23 results on '"Mohan, V."'
Search Results
2. High prevalence of diabetes and impaired glucose tolerance in India: National Urban Diabetes Survey
- Author
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Ramachandran, A., primary, Snehalatha, C., additional, Kapur, A., additional, Vijay, V., additional, Mohan, V., additional, Das, A. K., additional, Rao, P. V., additional, Yajnik, C. S., additional, Prasanna Kumar, K. M., additional, and Nair, Jyotsna D., additional
- Published
- 2001
- Full Text
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3. Intimal medial thickness of the carotid artery in South Indian diabetic and non-diabetic subjects: the Chennai Urban Population Study (CUPS)
- Author
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Mohan, V., primary, Ravikumar, R., additional, Shanthi Rani, S., additional, and Deepa, R., additional
- Published
- 2000
- Full Text
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4. Family studies of non-insulin-dependent diabetes mellitus in South Indians
- Author
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McCarthy, M. I., primary, Hitman, G. A., additional, Shields, D. C., additional, Morton, N. E., additional, Snehalatha, C., additional, Mohan, V., additional, Ramachandran, A., additional, and Viswanathan, M., additional
- Published
- 1994
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5. Anthropometric measures and glucose levels in a large multi-ethnic cohort of individuals at risk of developing type 2 diabetes.
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Koning, L., Gerstein, H., Bosch, J., Diaz, R., Mohan, V., Dagenais, G., Yusuf, S., and Anand, S.
- Abstract
We determined: (1) which of BMI, waist circumference, hip circumference and WHR has the strongest association and explanatory power for newly diagnosed type 2 diabetes and glucose status; and (2) the impact of considering two measures simultaneously. We also explored variation in anthropometric associations by sex and ethnicity. We performed cross-sectional analysis of 22,293 men and women who were from five ethnic groups and 21 countries, and at risk of developing type 2 diabetes. Standardised anthropometric associations with type 2 diabetes and AUC of glucose status from OGTT (AUC
OGTT ) were determined using multiple regression. Explanatory power was assessed using the c-statistic and adjusted r2 . An increase in BMI, waist circumference or WHR had similar positive associations with type 2 diabetes, AUCOGTT and explanatory power after adjustment for age, sex, smoking and ethnicity ( p < 0.01). However, using BMI and WHR together resulted in greater explanatory power than with other models ( p < 0.01). Associations were strongest when waist circumference and hip circumference were used together, a combination that had greater explanatory power than other models except for BMI and WHR together ( p < 0.01). Results were directionally similar according to sex and ethnicity; however, significant variations in associations were observed among these subgroups. The combination of BMI and WHR, or of waist circumference and hip circumference has the best explanatory power for type 2 diabetes and glucose status compared with a single anthropometric measure. Measurement of waist circumference and hip circumference is required to optimally identify people at risk of type 2 diabetes and people with elevated glucose levels. [ABSTRACT FROM AUTHOR]- Published
- 2010
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6. Positive association in the absence of linkage suggests a minor role for the glucokinase gene in the pathogenesis of Type 2 (non-insulin-dependent) diabetes mellitus amongst South Indians.
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McCarthy, M., Hitchins, M., Hitman, G., Cassell, P., Hawrami, K., Morton, N., Mohan, V., Ramachandran, A., Snehalatha, C., and Viswanathan, M.
- Abstract
Mutations of the glucokinase gene have been implicated in the development of glucose intolerance in pedigrees with maturity-onset diabetes of the young. However, the contribution of the glucokinase gene to the aetiology of common Type 2 (non-insulin-dependent) diabetes mellitus is uncertain. We have studied the role of the glucokinase gene in the pathogenesis of Type 2 diabetes in South Indians, using both population-association and linkage methodology. A pair of CA-repeat sequences (GCK(3′) and GCK(5′)) straddling the glucokinase gene were employed as markers, each subject being typed using the polymerase chain reaction and polyacrylamide gel electrophoresis. Comparisons of allele frequencies at these markers were made between 168 Type 2 diabetic subjects and 70 racially-matched control subjects. No differences in allele frequencies were apparent at the GCK(5′) marker; however, there were significant differences in allele frequencies at the GCK(3′) marker between the Type 2 diabetic subjects and control subjects ( χ=11.6, df=3, p=0.009) with an increase of the z allele (78.0% vs 66.4%) and a decrease of the z+2 allele (13.7% vs 25.0%) amongst the diabetic subjects. Linkage between glucose intolerance and the glucokinase gene was studied in 53 nuclear pedigrees under a variety of genetic models. Linkage was excluded (lod score <−2) at a recombination fraction of zero under five of the ten models used and highly unlikely (−2 < lod score <−1) under the others. The combination of positive association and negative linkage suggests that glucokinase acts as a minor gene influencing the development of Type 2 diabetes within this population. [ABSTRACT FROM AUTHOR]
- Published
- 1993
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7. A genetic study of retinopathy in South Indian Type 2 (non-insulin-dependent) diabetic patients.
- Author
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Hawrami, K., Mohan, R., Mohan, V., and Hitman, G.
- Abstract
Genetic marker studies in diabetic retinopathy are controversial and frequently complicated by possible independent associations of Type 1 (insulin-dependent) diabetes mellitus with the markers so far analysed. We have looked for associations of candidate genes with retinopathy in South Indian Type 2 (non-insulin-dependent) diabetic patients; patients were subdivided into those with exudative maculopathy ( n=53), proliferative retinopathy ( n=40) and patients free from diabetic retinopathy with a minimum disease duration of 15 years ( n=45). DNA was extracted from blood samples and studied by Southern blot hybridisation techniques and the following probe enzyme combinations: HLA-DQB1; Taq 1, HLA-DQA1; Taq 1, HLA-DRA; Bgl II, insulin gene hypervariable region; Pvu II and the switch region of the immunoglobulin IgM heavy chain gene (Sμ); Sac I. Differences in genotype distributions between the study groups were only detected with the Sμ probe which detects polymorphism of both Sμ and Sα1 (the switch region of IgA). Two alleles of Sα1 were detected sized 7.4 kilobase and 6.9 kilobase. The frequency of 6.9 kilobase homozygotes was lower in proliferative retinopathy (19%) compared to patients free from diabetic retinopathy (54%, p=0.005) and exudative maculopathy (46%, p=0.03). This data suggests that there is a genetic predisposition to proliferative retinopathy in Type 2 (non-insulin-dependent) diabetes of South Indian origin and that this is determined by polymorphism of the heavy chain immunoglobulin genes located on chromosome 14. [ABSTRACT FROM AUTHOR]
- Published
- 1991
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8. The genetic predisposition to fibrocalculous pancreatic diabetes.
- Author
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Kambo, P., Hitman, G., Mohan, V., Ramachandran, A., Snehalatha, C., Suresh, S., Metcalfe, K., Ryait, B., and Viswanathan, M.
- Abstract
Fibrocalculous pancreatic diabetes (previously known as tropical pancreatic diabetes) is a rare cause of diabetes confined to countries within the tropical belt. The aetiology of fibrocalculous pancreatic diabetes is thought to be environmental although the agent(s) is unknown. We have investigated a possible genetic basis of this disease by looking for restriction fragment length polymorphisms of genes implicated in the aetiology of diabetes mellitus. Seventy-six Dravidian patients with fibrocalculous pancreatic diabetes were studied, and the restriction fragment length polymorphisms obtained compared to racially matched control subjects ( n=94), patients with Type 2 (non-insulin-dependent) diabetes ( n=87) and Type 1 (insulin-dependent) diabetes ( n=58). No association of fibrocalculous pancreatic diabetes was found with restriction fragment length polymorphisms of the insulin receptor gene. Although no association of fibrocalculous pancreatic diabetes was found with polymorphism of the HLA DRα/DQα/DXα genes, an association was found with the Taq 1 restriction fragment length polymorphisms of the DQβ gene (DQβ T2/T6 present in 39% of patients with fibrocalculous pancreatic diabetes compared to 19% in control subjects; p=0.01; corrected p value=0.04) which is similar to that found in Type 1 but not Type 2 diabetes. An association of fibrocalculous pancreatic diabetes was also found with the hypervariable region in the 5-prime flanking region of the insulin gene; 40% of patients possessed the class 3 allele compared to 9.5% of control subjects p=0.0001; corrected p value=0.0008). In Type 2 diabetes, similar results were obtained with 33% subjects possessing the class 3 allele ( p value compared to control subjects=0.0005; corrected p value=0.004). This study suggests that fibrocalculous pancreatic diabetes has a genetic component in its aetiology. Furthermore, its origin might be related to an individual with part of the genetic predisposition to diabetes (Type 1 or Type 2) who additionally has evidence of chronic calcific pancreatitis. [ABSTRACT FROM AUTHOR]
- Published
- 1989
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9. High prevalence of Type 2 (non-insulin-dependent) diabetes among the offspring of conjugal Type 2 diabetic parents in India.
- Author
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Viswanathan, M., Mohan, V., Snehalatha, C., and Ramachandran, A.
- Abstract
The prevalence of Type 2 (non-insulin-dependent) diabetes among offspring of conjugal Type 2 diabetic parents in India was determined by performing oral glucose tolerance tests. Diabetes was present in 50% of offspring, and 12% had impaired glucose tolerance according to the National Diabetes Data Group criteria. Thus, 62% of all offspring had abnormal glucose tolerance tests. This is the highest prevalence rate for diabetes among offspring of conjugal diabetic parents and might represent an ethnic variation of the genetic factors operating in Indian patients with Type 2 (non-insulin-dependent) diabetes. [ABSTRACT FROM AUTHOR]
- Published
- 1985
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10. Tropical pancreatic diabetes in South India: heterogeneity in clinical and biochemical profile.
- Author
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Mohan, V., Mohan, R., Susheela, L., Snehalatha, C., Bharani, G., Mahajan, V., Ramachandran, A., Viswanathan, M., and Kohner, E.
- Abstract
Clinical and biochemical studies were carried out in 33 patients with diabetes secondary to chronic calcific, non-alcoholic pancreatitis (tropical pancreatic diabetes) and in 35 Type 2 (non-insulin-dependent) diabetic patients and 35 nondiabetic subjects. Despite lower body mass indices, only 25% of patients with tropical pancreatic diabetes had clinical evidence of malnutrition. There was no history of cassava ingestion. Mean serum cholesterol concentration was significantly lower in the tropical pancreatic diabetic patients ( p<0.01) in comparison with the Type 2 diabetic patients or non-diabetic subjects, due to a significantly decreased concentration of LDL cholesterol ( p<0.01) and VLDL cholesterol ( p<0.05). Basal and post-glucose stimulated concentrations of serum C-peptide were highest in those pancreatic diabetic patients ( n=11) who responded to oral hypoglycaemic drugs, intermediate in the majority ( n=17), who were insulin dependent and ketosis resistant and negligible in a small sub-group ( n=5) who were ketosis prone. The occurrence of microangiopathy in pancreatic diabetic patients was common and similar to that in Type 2 diabetic patients. Thus, tropical pancreatic diabetes in South India appears to be heterogenous with respect to level of nutrition, severity of glucose intolerance, B-cell function, response to therapy and the occurrence of microvascular complications. [ABSTRACT FROM AUTHOR]
- Published
- 1985
- Full Text
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11. 35th Annual Meeting of the European Association for the Study of Diabetes
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Melander, A., Olsson, J., Lindberg, G., Salzman, A., Howard, T., Stang, P., Lydick, E., Emslie-Smith, A., Boyle, D. I. R., Evans, J. M. M., Macdonald, T. M., Bain, J., Sullivan, F., Juhl, C., Pørksen, N., Sturis, J., Hollingdal, M., Pincus, S., Veldhuis, J., Dejgaard, A., Schmitz, O., Kristensen, J. S., Frandsen, K. B., Bayer, Th., Müller, P., Dunning, B. E., Paladini, S., Gutierrez, C., Deacon, R., Valentin, M., Grunberger, G., Weston, W. M., Patwardhan, R., Rappaport, E. B., Sargeant, L. A., Wareham, N. J., Khaw, K. T., Zethelius, Björn, Lithell, Hans, Hales, C. Nicholas, Berne, Christian, Lakka, H.-M., Oksanen, L., Tuomainen, T.-P., Kontula, K., Salonen, J. T., Dekker, J. M., de Boks, P., de Vegt, F., Stehouwer, C. D. A., Nijpels, G., Bouter, L. M., Heine, R. J., Bruno, G., Cavallo-Perin, P., Bargero, G., D’Errico, N., Borra, M., Macchia, G., Pagano, G., Newton, R. W., Ruta, D. A., New, J. P., Wallace, C., Roxburgh, M. A., Young, R. J., Vaughan, N. J. A., Elliott, P., Brennan, G., Devers, M., MacAlpine, R., Steinke, D., Lawson, D. H., Decallonne, B., Casteels, K., Gysemans, C., Bouillon, R., Mathieu, C., Linn, Thomas, Strate, Christine, Schneider, Kerstin, Funda, D. P., Jirsa, M., Kozáková, H., Kaas, A., Kofronová, O., Tlaskalová-Hogenová, H., Buschard, K., Wanka, H., Hartmann, A., Kuttler, B., Rasmussen, S. B., Sørensen, T. S., Markholst, H., Petersen, J. S., Karounos, D., Dyrberg, T., Mabley, J. G., Haskó, G., Szabó, C., Seissler, J., Nguyen, T. B. T., Steinbrenner, H., Scherbaum, W. A., Cipriani, R., Gabriele, A., Sensi, M., Guidobaldi, L., Pantellini, F., Cerrito, M. G., Scarpa, S., Di Mario, U., Morano, S., Ceolotto, G., Iori, E., Baritono, E., Del Prato, S., Semplicini, A., Trevisan, R., Zerbini, G., Meregalli, G., Asnaghi, V., Tentori, F., Maestroni, A., Mangili, R., Marescotti, C., Vedovato, M., Tiengo, A., Tadjieva, J., Mankovsky, B. N., Van Aken, S., Raes, A., Vande Walle, J., Matthys, D., Craen, M., Hansen, H. P., Lund, S. S., Rossing, P., Jensen, T., Parving, H.-H., Andersen, S., Tarnow, L., Hansen, B. V., Trautner, C., Haastert, B., Ennenbach, N., Willich, S., Tabák, Á. Gy., Orchard, T. J., Spranger, J., Preissner, K. T., Schatz, H., Pfeiffer, A., Cantón, A., Burgos, R., Hernández, C., Lecube, A., Mesa, J., Segura, R. M., Mateo, C., Simó, R., Fathallah, L., Greene, D. A., Obrosova, I., Gilbert, R. E., Kelly, D. J., Cox, A. J., Berka-Wilkinson, J. L., Taylor, H. R., Panagiotopoulos, S., Lee, V., Jerums, G., Cooper, M. E., Hitman, G. A., Aganna, E., Ogunkolade, W. B., Rema, M., Deepa, R., Shanthi-Rani, C. S., Barakat, K., Kumarajeewa, T. R., Cassell, P. G., McDermott, M. F., Mohan, V., Ways, K., Bursell, S., Devries, T., Woodworth, J., Alatorre, C., King, G., Aiello, L. P., Karisen, A. E., Pavlovic, D., Nielsen, K., Jensen, J., Andersen, H. U., Pociot, F., Mandrup-Poulsen, T., Eizirik, D. L., Nerup, J., Lortz, S., Tiedge, M., Lenzen, S., Lally, F. J., Bone, A. J., Darville, M. I., Ho, Y.-S., Sternesjö, J., Sandler, S., Chen, M.-C., Schuit, F., Pipeleers, D. G., Merezak, S., Hardikar, A., Hoet, J. J., Remacle, C., Reusens, B., Bréant, B., Garofano, A., Czernichow, P., Kubota, N., Terauchi, Y., Miki, H., Tamemoto, H., Yamauchi, T., Nakano, R., Komeda, K., Eto, K., Tobe, K., Kimura, S., Kadowaki, T., Ide, T., Murakami, K., Tsunoda, M., Mochizuki, T., Ozanne, S. E., Nave, B. T., Wang, C. L., Dorling, M. W., Petry, C. J., Koopmans, S. J., van der Bent, C., Que, I., Radder, J. K., Sebokova, E., Sana, A. K., Klimes, I., Ruderman, N., Morviducci, L., Pastore, L., Morelli, S., Sagratella, E., Zorretta, D., Buongiomo, A., Tamburrano, G., Giaccari, A., Martinenghi, Sabina, De Angelis, Gabriella Cusella, Ravasi, Flavio, Bifari, Francesco, Bordignon, Claudio, Falqui, Luca, Kessler, A., Dransfeld, O., Sasson, S., Tomas, E., Zorzano, A., Eckel, J., Thorsby, P., Rosenfalck, A. M., Kjems, L., Hanssen, K. F., Madsbad, S., Birkeland, K. I., Hamilton-Wessler, M., Markussen, J., Bergman, R. N., Melki, V., Hanaire-Broutin, H., Bessières-Lacombe, S., Tauber, J.-P., Home, P. D., Lindholm, A., Riis, A., Rosenstock, J., Schwartz, S., Clark, C., Edwards, M., Donley, D., Swift, P., Mortensen, H. B., Lynggaard, H., Hougaard, P., Cull, C. A., Neil, H. A. W., Frighi, V., Manley, S. E., Holman, R. R., Turner, R. C., Steiner, G., Davis, W. A., Weeraratna, T., Bruce, D. G., Davis, T. M. E., Vergès, B., Duvillard, L., Pont, F., Florentin, E., Gambert, Ph., Benko, B., Ljubić, S., Turk, Z., Granić, M., März, W., Wollschläger, H., Klein, G., Neiss, A., Wehling, M., Huxtable, S. J., Saker, P. J., Walker, M., Frayling, T. M., Levy, J. C., O’Rahilly, S., Hattersley, A. T., McCarthy, M. I., Orecchio, A., Giacchini, A., Dominici, R., Canettieri, G., Trinti, B., Zani, M., Andreoli, M., Sciacchitano, S., de Silva, A. M., Whitecross, K., Pasco, J., Kotowicz, M., Nicholson, G., Zimmet, P., Boyko, E. J., Collier, G. R., Frittitta, L., Pizzuti, A., Argiolas, A., Graci, S., Goldfine, I. D., Bozzali, M., Ercolino, T., Costanzo, B., Iacoviello, L., Tassi, V., Trischitta, V., Wauters, M., Rankinen, T., Mertens, I., Chagnon, M., Bouchard, C., Van Gaal, L., Sivenius, K., Valve, R., Hakkarainen, V., Niskanen, L., Laakso, M., Uusitupa, M., Beridze, N., Japaridze, M., Kurashvili, R., Dundua, M., Kebuladze, G., Kazakhashvili, N., Offley-Shore, B., Thomas, B., Ghebremeskel, K., Crawford, M., Lowy, C., Eriksson, Ulf J., Martin Simán, C., Wisse, Bert, Gittenberger-de Groot, Adriana C., Wentzel, P., Eriksson, U. J., Wender-Ożegowska, E., Drews, K., Biczysko, R., Bronisz, A., Rość, D., Graczykowska-Koczorowska, A., Kotschy, M., Sokup, A., Kohnert, K. D., Besch, W., Strese, J., Frick, U., Zander, E., Kemer, W., Škrha, J., Kvasnička, J., Kalvodová, B., Hilgertová, J., Schatteman, K., Goossens, F., Scharpé, S., De Leeuw, I., Hendriks, D., Legakis, I. N., Panayiotou, D., Mountokalakis, Th. D., Enderle, M. D., Beckmann, P., Balletshofer, B., Rittig, K., Maerker, E., Volk, A., Meisner, C., Jacob, S., Matthaei, S., Häring, H. U., Rett, K., Ueda, K., Nakagawa, T., Shimajiri, Y., Kokawa, M., Matsumoto, E., Sasaki, H., Sanke, T., Nanjo, K., McKinnon, Caroline M., Macfarlane, Wendy M., Docherty, Kevin, Furukawa, N., Shirotani, T., Kishikawa, H., Kaneko, K., Araki, E., Shichiri, M., Prentki, M., Roduit, R., Susini, S., Buteau, J., Ejrnæs, A. M., Andersen, N. Aa., Osterhoff, M., Möhlig, M., Ortmann, J., Bikashaghi, F., Mayer, C., Bikashagi, F., Ackermans, M. T., Pereira Arias, A. M., Bisschop, P. H. L. T., Endert, E., Sauerwein, H. P., Romijn, J. A., Gastaldelli, A., Baldi, S., Pettiti, M., Natali, A., Frascerra, S., Camastra, S., Toschi, E., Ferrannini, E., Stingl, H., Krssak, M., Bischof, M. G., Krebs, M., Fürnsinn, C., Nowotny, P., Waldhäusl, W., Roden, M., Neeft, M., Meijer, A. J., Båvenholm, P., Pigon, J., Efendic, S., Kästenbauer, T., Sauseng, S., Sokol, G., Auinger, M., Irsigler, K., Abbott, C. A., Carrington, A. L., Faragher, B., Kulkarni, J., Van Ross, E. R. E., Boulton, A. J. M., Armstrong, D. G., Hadi, S., Nguyen, H. C., Harkless, L. B., Jirkovská, A., Kasalicky, P., Hosová, J., Skibova, J., Uccioli, L., Caselli, A., Giacomozzi, C., Macellari, V., Giurato, L., Lardieri, L., Menzinger, G., Pham, H. T., Rosenblum, B. I., Lyons, T. E., Giurini, J. M., Smakowski, P., Chrzan, J. S., Habershaw, G. M., Veves, A., Foster, A. M., Bates, M., Doxford, M., Edmonds, M. E., Kecha, O., Winkler, R., Martens, H., Collette, J., Lefèbvre, P. J., Greiner, D., Geenen, V., Atlan-Gepner, C., Naspetti, M., Valéro, R., Barad, M., Lepault, F., Vialettes, B., Naquet, P., de Galan, B., Netea, M. G., Hancu, N., Smits, P., Van der Meer, J. W. M., Osterbye, T., Jørgensen, K. H., Tranum-Jensen, J., Fredman, P., Høy, M., Bokvist, K., Olsen, H. L., Horn, T., Gromada, J., Laub, R., Lohmann, T., Hahn, H. J., Adler, T., Emmrich, F., Rabuazzo, A. M., Lupi, R., Dotta, F., Patanè, G., Marselli, L., Realacci, M., Piro, S., Del Guerra, S., Santangelo, C., Navalesi, R., Purrello, F., Marchetti, P., de Vos, P., Visser, L., de Haan, B. J., Klok, P., van Schilfgaarde, R., Poppema, S., Juang, J.-H., Kuo, C.-H., Hsu, B. R.-S., Nacher, V., Pérez, M., Biarnés, M., Raurell, M., Soler, J., Montanya, E., Ritzel, R., Maubach, J., Büsing, M., Becker, T., Klempnauer, J., Hücking, K., Schmiegel, W. H., Nauck, M. A., Bouček, P., Saudek, F., Adamec, M., Kožitarová, R., Jedináková, T., Vlasáková, Z., Skibová, J., Bartoš, V., Maffi, P., Bertuzzi, F., Aldrighetti, L., Taglietti, M. V., Castelnuovo, A., Pozza, G., Di Carlo, V., Secchi, A., Renier, G., Mamputu, J.-C., Gillespie, J. S., McMaster, D., Mercer, C., Trimble, E. R., Lecomte, M., Véricel, E., Paget, C., Ruggiero, D., Lagarde, M., Wiernsperger, N., Pricci, F., Leto, G., Amadio, L., Cordone, S., Iacobini, C., Catalano, S., Violi, F., Rotella, C. M., Pugliese, G., Zicari, A., Gradini, R., Sale, P., Pala, L., Cresci, B., Giannini, S., Manuelli, C., Dahlfors, G., Arnqvist, H. J., Gonelle-Gispert, C., Halnan, P. A., Sadoul, K., Wolter, S., Lang, J., Niwa, T., Yu, W., Hidaka, H., Senda, T., Niki, I., Fukasawa, T., Renstrom, E., Barg, S., Seward, E., Rorsman, P., Rutter, G. A., Molinete, M., Lilla, V., Ravazzola, M., Halban, P. A., Efanov, A. M., Bertorello, A. M., Zaitsev, S. V., Zwiller, J., Berggren, P.-O., MŞengül, A., Salman, F., Sargrn, M., Özer, E., Karşidaǧ, K., Salman, S., Gedik, S., Satman, İ., Dinççaǧ, N., Yılmaz, M. T., Lloyd, A., Hopkinson, P. K., Testa, M. A., Blonde, L., Turner, R. R., Hayes, J., Simonson, D. C., van der Ven, N. C. W., Lubach, C. H. C., Snoek, F. J., Mollema, E. D., van der Ploeg, H. M., Danne, T., Hoey, H., McGee, H., Fitzgerald, H., Lernmark, B., Thernlund, G., Fredin, K., Hägglöf, B., Lugari, R., Dell’Anna, C., Ugolotti, D., Dei Cas, A., Barilli, A. L., Sard, L., Marani, B., Iotti, M., Zandomeneghi, R., Gnudi, A., Kjems, L. L., Volund, Aa., Toft-Nielsen, M., Damholt, M. B., Hilsted, L., Hughes, T. E., Krarup, T., Holst, J. J., Young, A., Gottlieb, A., Fineman, M., Kolterman, O., Cancelas, J., García-Martínez, J. A., Villanueva-Peñacarrillo, M. L., Valverde, I., Malaisse, W. J., Filipsson, K., Ahrén, B., Balkan, B., Kwasnik, L., Battle, B., Li, X., Egan, J. M., Clocquet, A. R., Elahi, D., Petrella, E., Pricket, K., Petersen, K. F., Sullivan, J. T., Amatruda, J. M., Livingston, J. N., Shulman, G. I., Freyse, E.-J., Knospe, S., Glund, K., Demuth, H.-U., Walker, D., Malik, R. A., Reljanovic, M., Barada, A., Milicevic, Z., Tack, Cees J., Goldstein, David S., Van Huysen, C., Stevens, M. J., Cao, X., Sundkvist, G., Dahlin, L.-B., Eriksson, K.-F., Rosén, I., Lattimer, S. A., Sima, A. A. F., Sullivan, K., Shaw, J. E., de Courten, M. P., Zimmet, P. Z., Gourdy, P., Ruidavets, J. B., Arveiler, D., Amouyel, Ph., Bingham, A., Tauber, J. P., Lam, K. S. L., Wat, N. M. S., Lam, T. H., Janus, E. D., de Pablos, P., Rodriguez, F., Martínez, J., Sánchez, V., Santana, C., García, I., Macías, A., Levin, K., Hother-Nielsen, O., Henriksen, J. E., Beck-Nielsen, H., Brechtel, K., Machann, J., Koch, M., Nielsen, M., Löblein, K., Becker, R., Denignger, M., Renn, W., Machicao, F., Claussen, C. D., Schick, F., Diraison, F., Moulin, P., Beylot, M., Thams, P., Capito, K., Eliasson, Lena, Barg, Sebastian, Göpel, Sven, Kanno, Takahiro, Renström, Erik, Meda, P., Charollais, A., Gjnovci, A., Calabrese, A., Wonkam, A., Caton, D., Wisznievski, L., Serre, V., Cogne, F., Bauquis, J., Bosco, D., Huarte, J., Herrera, P., Gotfredsen, C. 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J., Schiaffini, R., Pantaleo, A., Battocletti, T., Vaccari, V., Brufani, C., Martuscelli, E., Gargiulo, P., Nieszner, E., Posa, I., Kocsis, E., Préda, I., Pogatsa, G., Koltai, M. Z. S., Stefanidis, A., Manoussakis, S., Handanis, S., Zairis, M., Vitalis, D., Dadiotis, L., Fiorina, P., La Rocca, E., Astorri, E., Rossetti, C., Lucignani, G., Giudici, D., Castoldi, R., Mazarakis, N., Giagiakou, E., Karavidas, A., Agellou, A., Karamani, O., Matsakas, E., Caviezel, F., Morricone, L., Ranucci, M., Denti, S., Cazzaniga, A., Enrini, R., Isgrò, G., González de Molina, F. J., Sala, J., Masià, R., Marrugat, J., Kruszewski, P., Wolnik, B., Bieniaszewski, L., Świerblewska, E., Semetkowska-Jurkiewicz, E., Krupa-Wojciechowska, B., Vasilikos, P. G., Alaveras, A. E. G., Anastasopoulos, N. G., Chala, E., Sidira, M., Christakopoulos, P. D., Poulsen, P. L., Hansen, K. W., Ebbehøj, E., Knudsen, S. T., Mogensen, C. E., Ramu, Y., Vidyullatha, Y., Strojek, K., Gorska, J., Morawin, E., Ritz, E., Ciavarella, A., Malini, P. L., Strocchi, E., Fiumi, N., Ambrosioni, E., Idzior-Waluś, B., Stevens, L., McEneny, J., O’Kane, M. J., Moles, K. W., McMaster, C., Young, I. S., Leonhardt, W., Konstadelou, E., Gürlek, Alper, Soedamah-Muthu, S., Taskinen, M. R., Ehnholm, C., Wägner, A., Bayen, Laia, Rigla, M., Ortega, E., Caixàs, A., Mestrón, A., Ordóñez, J., Pérez, A., Sotiropoulou, G., Servais, P. L., Bertolotto, A., Pilo, M., Suchánková, G., Andratschke, S., Tschöp, M., Strasburger, C.-J., Rizzo, L., Aerts, P., Vinckx, M., Ansquer, J. C., Ryan, M., Buter, H., Navis, G. J., de Jong, P. E., de Zeeuw, D., Carreras, G., Giménez, G., Pou, J. M., Howorka, K., Gabriel, M., Pumprla, J., Köves, A., Bhowmik, N. B., Haque, A., Rahman, A., Paleari, F., Gamba, P., Mauri, G., Rovaris, G., Giannattasio, C., Piatti, M. L., Zincone, A., Cavaletti, G., Mancia, G., Lan, S., Arezzo, J., Gerber, R. A., Klioze, S. S., Saponara, C., Tartaglione, T., Cercone, S., Caputo, S., Meloni, T., Brunetti, D., Di Lazzaro, V., Xu, G., Jiang, H. Y., Shy, M. E., Sugimoto, K., Zhang, W.-X., Kuchmerovskaya, T., Donchenko, G., Shymansky, I., Kuchmerovsky, N., Pakyrbaeva, L., Cameron, N. E., Keegan, A., Cotter, M. A., Mirrlees, D., Smale, S. E., Biessels, G. J., Duis, S. E. J., Kamal, A., Gispen, W. H., Carrington, A., Carman, S., Smiarowski, H., Lavoie, D., Sawicki, D., Sabetta, A., Litchfield, J., Van Zandt, M., Sredy, J., Smirnova, V., Strokov, I., Ivanova, L., Ichunina, A., Nakamura, J., Nakayama, M., Hamada, Y., Chaya, S., Kato, K., Kasuya, Y., Mizubayashi, R., Miwa, K., Yasuda, Y., Kamiya, H., Hotta, N., Bíró, K., Kukorelli, T., Szilágyi, N., Kürthy, M., Komáromy, A., Mogyorosi, T., Nagy, K., Çakir, M., Baskal, N., Güllü, S., Elhan, A. H., Erdogan, G., Ziegler, D., Piolot, R., Neubauer, J., Senesi, B., Bonetti, R., Napolitano, A., Canepa, F., Ottonello, P., Schabmann, A., Giménez-Pérez, G., Arroyo, J. A., López, T., Ponz, E., Mauricio, D., Diem, P., Zanchin, L., Suter, S. L., Lefrandt, J. D., Smit, A., van Roon, A. M., Dullaart, R., Voita, D., Mackevics, V., Vitols, A., Lengyel, Cs., Farkas, Gy., Török, T., Légrády, P., Várkonyi, T. T., Kardos, A., Gingl, Z., Kempler, P., Rudas, L., Lonovics, J., Marchand, M., Stevens, L. K., Tarnás, Gy., Estrella, F., Christensen, N. J., Keresztes, K., Barna, I., Hermányi, Zs., Vargha, P., Bonnevie, L., Chanudet, X., Larroque, P., Tutuncu, N. Bascil, Deger, A., Batur, M. K., Yildirir, A., Onalan, O., Aksöyek, S., Kabakçι, G., Erbaş, T., Galicka-Latała, D., Surdacki, A., Gerritsen, J., TenVoorde, B. J., Heethaar, R. M., Tagawa, T. S., Kodama, M., Yoshioka, R., Yamasaki, Y., Didangelos, T., Athyros, V., Kontopoulos, A., Papageorgiou, A., Karamitsos, D., Lacigová, S., Rušavý, Z., Kárová, R., Perrild, H., Kay, L., Jørgensen, T., Bień, A. I., Witek, P., Geraldes, Elizabete, Rodrigues, D., Pereira, L., Doménech, A., Leitão, P., Anagnostopoulos, D., Foster, A. V. M., Nag, S., Barsoum, M., Lewis, G., Dunlop, N., Connolly, V., Bilous, R., Kelly, W., Chantelau, E., Gede, A., Sharman, D., O’Halloran, D., Best, C., Abbas, Z. G., Lutale, J., Gill, G. V., Jarvis, W. R., Archibald, L. K., Corcoran, S., Mansell, J., Pibworth, L., Terada, H., Shiba, T., Utugi, N., Utugi, T., Blum, M., Strobel, J., Höffken, K., Razvi, F. M., Kritzinger, E. E., Taylor, K., Jones, S., Illahi, W., Grüβer, M., Hartmann, P., Hoffstadt, K., van Leiden, H. A., Moll, A. C., Polak, B. C. P., Pietragalla, G. B., Maurino, M., Montanaro, M., Karadeniz, Ş., Tommasini, P., Quadrini, C., Demiraj, V., Rispoli, E., Ota, A., Takama, H., Saito, N., Hemández, C., Lepore, D., Antico, L., Giardina, B., Franconi, F., Michoud, E., Chamot, S., Riva, Ch., Hammes, H.-P., Renner, O., Breier, G., Lin, J., Alt, A., Betzholtz, C., Bretzel, R. G., Manti, R., Gallo, M., Molinar Hin, A., Brignardello, E., Boccuzzi, G., Li, Shanfang, Xiang, Kunsan, Zhang, Rugeng, Shangguan, Xinhong, Wu, Jianrong, Donnan, P. T., Broomhall, J., Hunter, K., Morris, A. D., Ioannidis, G., Peppa, M., Rontogianni, E., Kallifronas, M., Lekatsas, I., Chrysanthopoulou, G., Anthopoulos, L., Kesse, M., Thalassinos, N., Neves, C., Medina, J. L., Lopes, F., Yılmaz, M., Güvener, N., Güvener, M., Kocagöz, T., Böke, E., Paşaoglu, I., Bascil Tutuncu, N., Oto, A., Karvonen, M. K., Koulu, M., Pesonen, U., Mercuri, M., Rauramaa, R., Rutter, M. K., Kestevan, P., McComb, J. M., Marshall, S. M., Sobieska, M., Wiktorowicz, K., Kanters, S. D. J. M., Banga, J. D., Algra, A., Frijns, C. J. M., Beutler, J. J., Fijnheer, R., Nicoloff, G., Baydanoff, S., Stanimirova, N., Petrova, Ch., Lario, S., Campistol, J. M., Cases, A., Clària, J., Iñigo, P., Esmatjcs, E., Sármán, B., Tóth, M., Kocsis, I., Somogyi, A., Bumbure, A., Jachimowicz, K., Samson, J., Tomasiak, M., Sobol, A., Stańczyk, L., Watala, C., Stradina, P., Wiśniewska-Jarosińska, M., Marciniak, D., Więcławska, B., Watała, C., Golański, J., Zinnat, R., Mahmud, I., Büyükasik, Yahya, Demiroğlu, H., Szczepanik, A., Skowroński, M., Murawska, A., Meeking, D. R., Allard, S., Munday, J., Chowienczyk, P., Shaw, K. M., Cummings, M. H., Šimková, R., Jirsa, M., Hadoke, P. W. F., McIntyre, C. A., Jones, G. C., Williams, B. C., Elliott, A. I., McKnight, J. A., Pernow, J., Bombonato, G. C., Finucci, G. F., Zotta, L., Senses, V., Ozyazgan, S., Ince, E., Tunçdemir, M., Oztürk, M., Sultuybek, G., Akkan, A. G., Özyazgan, S., Unlücerci, Y., Bekpınar, S., Meyer, M. F., Lee, B. C., Shore, A. C., Humphreys, J. M., Tooke, J. E., Dell’Omo, G., Giovannitti, G., Caricato, F., Mariani, M., Pedrinelli, R., Kiviet-Boehm, C., Schwelling, V., Matthäei, S., Pfohl, M., McInerney, D., Itoh, H., Ohno, T., Katoh, N., Baumgartner-Parzer, S., Artwohl, M., Graier, W., Ludwig, C., Tachi, Y., Bannai, C., Shinohara, M., Shimpuku, H., Ohura, K., Bertacca, A., Sasvári, M., Szaleczki, E., Pusztai, P., Boes, U., Klaus, E., Dittrich, P., Wagner, Z., Wittmann, I., Pótó, L., Wagner, L., Mazák, I., Nagy, J., Feletto, F., Taboga, C., Tonutti, L., Lizzio, S., Russo, A., Selmo, V., Ceriello, A., Lekakis, J., Papamichael, C. M., Stamatelopoulos, K., Stamatelopoulos, S., Yillar, D. O., Gay, M., Lillaz, E., Passaro, A., Vanini, A., Calzoni, F., D’Elia, K., Carantoni, M., Zuliani, G., Fellin, R., Solini, A., Chwatko, G., Bald, E., Dramais, A.-S., Wallemacq, P. E., Vandeleene, B., Ciaria, M. V., Ariano, M., Strom, R., Gibney, J., Weiss, U., Turner, B., O’Gorman, P., Watts, G., Powrie, J., Crook, M., Shaw, K., and Cummings, M.
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- 1999
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12. Serum immunoreactive insulin responses to a glucose load in Asian Indian and European Type 2 (non-insulin-dependent) diabetic patients and control subjects.
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Mohan, V., Sharp, P., Cloke, H., Burrin, J., Schumer, B., and Kohner, E.
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The serum immunoreactive insulin response to an oral glucose load was estimated in 15 Asian Indian and 29 European non-diabetic subjects, and in 45 Asian Indian and 72 European Type 2 (non-insulin-dependent) diabetic patients. In the non-diabetic group, basal insulin values were higher in the Asian Indians than the Europeans (16.7 ± 3.0 vs. 6.9 ± 0.7 mU/l, p < 0.001), and remained higher throughout the glucose tolerance test. Total insulin response was also higher in the Asian Indians ( p < 0.001), and linear regression analysis revealed basal insulin, body mass index and race to be important predictors of insulin response. Amongst the diabetic patients, basal insulin values were again higher in the Asian Indians compared with the Europeans (18.0±5.0 vs. 11.5±0.9 mU/l, p<0.05). Total insulin response was also greater ( p < 0.01). Linear regression analysis revealed the basal insulin value to be the only significant predictor of insulin response. The results demonstrate higher insulin levels in Asian Indians than Europeans in both normal subjects and Type 2 diabetic subjects. The insulin response to a glucose load is also greater in the Asian Indians. In the control subjects, ethnic differences contribute to this response, whereas in the diabetic patients this is a function of the elevated basal insulin values of the Asian Indians. [ABSTRACT FROM AUTHOR]
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- 1986
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13. Tropical malnutrition diabetes
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McMillan, Donald E., primary and Mohan, V., additional
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- 1986
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14. Glycaemic control is still central in the hierarchy of priorities in type 2 diabetes management.
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Khunti K, Zaccardi F, Amod A, Aroda VR, Aschner P, Colagiuri S, Mohan V, and Chan JCN
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A panel of primary care and diabetes specialists conducted focused literature searches on the current role of glycaemic control in the management of type 2 diabetes and revisited the evolution of evidence supporting the importance of early and intensive blood glucose control as a central strategy to reduce the risk of adverse long-term outcomes. The optimal approach to type 2 diabetes management has evolved over time as the evidence base has expanded from data from trials that established the role of optimising glycaemic control to recent data from cardiovascular outcomes trials (CVOTs) demonstrating organ-protective effects of newer glucose-lowering drugs (GLDs). The results from these CVOTs were derived mainly from people with type 2 diabetes and prior cardiovascular and kidney disease or multiple risk factors. In more recent years, earlier diagnosis in high-risk individuals has contributed to the large proportion of people with type 2 diabetes who do not have complications. In these individuals, a legacy effect of early and optimal control of blood glucose and cardiometabolic risk factors has been proven to reduce cardiovascular and kidney disease events and all-cause mortality. As there is a lack of RCTs investigating the potential synergistic effects of intensive glucose control and organ-protective effects of newer GLDs, this article re-evaluates the evolution of the scientific evidence and highlights the importance of integrating glycaemic control as a pivotal early therapeutic goal in most people with type 2 diabetes, while targeting existing cardiovascular and kidney disease. We also emphasise the importance of implementing multifactorial management using a multidisciplinary approach to facilitate regular review, patient empowerment and the possibility of tailoring interventions to account for the heterogeneity of type 2 diabetes., (© 2024. The Author(s).)
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- 2024
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15. Correction to: Young-onset diabetes in Asian Indians is associated with lower measured and genetically determined beta cell function.
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Siddiqui MK, Anjana RM, Dawed AY, Martoeau C, Srinivasan S, Saravanan J, Madanagopal SK, Taylor A, Bell S, Veluchamy A, Pradeepa R, Sattar N, Venkatesan R, Palmer CNA, Pearson ER, and Mohan V
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- 2022
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16. Young-onset diabetes in Asian Indians is associated with lower measured and genetically determined beta cell function.
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Siddiqui MK, Anjana RM, Dawed AY, Martoeau C, Srinivasan S, Saravanan J, Madanagopal SK, Taylor A, Bell S, Veluchamy A, Pradeepa R, Sattar N, Venkatesan R, Palmer CNA, Pearson ER, and Mohan V
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- Asian People genetics, Cross-Sectional Studies, Humans, India epidemiology, Obesity genetics, Overweight genetics, Risk Factors, Diabetes Mellitus, Type 2 epidemiology, Diabetes Mellitus, Type 2 genetics, Insulin Resistance genetics
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Aims/hypothesis: South Asians in general, and Asian Indians in particular, have higher risk of type 2 diabetes compared with white Europeans, and a younger age of onset. The reasons for the younger age of onset in relation to obesity, beta cell function and insulin sensitivity are under-explored., Methods: Two cohorts of Asian Indians, the ICMR-INDIAB cohort (Indian Council of Medical Research-India Diabetes Study) and the DMDSC cohort (Dr Mohan's Diabetes Specialties Centre), and one of white Europeans, the ESDC (East Scotland Diabetes Cohort), were used. Using a cross-sectional design, we examined the comparative prevalence of healthy, overweight and obese participants with young-onset diabetes, classified according to their BMI. We explored the role of clinically measured beta cell function in diabetes onset in Asian Indians. Finally, the comparative distribution of a partitioned polygenic score (pPS) for risk of diabetes due to poor beta cell function was examined. Replication of the genetic findings was sought using data from the UK Biobank., Results: The prevalence of young-onset diabetes with normal BMI was 9.3% amongst white Europeans and 24-39% amongst Asian Indians. In Asian Indians with young-onset diabetes, after adjustment for family history of type 2 diabetes, sex, insulin sensitivity and HDL-cholesterol, stimulated C-peptide was 492 pmol/ml (IQR 353-616, p<0.0001) lower in lean compared with obese individuals. Asian Indians in our study, and South Asians from the UK Biobank, had a higher number of risk alleles than white Europeans. After weighting the pPS for beta cell function, Asian Indians have lower genetically determined beta cell function than white Europeans (p<0.0001). The pPS was associated with age of diagnosis in Asian Indians but not in white Europeans. The pPS explained 2% of the variation in clinically measured beta cell function, and 1.2%, 0.97%, and 0.36% of variance in age of diabetes amongst Asian Indians with normal BMI, or classified as overweight and obese BMI, respectively., Conclusions/interpretation: The prevalence of lean BMI in young-onset diabetes is over two times higher in Asian Indians compared with white Europeans. This phenotype of lean, young-onset diabetes appears driven in part by lower beta cell function. We demonstrate that Asian Indians with diabetes also have lower genetically determined beta cell function., (© 2022. The Author(s).)
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- 2022
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17. Lifetime risk of diabetes in metropolitan cities in India.
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Luhar S, Kondal D, Jones R, Anjana RM, Patel SA, Kinra S, Clarke L, Ali MK, Prabhakaran D, Kadir MM, Tandon N, Mohan V, and Narayan KMV
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- Adult, Age Distribution, Diabetes Mellitus diagnosis, Diabetes Mellitus mortality, Disease-Free Survival, Female, Humans, Incidence, India epidemiology, Life Expectancy, Male, Markov Chains, Middle Aged, Models, Theoretical, Obesity epidemiology, Prevalence, Risk Assessment, Risk Factors, Sex Distribution, Time Factors, Young Adult, Diabetes Mellitus epidemiology, Urban Health
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Aims/hypothesis: We aimed to estimate the lifetime risk of diabetes and diabetes-free life expectancy in metropolitan cities in India among the population aged 20 years or more, and their variation by sex, age and BMI., Methods: A Markov simulation model was adopted to estimate age-, sex- and BMI-specific lifetime risk of developing diabetes and diabetes-free life expectancy. The main data inputs used were as follows: age-, sex- and BMI-specific incidence rates of diabetes in urban India taken from the Centre for Cardiometabolic Risk Reduction in South Asia (2010-2018); age-, sex- and urban-specific rates of mortality from period lifetables reported by the Government of India (2014); and prevalence of diabetes from the Indian Council for Medical Research INdia DIABetes study (2008-2015)., Results: Lifetime risk (95% CI) of diabetes in 20-year-old men and women was 55.5 (51.6, 59.7)% and 64.6 (60.0, 69.5)%, respectively. Women generally had a higher lifetime risk across the lifespan. Remaining lifetime risk (95% CI) declined with age to 37.7 (30.1, 46.7)% at age 60 years among women and 27.5 (23.1, 32.4)% in men. Lifetime risk (95% CI) was highest among obese Indians: 86.0 (76.6, 91.5)% among 20-year-old women and 86.9 (75.4, 93.8)% among men. We identified considerably higher diabetes-free life expectancy at lower levels of BMI., Conclusions/interpretation: Lifetime risk of diabetes in metropolitan cities in India is alarming across the spectrum of weight and rises dramatically with higher BMI. Prevention of diabetes among metropolitan Indians of all ages is an urgent national priority, particularly given the rapid increase in urban obesogenic environments across the country. Graphical abstract.
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- 2021
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18. Impact of age at type 2 diabetes mellitus diagnosis on mortality and vascular complications: systematic review and meta-analyses.
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Nanayakkara N, Curtis AJ, Heritier S, Gadowski AM, Pavkov ME, Kenealy T, Owens DR, Thomas RL, Song S, Wong J, Chan JC, Luk AO, Penno G, Ji L, Mohan V, Amutha A, Romero-Aroca P, Gasevic D, Magliano DJ, Teede HJ, Chalmers J, and Zoungas S
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- Age of Onset, Cerebrovascular Disorders epidemiology, Cerebrovascular Disorders etiology, Coronary Disease epidemiology, Coronary Disease etiology, Diabetes Mellitus, Type 2 complications, Diabetic Angiopathies etiology, Diabetic Nephropathies epidemiology, Diabetic Nephropathies etiology, Diabetic Neuropathies epidemiology, Diabetic Neuropathies etiology, Diabetic Retinopathy epidemiology, Diabetic Retinopathy etiology, Humans, Mortality, Odds Ratio, Peripheral Vascular Diseases epidemiology, Peripheral Vascular Diseases etiology, Diabetes Mellitus, Type 2 diagnosis, Diabetic Angiopathies epidemiology
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Aims/hypothesis: Few studies examine the association between age at diagnosis and subsequent complications from type 2 diabetes. This paper aims to summarise the risk of mortality, macrovascular complications and microvascular complications associated with age at diagnosis of type 2 diabetes., Methods: Data were sourced from MEDLINE and All EBM (Evidence Based Medicine) databases from inception to July 2018. Observational studies, investigating the effect of age at diabetes diagnosis on macrovascular and microvascular diabetes complications in adults with type 2 diabetes were selected according to pre-specified criteria. Two investigators independently extracted data and evaluated all studies. If data were not reported in a comparable format, data were obtained from authors, presented as minimally adjusted ORs (and 95% CIs) per 1 year increase in age at diabetes diagnosis, adjusted for current age for each outcome of interest. The study protocol was recorded with PROSPERO International Prospective Register of Systematic Reviews (CRD42016043593)., Results: Data from 26 observational studies comprising 1,325,493 individuals from 30 countries were included. Random-effects meta-analyses with inverse variance weighting were used to obtain the pooled ORs. Age at diabetes diagnosis was inversely associated with risk of all-cause mortality and macrovascular and microvascular disease (all p < 0.001). Each 1 year increase in age at diabetes diagnosis was associated with a 4%, 3% and 5% decreased risk of all-cause mortality, macrovascular disease and microvascular disease, respectively, adjusted for current age. The effects were consistent for the individual components of the composite outcomes (all p < 0.001)., Conclusions/interpretation: Younger, rather than older, age at diabetes diagnosis was associated with higher risk of mortality and vascular disease. Early and sustained interventions to delay type 2 diabetes onset and improve blood glucose levels and cardiovascular risk profiles of those already diagnosed are essential to reduce morbidity and mortality. Graphical abstract.
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- 2021
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19. Variation at the DPP4 locus influences apolipoprotein B levels in South Asians and exhibits heterogeneity in Europeans related to BMI.
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Bailey SD, Xie C, Paré G, Montpetit A, Mohan V, Yusuf S, Gerstein H, Engert JC, and Anand SS
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- Adult, Asian People, Case-Control Studies, Diabetes Mellitus, Type 2 blood, Diabetes Mellitus, Type 2 genetics, Female, Humans, Male, Middle Aged, Polymorphism, Single Nucleotide genetics, White People, Apolipoproteins B blood, Body Mass Index, Dipeptidyl Peptidase 4 genetics
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Aims/hypothesis: Dyslipidaemia, a common feature of type 2 diabetes, is characterised by an increase in atherogenic particles, quantifiable through apolipoprotein B (ApoB) levels. Genetic studies of lipid levels have focused on Europeans; a study in South Asians could identify novel genes., Methods: We tested 31,739 single nucleotide polymorphisms (SNPs) from ∼ 2,000 genes in 2,573 South Asians from the epidemiological arm of the Diabetes Reduction Assessment with Ramipril and Rosiglitazone Medication (DREAM) study (EpiDREAM) for association with ApoB and we tested two novel associations for replication in 1,181 South Asians from the INTERHEART case-control study., Results: The SNP, rs4664443, within DPP4 was associated with ApoB (p = 7.98 × 10(-5)) in EpiDREAM. The observed association was replicated in the INTERHEART South Asians (one-sided p = 9.65 × 10(-3); combined two-sided p = 4.68 × 10(-6)). The rs4664443 SNP was not associated with ApoB among five other EpiDREAM ethnicities. However, because South Asians had a significantly lower mean BMI compared with other EpiDREAM ethnicities, we tested for and found an interaction between rs4664443 and BMI for ApoB among the Europeans, the largest subgroup in EpiDREAM (p = 4.14 × 10(-3) for interaction), observing an association with ApoB in Europeans with a BMI <25 kg/m(2) (p = 2.35 × 10(-3)), but not with a BMI ≥ 25 kg/m(2) (p = 0.21). The association between rs4664443 and ApoB among all EpiDREAM individuals with BMI <25 kg/m(2) was significant (n = 2,972; p = 1.44 × 10(-5)) compared with those with a BMI ≥ 25 kg/m(2) (n = 11,559; p = 0.81), and there was evidence of association among all genotyped individuals with a BMI <25 kg/m(2), including the INTERHEART South Asians (n = 3,601; p = 9.52 × 10(-7))., Conclusion/interpretation: Variation at the DPP4 locus is associated with ApoB in South Asians and displays heterogeneity related to BMI in other ethnicities.
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- 2014
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20. HbA1c, fasting and 2 h plasma glucose in current, ex- and never-smokers: a meta-analysis.
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Soulimane S, Simon D, Herman WH, Lange C, Lee CM, Colagiuri S, Shaw JE, Zimmet PZ, Magliano D, Ferreira SR, Dong Y, Zhang L, Jorgensen T, Tuomilehto J, Mohan V, Christensen DL, Kaduka L, Dekker JM, Nijpels G, Stehouwer CD, Lantieri O, Fujimoto WY, Leonetti DL, McNeely MJ, Borch-Johnsen K, Boyko EJ, Vistisen D, and Balkau B
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- Humans, Blood Glucose metabolism, Fasting blood, Glycated Hemoglobin metabolism, Smoking blood, Smoking metabolism
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Aims/hypothesis: The relationships between smoking and glycaemic variables have not been well explored. We compared HbA1c, fasting plasma glucose (FPG) and 2 h plasma glucose (2H-PG) in current, ex- and never-smokers., Methods: This meta-analysis used individual data from 16,886 men and 18,539 women without known diabetes in 12 DETECT-2 consortium studies and in the French Data from an Epidemiological Study on the Insulin Resistance Syndrome (DESIR) and Telecom studies. Means of three glycaemic variables in current, ex- and never-smokers were modelled by linear regression, with study as a random factor. The I (2) statistic was used to evaluate heterogeneity among studies., Results: HbA1c was 0.10% (95% CI 0.08, 0.12) (1.1 mmol/mol [0.9, 1.3]) higher in current smokers and 0.03% (0.01, 0.05) (0.3 mmol/mol [0.1, 0.5]) higher in ex-smokers, compared with never-smokers. For FPG, there was no significant difference between current and never-smokers (-0.004 mmol/l [-0.03, 0.02]) but FPG was higher in ex-smokers (0.12 mmol/l [0.09, 0.14]). In comparison with never-smokers, 2H-PG was lower (-0.44 mmol/l [-0.52, -0.37]) in current smokers, with no difference for ex-smokers (0.02 mmol/l [-0.06, 0.09]). There was a large and unexplained heterogeneity among studies, with I (2) always above 50%; I (2) was little changed after stratification by sex and adjustment for age and BMI. In this study population, current smokers had a prevalence of diabetes that was 1.30% higher as screened by HbA1c and 0.52% lower as screened by 2H-PG, in comparison with never-smokers., Conclusion/interpretation: Across this heterogeneous group of studies, current smokers had a higher HbA1c and lower 2H-PG than never-smokers. This will affect the chances of smokers being diagnosed with diabetes.
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- 2014
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21. Prevalence of diabetes and prediabetes (impaired fasting glucose and/or impaired glucose tolerance) in urban and rural India: phase I results of the Indian Council of Medical Research-INdia DIABetes (ICMR-INDIAB) study.
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Anjana RM, Pradeepa R, Deepa M, Datta M, Sudha V, Unnikrishnan R, Bhansali A, Joshi SR, Joshi PP, Yajnik CS, Dhandhania VK, Nath LM, Das AK, Rao PV, Madhu SV, Shukla DK, Kaur T, Priya M, Nirmal E, Parvathi SJ, Subhashini S, Subashini R, Ali MK, and Mohan V
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- Adult, Aged, Blood Glucose analysis, Comorbidity, Cross-Sectional Studies, Female, Humans, Hypertension epidemiology, India epidemiology, Male, Middle Aged, Obesity, Abdominal epidemiology, Prevalence, Sex Factors, Young Adult, Diabetes Mellitus epidemiology, Health Surveys statistics & numerical data, Prediabetic State epidemiology, Rural Population statistics & numerical data, Urban Population statistics & numerical data
- Abstract
Aims/hypothesis: This study reports the results of the first phase of a national study to determine the prevalence of diabetes and prediabetes (impaired fasting glucose and/or impaired glucose tolerance) in India., Methods: A total of 363 primary sampling units (188 urban, 175 rural), in three states (Tamilnadu, Maharashtra and Jharkhand) and one union territory (Chandigarh) of India were sampled using a stratified multistage sampling design to survey individuals aged ≥ 20 years. The prevalence rates of diabetes and prediabetes were assessed by measurement of fasting and 2 h post glucose load capillary blood glucose., Results: Of the 16,607 individuals selected for the study, 14,277 (86%) participated, of whom 13,055 gave blood samples. The weighted prevalence of diabetes (both known and newly diagnosed) was 10.4% in Tamilnadu, 8.4% in Maharashtra, 5.3% in Jharkhand, and 13.6% in Chandigarh. The prevalences of prediabetes (impaired fasting glucose and/or impaired glucose tolerance) were 8.3%, 12.8%, 8.1% and 14.6% respectively. Multiple logistic regression analysis showed that age, male sex, family history of diabetes, urban residence, abdominal obesity, generalised obesity, hypertension and income status were significantly associated with diabetes. Significant risk factors for prediabetes were age, family history of diabetes, abdominal obesity, hypertension and income status., Conclusions/interpretations: We estimate that, in 2011, Maharashtra will have 6 million individuals with diabetes and 9.2 million with prediabetes, Tamilnadu will have 4.8 million with diabetes and 3.9 million with prediabetes, Jharkhand will have 0.96 million with diabetes and 1.5 million with prediabetes, and Chandigarh will have 0.12 million with diabetes and 0.13 million with prediabetes. Projections for the whole of India would be 62.4 million people with diabetes and 77.2 million people with prediabetes.
- Published
- 2011
- Full Text
- View/download PDF
22. Long-term effect of rosiglitazone and/or ramipril on the incidence of diabetes.
- Author
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Gerstein HC, Mohan V, Avezum A, Bergenstal RM, Chiasson JL, Garrido M, MacKinnon I, Rao PV, Zinman B, Jung H, Joldersma L, Bosch J, and Yusuf S
- Subjects
- Aged, Diabetes Mellitus prevention & control, Female, Humans, Male, Middle Aged, Rosiglitazone, Diabetes Mellitus drug therapy, Hypoglycemic Agents therapeutic use, Ramipril therapeutic use, Thiazolidinediones therapeutic use
- Abstract
Aims/hypothesis: The Diabetes Reduction Assessment with Ramipril and Rosiglitazone Medication (DREAM) trial reported that 3 years of therapy with rosiglitazone reduced the primary outcome of diabetes or death by 60%. Here we investigated whether an effect on diabetes prevention persists more than 1.5 years after therapy has been discontinued., Methods: The DREAM On passive follow-up study was conducted at 49 of the 191 DREAM sites. Consenting participants were invited to have a repeat OGTT 1-2 years after active therapy ended. A diagnosis of diabetes at that time was based on either a fasting or 2 h plasma glucose level of ≥7.0 mmol/l or ≥11.1 mmol/l, respectively, or a confirmed diagnosis by a non-study physician. Regression to normoglycaemia was defined as a fasting and 2 h plasma glucose level of <6.1 mmol/l and <7.8 mmol/l, respectively., Results: After a median of 1.6 years after the end of the trial and 4.3 years after randomisation, rosiglitazone participants had a 39% lower incidence of the primary outcome (hazard ratio [HR] 0.61, 95% CI 0.53-0.70; p < 0.0001) and 17% more regression to normoglycaemia (95% CI 1.01-1.34; p = 0.034). When the analysis was restricted to the passive follow-up period, a similar incidence of both the primary outcome and regression was observed in people from both treatment groups (HR 1.00, 95% CI 0.81-1.24 and HR 1.14, 95% CI 0.97-1.32, respectively). Similar effects were noted when new diabetes was analysed separately from death. Ramipril did not have any significant long-term effect., Conclusions/interpretation: Time-limited exposure to rosiglitazone reduces the longer term incidence of diabetes by delaying but not reversing the underlying disease process.
- Published
- 2011
- Full Text
- View/download PDF
23. Anthropometric measures and glucose levels in a large multi-ethnic cohort of individuals at risk of developing type 2 diabetes.
- Author
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de Koning L, Gerstein HC, Bosch J, Diaz R, Mohan V, Dagenais G, Yusuf S, and Anand SS
- Subjects
- Adult, Body Mass Index, Cross-Sectional Studies, Diabetes Mellitus, Type 2 ethnology, Female, Glucose Tolerance Test, Humans, Linear Models, Male, Middle Aged, Risk Factors, Waist Circumference, Blood Glucose, Diabetes Mellitus, Type 2 blood, Diabetes Mellitus, Type 2 epidemiology
- Abstract
Aims/hypotheses: We determined: (1) which of BMI, waist circumference, hip circumference and WHR has the strongest association and explanatory power for newly diagnosed type 2 diabetes and glucose status; and (2) the impact of considering two measures simultaneously. We also explored variation in anthropometric associations by sex and ethnicity., Methods: We performed cross-sectional analysis of 22,293 men and women who were from five ethnic groups and 21 countries, and at risk of developing type 2 diabetes. Standardised anthropometric associations with type 2 diabetes and AUC of glucose status from OGTT (AUC(OGTT)) were determined using multiple regression. Explanatory power was assessed using the c-statistic and adjusted r (2)., Results: An increase in BMI, waist circumference or WHR had similar positive associations with type 2 diabetes, AUC(OGTT) and explanatory power after adjustment for age, sex, smoking and ethnicity (p < 0.01). However, using BMI and WHR together resulted in greater explanatory power than with other models (p < 0.01). Associations were strongest when waist circumference and hip circumference were used together, a combination that had greater explanatory power than other models except for BMI and WHR together (p < 0.01). Results were directionally similar according to sex and ethnicity; however, significant variations in associations were observed among these subgroups., Conclusions/interpretation: The combination of BMI and WHR, or of waist circumference and hip circumference has the best explanatory power for type 2 diabetes and glucose status compared with a single anthropometric measure. Measurement of waist circumference and hip circumference is required to optimally identify people at risk of type 2 diabetes and people with elevated glucose levels.
- Published
- 2010
- Full Text
- View/download PDF
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