test, Caspase 3, Cholesterol, Receptors, Adiponectin, Signal Transduction, Genetically modified mouse, medicine.medical_specialty, Normal diet, Blotting, Western, Biophysics, Mice, Transgenic, Biology, Diet, High-Fat, Article, Diabetes Mellitus, Experimental, Insulin resistance, Internal medicine, medicine, Animals, Muscle, Skeletal, Molecular Biology, Pancreas, Crosses, Genetic, Triglycerides, Adiponectin, Triglyceride, Body Weight, Cell Biology, Hypertrophy, Glucose Tolerance Test, medicine.disease, Endocrinology, chemistry, Gene Expression Regulation, Insulin Receptor Substrate Proteins, Insulin Resistance, Biomarkers
Abstract

Background Overexpression of adiponectin receptor 1 in macrophages can physiologically modulate metabolic activities in vivo by enhancing adiponectin actions in distal metabolically active tissues. To investigate the effects of enhanced adiponectin actions in TALLYHO (TH) diabetic mouse model, we crossed the adiponectin receptor 1 macrophage-specific transgenic mice (AdR1-TG) with the TALLYHO diabetic mice (TH) to examine the changes of lipid accumulation and insulin sensitivity in these mice. Methods AdR1-TG/TH and the control WT/TH mice were fed either normal diet or high fat diet for 28 weeks. Whole body weights of these mice were measured and mouse sera were analyzed for the levels of cholesterol, triglyceride, and free fatty acids. Glucose tolerance testing (GTT) and insulin tolerance testing (ITT) in these mice were performed to investigate systemic insulin sensitivity in vivo. Molecular markers for insulin signaling pathway in mouse skeletal muscle tissues, IRS-1 and AKT, were examined. Mouse serum insulin levels were measured and Sirt1 gene expression in mouse pancreatic tissues was also quantified related to the insulin secretion. The Caspase 3 protein levels were analyzed by Western blot methods. Results Compared to the control WT/TH mice, AdR1-TG/TH mice showed significantly lower body weights under either normal diet or high fat diet and the mouse serum levels of cholesterol, triglyceride and free fatty acids were significantly decreased in the transgenic crossed mice when compared to those from the control mice. Improved GTT and ITT tests indicating increased systemic insulin sensitivity in the transgenic crossed mice demonstrated the enhanced adiponectin actions on the systemic metabolism in vivo. The increases of insulin secretion and its related gene expression were also detected in the transgenic crossed mice. In contrast, the control mice showed hypertrophy pancreases companying with high apoptosis gene expression. These results suggest that enhanced adiponectin actions by overexpressing adiponectin receptor 1 in macrophages can provide unique interactions with the metabolic tissues/cells, improving lipid accumulation and insulin sensitivity in TALLYHO diabetic mice.

Published
2013

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