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9. High GADA titer increases the risk of insulin requirement in LADA patients: a 7-year follow-up (NIRAD study 7)

Author

Zampetti, S., Campagna, G., Tiberti, C., Songini, M., Arpi, Ml., De Simone, G., Cossu, E., Cocco, L., Osborn, J., Bosi, E., Giorgino, F., Spoletini, M., Buzzetti, R., NIRAD Study Group, Adda, G, Di Lembo, S, Aglialoro, A, Cattaneo, A, Scassi, V, Anichini, R, Arcangeli, A, Arpi, Ml, Bardini, Rg, Basciano, P, Bracaccia, M, Pistoni, S, Bracaglia, D, Borzı, V, Emanuele, V 2nd, Cannata, F, Capitano, G, Cignarelli, M, Piemontese, S, Capuano, G, Carro, S, Cazzalini, C, Cocco, L, Ciccarone, Am, Cicioni, G, Cossu, E, Sano, F, Cucinotta, D, Di Benedetto, A, De Mattia, G, Mollica, Mr, De Cosmo, S, Minenna, A, Dei Cas, A, De Simone, G, Di Berardino, P, Dotta, F, Contini, V, Franzetti, I, Frontoni, S, Gadaleta, G, Galeone, G, Magiar, Av, Garofano, Mr, Gentile, S, Guarino, G, Giansanti, R, Genovese, S, Giancaterini, A, Leotta, S, Gianni, E, Burrafato, S, Giordano, C, Gigante, A, Cicalo, A, Giorgino, F, Gnasso, A, Fiaschi, E, Grossi, G, Deverardinis, F, Ianni, L, Iovine, C, Lauro, R, Federici, M, Spallone, V, Lo Presti, A, Scarpetta, Am, Lunari, R, Manna, R, Margotta, A, Mantovani, E, Matteoli, Mc, Matteucci, E, Chiesi, F, Maran, A, Mascetti, P, Quintana, T, Mazzucca, P, Melga, P, Cordera, R, Meloncelli, I, Morano, S, Morviducci, L, Nannipieri, M, Parillo, M, Pacifico, A, Pascal, G, Papini, E, Graziano, F, Passaro, A, Pata, P, Pontiroli, Ae, Pozzilli, P, Cipolloni, L, Guglielmi, C, Puccio, L, Raffa, Lm, Richini, D, Romano, R, Rotella, C, Santantonio, G, Sbriglia, Ms, Songini, M, Cau, V, Scorsone, A, Taboga, C, Tatti, P, Turco, A, Trovati, M, Fiori, E, Vasta, M, Vitale, F, Zavaroni, D, Buzzetti, R, Bosi, E, Giaccari, A, Di Pietro, S, Suraci, C, Locatelli, M, Bazzigaluppi, E, Falorni, A, Tiberti, C, Capizzi, M, Marandola, L, and Petrone, A.

Subjects
Male, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Type 2 diabetes, Logistic regression, LADA, Settore MED/13 - Endocrinologia, Endocrinology, Insulin, Glutamate Decarboxylase, Medicine (all), Diabete di tipo 1, autoanticorpi, GADA, LADA, Titrimetry, General Medicine, Middle Aged, Diabetes and Metabolism, Titer, Female, Type 2, Type 1, Adult, Risk, medicine.medical_specialty, medicine.drug_class, autoanticorpi, Socio-culturale, GADA, Diabete di tipo 1, Internal medicine, Diabetes mellitus, Diabetes Mellitus, medicine, Humans, Hypoglycemic Agents, Aged, Autoantibodies, Case-Control Studies, Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, Follow-Up Studies, business.industry, Autoantibody, Case-control study, medicine.disease, Sulfonylurea, business
Abstract

ObjectiveThe aim of this study was to determine whether glutamic acid decarboxylase antibody (GADA) titer and other clinical parameters could define the risk of progression to insulin therapy in latent autoimmune diabetes in adults (LADA) patients during a 7-year follow-up.MethodsThis study involved 220 LADA and 430 type 2 diabetes subjects followed up for 7 years from the time of GADA screening to evaluate their progression toward insulin therapy. Kaplan–Meier curves and multivariate logistic regression analysis were performed to identify the markers capable of influencing this progression.ResultsDuring the follow-up, the drop out was 4% in both groups. A total of 119 (56.1%) out of 212 LADA patients required insulin during the 7 years of follow-up. The Kaplan–Meier plots showed that 74/104 (71.1%) of high GADA titer required insulin compared with 45/108 (41.6%) of low GADA titer and with 86/412 (20.9%) of type 2 diabetes (P2and IA-2ICand zinc transporter 8 (ZnT8) positivity were also shown as the markers of faster progression (PPPConclusionsHigh GADA titer, BMI ≤ 25, ZnT8 and IA-2ICpositivity and sulfonylurea treatment, in the first year from diagnosis, significantly increase the progression toward insulin requirement in LADA patients.

Published
2014
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10. Effect of Sibutramine on Cardiovascular Outcomes in Overweight and Obese Subjects

Author

James, Wp, Caterson, Id, Coutinho, W, Finer, N, VAN GAAL LF, Maggioni, Ap, TORP-PEDERSEN, C, Sharma, Am, Shepherd, Gm, Rode, Ra, Renz, Cl, Van Gaal LF, Torp-Pedersen, C, Pepine, C, Pocock, S, Drexler, H, Swedberg, K, Sleight, P, Armstrong, P, Kerr, D, Dagenais, G, Brophy, J, Avezum, A, Bogaty, P, Fabbri, G, Galli, M, Hildebrandt, P, Mann, J, Ostergren, J, Sherman, D, Zannad, F, Colquhoun, D, Hollanders, G, e Forti A, Costa, Cifkova, R, Toubro, S, Ziegler, O, Scherbaum, Wa, Jordan, J, Halmy, L, Ferrannini, E, Santini, F, Gonzalez, C, Narkiewicz, K, Hancu, N, Payer, J, Pascual, J, Wilding, J, Campbell, L, Carey, D, Gerstman, M, Karrasch, J, Lefkovits, J, Marks, J, Marks, S, Moses, R, Phillips, P, Proietto, J, Roberts, D, Roberts-Thomson, P, Shaw, J, Simpson, R, Singh, B, Singleton Jeffries, W, Stuckey, B, Boland, J, Brohet, C, Coucke, F, Dendale, P, Jouret, G, Kolanowski, J, Kutnowski, M, Martens, F, Muls, E, Peiffer, F, Penninckx, H, Scheen, A, Schoors, D, Vaerenberg, M, Van Cleemput, J, Van Crombrugge, P, Van Kuyk, M, Verhaegen, A, Wollaert, B, de Albuquerque DC, Appolinario, J, de Godoy Matos AF, Gross, Jl, Halpern, A, Kerr Saraiva JF, Milagres, R, Repetto, G, Suplicy, Hl, Zanella, Mt, Bednarova, J, Cepelak, V, Cerny, P, Hainer, V, Havranek, P, Homza, M, Jansa, P, Karlicek, M, Kolesar, J, Kotik, I, Kucera, D, Kuchar, J, Kunc, M, Kvapil, M, Linhart, A, Machova, V, Matuska, J, Oral, I, Pavlas, J, Pesatova, S, Povolny, J, Semrad, B, Smetana, K, Soucek, M, Svacina, S, Tesinsky, P, Urbanek, R, Wasserburger, B, Zachoval, R, Zahumensky, E, Zidkova, E, Astrup, A, Dominguez, H, Faber, J, Hilderbrant, P, Kober, L, Perrild, H, Richelsen, B, Sogaard, P, Svendsen, Ol, Urhammer, S, Archambeaud, F, Basdevant, A, Borys, Jm, Bringer, J, Brunetiere, C, Charpentier, G, Cocaul-André, M, Dabadie, H, Dubreuil, A, Estour, B, Gautier, Jf, Gibault, T, Halimi, S, Hespel, Jp, Issa Sayegh, M, Krempf, M, Laville, M, Lecerf, Jm, Louvet, Jp, Penfornis, A, Ritz, P, Schlienger, Jl, Schmitt, B, Valensi, P, Baar, M, Beermann, J, Bock, M, Boenner, G, Dammann, Hg, Diehm, C, Ditschuneit, H, Gadow, J, Gehlhar, S, Gessner, S, Guthersohn, A, Hamann, A, Hanefeld, M, Hasenfuss, G, Herzner, A, Heun, Kc, Heufelder, Ae, Hohensee, H, Jacob, S, Krings, P, Krätzig, B, Krosse, B, Lehmann, Rt, Mindt-Prüfert, S, Maisch, B, Pfeiffer, Af, Richard, F, Rose, B, Schmidt, E, Scholze, J, Schreckenberg, A, Stuebler, P, Walter, J, Wirth, A, Wunderlich, J, Abraham, G, Altorjay, A, Augusztin, G, Csaszar, A, Czuriga, I, Dinnyes, J, Gero, L, Gyimesi, A, Janosi, A, Kovacs, I, Liziczai, I, Majtenyi, A, Medvegy, M, Nadhazi, Z, Pados, G, Polak, G, Ronaszeki, A, Sido, Z, Simon, K, Anzà, C, Bevilacqua, M, Bosello, O, Chiariello, M, Cordera, R, Ferrari, E, Frittitta, L, Giorgino, R, Liuzzi, A, Malinverni, C, Di Mario, U, Melchionda, N, Occhi, G, Perticone, F, Pinchera, A, Pinelli, G, Rovera, G, Santeusanio, F, Urbinati, S, Alpizar-Salazar, M, Carrillo-Ortega, E, Fanghanel Salmon, G, Laviada-Molina, Ha, Madero, Ma, Rodriguez, G, Saldate, C, Sanchez-Castillo, Cp, Violante, Rm, Wacher, N, Zayas-Jaime, Fj, Zuniga-Guajardo, S, Adamiec, R, Banasiak, W, Chrusciel, P, Derlaga, B, Gebala, A, Gessek, J, Janik, K, Janion, M, Kalina, Z, Kozlowski, A, Kusnierz, B, Majcher, Z, Miekus, P, Niegowska, J, Okopien, B, Ostrowska, L, Pasowicz, M, Piepiorka, M, Pluta, W, Polaszewska-Muszynska, M, Ponikowski, P, Pupek-Musialik, D, Sawicki, A, Sobocik, H, Stankiewicz, A, Szpajer, M, Trojnar, R, Tykarski, A, Wrabec, K, Wyrzkowski, B, Zahorska-Markiewicz, B, Zalewski, M, Carrageta, M, Mendes Pedro MM, Parente Martins LM, dos Santos, L, Babes, A, Creteanu, G, Dan, Ga, Dragulescu, Si, Graur, M, Tirgoviste, Ci, Morosanu, M, Mota, M, Paveliu, Fs, Radoi, M, Ranetti, A, Totoian, I, Andre, I, Bugan, V, Cencarik, J, Csala, L, Farsky, S, Gonsorcik, J, Kamensky, G, Kmec, J, Krahulec, B, Kurian, R, Macek, V, Majercak, I, Micko, K, Mokan, M, Riecansky, I, Sojka, G, Uhliar, R, Urgeova, L, Vancik, J, Baro, Fm, Barrios Merino, A, Borras, Jl, Caixas, A, Cuatrecasas Cambra, G, Dominguez Escribano JR, Duran Garcia, S, Escobar-Jimenez, L, Esteva de Antonio, I, Formiguera Sala, X, Garcia-Luna, Pp, Garcia Robles, R, Gonzalez Albarran, O, Hernandez-Mijares, A, Martin Hidalgo, A, Masmiquel Comas, L, Morales Perez, F, Moreno Esteban, B, Pascual Izuel JM, Redon Mas, J, Ricart, W, Rubio, Ma, Ruilope, Lm, Salas-Salvado, J, Terroba Larumbe, M, Tinahones, F, de la Torre Casares ML, Vidal Cortada, J, Zuniga-Perez Lemaur, M, Abdulhakim, Ee, Adler, A, Barnett, Ah, Bodmer, C, Campbell, Iw, Chowdhury, T, Cleland, J, Cook, Rc, Dinneen, S, Donnachie, H, Haslam, Dw, Hillis, Gs, Horne, M, Howarth, Dj, Hughes, E, Jackson, S, Jones, Sc, Jones, Th, Kumar, S, Lean, M, Maroni, J, Mcinnes, G, Middleton, A, Morris, A, Newcombe, G, O'Kane, Kp, Pavel, Ic, Pawa, R, Perry, C, Pitts, C, Raja, A, Reckless, J, Robinson, J, Sarmiento, R, Soo, Sc, Taylor, S, Thomas, Ho, Thomson, Ma, and Wilkins, M.

Subjects
Male, medicine.medical_specialty, Myocardial Infarction, Blood Pressure, Kaplan-Meier Estimate, Type 2 diabetes, Klinikai orvostudományok, Placebo, law.invention, Double-Blind Method, Randomized controlled trial, Weight loss, law, Internal medicine, Appetite Depressants, medicine, Humans, Obesity, Myocardial infarction, Stroke, Aged, business.industry, Hazard ratio, Orvostudományok, General Medicine, Middle Aged, Overweight, medicine.disease, Surgery, Diabetes Mellitus, Type 2, Cardiovascular Diseases, Cardiology, Female, Human medicine, medicine.symptom, business, Cyclobutanes, Sibutramine, medicine.drug
Abstract

Background The long-term effects of sibutramine treatment on the rates of cardiovascular events and cardiovascular death among subjects at high cardiovascular risk have not been established. Methods We enrolled in our study 10,744 overweight or obese subjects, 55 years of age or older, with preexisting cardiovascular disease, type 2 diabetes mellitus, or both to assess the cardiovascular consequences of weight management with and without sibutramine in subjects at high risk for cardiovascular events. All the subjects received sibutramine in addition to participating in a weight-management program during a 6-week, single-blind, lead-in period, after which 9804 subjects underwent random assignment in a double-blind fashion to sibutramine (4906 subjects) or placebo (4898 subjects). The primary end point was the time from randomization to the first occurrence of a primary outcome event (nonfatal myocardial infarction, nonfatal stroke, resuscitation after cardiac arrest, or cardiovascular death). Results The mean duration of treatment was 3.4 years. The mean weight loss during the lead-in period was 2.6 kg; after randomization, the subjects in the sibutramine group achieved and maintained further weight reduction (mean, 1.7 kg). The mean blood pressure decreased in both groups, with greater reductions in the placebo group than in the sibutramine group (mean difference, 1.2/1.4 mm Hg). The risk of a primary outcome event was 11.4% in the sibutramine group as compared with 10.0% in the placebo group (hazard ratio, 1.16; 95% confidence interval [CI], 1.03 to 1.31; P=0.02). The rates of nonfatal myocardial infarction and nonfatal stroke were 4.1% and 2.6% in the sibutramine group and 3.2% and 1.9% in the placebo group, respectively (hazard ratio for nonfatal myocardial infarction, 1.28; 95% CI, 1.04 to 1.57; P=0.02; hazard ratio for nonfatal stroke, 1.36; 95% CI, 1.04 to 1.77; P=0.03). The rates of cardiovascular death and death from any cause were not increased. Conclusions Subjects with preexisting cardiovascular conditions who were receiving long-term sibutramine treatment had an increased risk of nonfatal myocardial infarction and nonfatal stroke but not of cardiovascular death or death from any cause. (Funded by Abbott; ClinicalTrials.gov number, NCT00234832.)

Published
2010
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11. Serum levels of osteopontin predict diabetes remission after bariatric surgery.

Author

CarboneThe author names have been tagged as given names and surnames (surnames are highlighted in teal color). Please confirm if they have been identified correctly.-->, F-->., Adami, G-->., Liberale, L., Bonaventura, A-->., Bertolotto, M-->., Andraghetti, G-->., Scopinaro, N-->., Camerini, G.B., Papadia, F.S., Cordera, R., Dallegri, F., and Montecucco, F-->.

Subjects
GASTRIC bypass, BARIATRIC surgery, TYPE 2 diabetes, OSTEOPONTIN, WEIGHT loss, DIABETES
Abstract

-->Bariatric surgery has been shown to effectively improve glycaemic control in morbidly obese subjects. However, the molecular bases of this association are still elusive and may act independently of weight loss. Here, our retrospective study has investigated the inflammatory molecule osteopontin (OPN) as a potential predictor of type 2 diabetes mellitus (T2DM) remission. -->Baseline serum levels of OPN were analyzed in 41 T2DM patients who underwent bariatric surgery. Anthropometric measures and biochemical variables, including insulin sensitivity indices (HOMA2), were assessed at baseline and at 1 and -->3 years after surgery. -->At baseline, patients who experienced T2DM remission had increased waist circumference, body weight and BMI, and higher serum OPN, compared with non-remitters. Patients with and without T2DM remission improved their lipid and glucose profiles, although insulin -->resistance indices were only improved in the T2DM remission group. In the overall cohort of both T2DM remission and non-remission patients, baseline circulating levels of OPN significantly correlated with reductions of body weight and BMI over time, and insulin sensitivity improved as well. However, only the HOMA2-%S remained independently associated with serum OPN on multivariate linear regression analysis (B: 0.227, 95% CI: 0.067–0.387, β = 0.831; P --> = 0.010). Baseline values of OPN predicted 3-year T2DM remission independently of body weight loss, lower BMI and duration of diabetes (OR: 1.046, 95% CI: 1.004–1.090; P --> = 0.033). -->Although larger studies are still needed to confirm our preliminary results, pre -->-operative OPN serum levels might be useful for predicting 3-year T2DM remission independently of weight loss in patients undergoing bariatric surgery. [ABSTRACT FROM AUTHOR]

Published
2019
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15. Sulfonylurea treatment of type 2 diabetic patients does not reduce the vasodilator response to ischemia.

Author

Spallarossa, Paolo, Rossettin, Pierfranco, Cordone, Stefano, Olivotti, Luca, Brunelli, Claudio, Schiavo, Mara, Cordera, Renzo, Spallarossa, P, Schiavo, M, Rossettin, P, Cordone, S, Olivotti, L, Cordera, R, and Brunelli, C

Subjects
GLIBENCLAMIDE, DIET therapy, TYPE 2 diabetes treatment, ISCHEMIA
Abstract

Objective: Sulfonylureas block the activation of vascular potassium-dependent ATP channels and impair the vasodilating response to ischcmia in nondiabetic individuals, but it is not know whether this occurs in type 2 diabetic patients under chronic treatment with these drugs. Glimepiride, a new sulfonylurea, apparently has no cardiovascular interactions. The aim of our study was to compare the effect of the widely used compound glibenclamide, the pancreas-specific glimepiride, and diet treatment alone on brachial artery response to acute forearm ischemia.Research Design and Methods: Brachial artery examination was performed by a high-resolution ultrasound technique on 20 type 2 diabetic patients aged mean +/- SD) 67 +/- 2 years and on 18 nondiabetic patients matched for age, hypertension, and dislipidemia. Diabetic subjects underwent three separate evaluations at the end of each 8-week treatment period, during which they received glibenclamide, glimepiride, or diet alone according to crossover design. Scans were obtained before and after 4.5 min of forearm ischemia. Postischemic vasodilation and hyperemia were expressed as percent variations in vessel diameter and blood flow.Results: Postischemic vasodilation and hyperemia were, respectively, 5.42 +/- 0.90 and 331 +/- 38% during glibenclamide, 5.46 +/- 0.69 and 326 +/- 28% during glimepiride, and 5.17 +/- 0.64 and 357 +/- 35% during diet treatment (NS). These results were similar to those found in the nondiabetic patients (6.44 +/- 0.68 and 406 +/- 42%, NS).Conclusions: In type 2 diabetic patients, the vasodilating response to forearm ischemia was the same whether patients were treated with diet treatment alone or with glibenclamide or glimepiride at blood glucose-lowering equipotent closes. [ABSTRACT FROM AUTHOR]

Published
2001
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22. Serum leptin and weight loss in severely obese patients undergoing biliopancreatic diversion.

Author

Adami, G F, Cordera, R, Campostano, A, Bressani, A, Cella, F, and Scopinaro, N

Subjects
*LEPTIN, *INGESTION, *OBESITY
Abstract

OBJECTIVE: To evaluate the influence of body fat and food intake on serum leptin concentration. DESIGN: Longitudinal study of a group of obese patients prior to and at, long term follow-up, after biliopancreatic diversion (BPD), when body weight was steadily reduced and food consumption was similar to or greater than preoperatively. RESULTS: In obese patients, very high serum leptin concentrations were found. Following the operation, with the body weight stable and normalized, a sharp fall of serum leptin concentration had occurred, with values returned to normal range. CONCLUSION: The changes in serum leptin concentration observed in the long term after weight loss are substantially accounted for by the loss of body fat and appear unrelated to the reduction of oral food intake. [ABSTRACT FROM AUTHOR]

Published
1998
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33. Caveolin-1 is essential for glimepiride-induced insulin secretion in the pancreatic βTC-6 cell line

Author

Puddu, A., Salani, B., Cordera, R., Viviani, G.L., and Maggi, D.

Subjects
*BIOLOGICAL transport, *CELL lines, *INSULIN, *PANCREATIC secretions
Abstract

Abstract: The KATP channels play a pivotal role in the complex mechanism of insulin secretion. KATP channels represent the target of sulphonylureas, a class of drugs widely used in type 2 diabetes to stimulate insulin secretion. We previously showed that caveolin-1 depletion impairs action of the sulphonylurea glimepiride in human endothelial cells. The aim of this work was to investigate the possible role of caveolin-1 in glimepiride-induced insulin secretion. Caveolin-1 was depleted using siRNA method in the pancreatic βTC-6 cell line. Then stimulation of insulin secretion was performed with different secretagogues (glucose, KCl, and glimepiride). Here, we show that βTC-6 caveolin-1 depleted cells maintained high rate of insulin secretion after KCl, but not after glucose and glimepiride stimulation. Moreover, we find a direct interaction between caveolin-1 and Kir6.2, one of the KATP channel subunit. These results demonstrate that Cav-1 plays a critical role for glucose and sulfonylurea-stimulated insulin secretion. [Copyright &y& Elsevier]

Published
2008
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34. IGF-I induced rapid recruitment of integrin β1 to lipid rafts is Caveolin-1 dependent

Author

Salani, B., Briatore, L., Contini, P., Passalacqua, M., Melloni, E., Paggi, A., Cordera, R., and Maggi, D.

Subjects
*SOMATOMEDIN, *INTEGRINS, *MEMBRANE proteins, *CELL membranes, *GENETIC regulation, *CELL lines, *IMMUNOFLUORESCENCE, *FLOW cytometry
Abstract

Abstract: Caveolin-1 (Cav-1) regulates both insulin like growth factor receptor (IGF-IR) and integrin β1 function. However, the role of Cav-1 in IGF-IR/integrin β1 cross talk remains to be established. In this study, we observed that IGF-I did not induce integrin β1 internalization but its plasma membrane reorganization. In particular, we found a rapid and transient association between integrin β1 and Cav-1 followed by the enrichment of integrin β1 in lipid rafts. To determine the role of Cav-1 in this process, we transfected Hacat cells with small interfering RNA specific for Cav-1 (siRNA-Cav-1) and with a scrambled siRNA as control (siRNA-Ctr). Cav-1 down regulated Hacat cells were then stimulated with IGF-I and analyzed by immunofluorescence and flow cytometry. We found that Cav-1 silencing abolished the recruitment of integrin β1 to lipid rafts in the presence of IGF-I. These data demonstrate that IGF-IR/integrin β1 cross talk is followed by integrin β1 lipid raft compartmentalization and that Cav-1 is required for this process. [Copyright &y& Elsevier]

Published
2009
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