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6. Genetic mapping of a susceptibility locus for insulin-dependent diabetes mellitus on chromosome 11q

Author

Hashimoto, L., Habita, C., Beressl, J. P., Delepine, M., Besse, C., Cambon-Thomsen, A., Deschamps, I., Rotter, J.I., Djoulah, S., James, M.R., Froguel, P., Weissenbach, J., Lathrop, G.M., and Julier, C.

Subjects
Type 1 diabetes -- Genetic aspects, Chromosome mapping -- Observations, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

A genome-wide linkage study of insulin-dependent diabetes mellitus (IDDM) using microsatellite markers, obtained from genothon maps and other informative markers derived using polymerase chain reaction analysis, localizes an unidentified susceptibility locus for IDDM. The locus is present in the FGF3 gene area on the chromosome 11Q. Genetic linkage studies also facilitate the identification of susceptibility loci in other multifactorial disorders.

Published
1994

9. Insulin-IGF2 region on chromosome 11p encodes a gene implicated in HLA-DR4-dependent diabetes susceptibility

Author

Julier, C., Hyer, R.N., Davies, J., Merlin, F., Soularue, P., Briant, L., Cathelineau, G., Deschamps, I., Rotter, J.I., Froguel, P., Boitard, C., Bell, J.I., and Lathrop, G.M.

Subjects
Insulin -- Genetic aspects, Histocompatibility antigens -- Health aspects, Ir genes -- Health aspects, Major histocompatibility complex -- Health aspects, Type 1 diabetes -- Genetic aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Chromosomal DNA is a complicated affair; in addition to the DNA sequences that specify the amino-acid sequence of protein molecules, there are DNA sequences involved in the regulation of the genes, as well as DNA sequences for which there is no known function. There is a class of alleles (DNA variants which might occur at a particular location on the chromosome) that are associated with insulin-dependent diabetes. These alleles are located on chromosome 11, near the location of the gene for insulin. However, family studies have failed to show that the inheritance of these alleles is associated with the development of diabetes in offspring. Taking a new tack, researchers have found that the inheritance of these genes influences the development of diabetes in some people, but not others. Specific genes of the major histocompatibility complex on chromosome 6 are known to be preferentially associated with many human diseases. When researchers analyzed the inheritance of the alleles on chromosome 11 near the insulin gene, they found that the alleles were an important determinant of insulin-dependent diabetes only for subjects with the gene for the class II histocompatibility molecule HLA-DR4. Subjects who have not inherited the HLA-DR4 gene do not experience an increased risk of diabetes from the gene alleles under question. Curiously, having the HLA-DR4 gene makes no difference if the risky genes are inherited from the mother. Increased risk of diabetes was seen only in individuals who not only had the HLA-DR4 gene, but inherited the risky alleles from their fathers. This observation may provide an explanation for the increased risk of diabetes observed among the children whose fathers have diabetes. It is known that the genetic alleles under study in the present report do not alter the structure of insulin itself. It is suspected, therefore, that these genes change the regulation of the production of insulin. It is also possible, however, that these genes may alter insulin-like growth factor 2 or some other gene that is located in the same general region of the short arm of chromosome 11. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1991

14. Second Annual Meeting of the European Association for the Study of Diabetes abstracts: Second part Aarhus, Denmark, July 6–8, 1966

Author

Ireland, J. T., Patnaik, B. K., Duncan, L. J. P., Jaksic, Z., Jakob, A., Lauper, N., Flury, R., Labhart, A., Froesch, E. R., Jarrett, R. J., Keen, H., Track, N., Jervell, J., Vallance-Owen, J., Bajaj, J. S., Jørgensen, K., Binder, C., Nielsen, Aa. V., Kammerer, L., Bretán, M., Nemsánszky, L., Jakab, L., Virág, III, S., Virag, S., Keat, E., Kerp, L., Kieling, F., Steinhilber, S., Keep, L., Knick, B., Korec, R., Korp, W., Lalouschek, L., Levett, R. E., Summer, K., Krentz, K., Kristensen, M., Kuhlencordt, Friedrich, Kuhlencordt, F., Kühnau, Jr., J., Meyer, H. -W., Lambert, A. E., Hoet, J. J., Lambotte, L., Shoemaker, W. C., Lefebvre, P., Lenti, G., Pellegrini, A., Pagano, G., Brotzu, M. V., Sirigu, F., Lestradet, H., Deschamps, I., Liebermeister, H., Rüenauver, R., Grüneklee, D., Schilling, W., Jahnke, K., Daweke, H., Löffler, G., Weinges, K. F., Lopez-Quijada, C., R-Candela, J. L., Loubatieres, A., Mariani, M. M., Alric, R., Lowy, C., Rubenstein, A. H., Weight, A. D., Martin, T. J., Russell, T., Luft, R., Madison, L., Cerasi, E., von Euler, U. S., Margolis, A., Bugala, I., Marasek, L., Marks, Vincent, Howorth, P. J. N., Samols, Ellis, Greenwood, F. C., Mazzi, C., Melani, F., Lawecki, J., Bartelt, K. M., Pfeiffer, E. F., Menzinger, G., Fallucca, F., Aliberti, L., Andreani, D., Meyer, U. A., Miki, E., Elliott P., Milani R., Bianchessi, M., Mirouze, J., Cartry, E., Saade, F., Jaffiol, C., Montenero, P., Denatone, P., Donatone, E., Ørskov, H., Östman, J., Øye, I., Sinclair, D., Pallardo, L. F., Cartillo-Olivares, J., Guijo, J., Garrido, J. M. Garcia, Castillo-Olivares, J., Matute, J. L., Pathe, G., Comtesse, G., Polge, U., Contesse, G., Pavel, I., Pieptes, R., Pedebsen, Jørgen, Pedersen, L. Mølsted, Jørgensen, K. R., Penchev, I., Piancino, G., Martini, P. P., Cravetto, C. A., Pieri, A., Scarpelli, P. T., Pihl, E., Falkmer, S., Pometta, D., Tatot, J., Rees, S. B., Kuwabara, T., Taton, J., Rees, S. B., Poulsen, J. E., Werner, A. U., Pozza, G., Ghidoni, A., Sanesi, E., Quinto, P., Flamigni, O., Tirelli, R., Flamingni, C., Rafaelsen, Ole J., Lyngsoe, J., Deckert, T., Reske-Nielsen, Edith, Lundbæk, Knud, Roderiguez-Minon, J. L., Rosell-Perez, M., Hedeskov, C. J., Esmann, V., Rosselin, G., Tchobroutsky, G., Freychet, P., Assan, R., Derot, M., Rudas, Barbara, Liebermeisteb, H., Salinas, Matilde, R-Candela, J. L., Samols, E., Tyler, J., Marks, V., Schliack, V., Skovborg, F., Schlichtkrull, J., Ditzel, J., Skrabalo, Z., Stavljenic, A., Crepinko, I., Dimitrov, N., Sönksen, P. H., Ellis, J. P., Greenwood, F., Nabarro, J. D. N., Söling, H. D., Zahlten, R., Willms, B., Stauffacher, W., Jeanrenaud, B., Sutter, B. Ch. J., Meyer, V., Mialhe, P., Thomas, K., de Gasparo, M., Toussaint, D., Gepts, W., Pickering, G. W., Fraser, J. A., Travia, L., Dalla Torre, L., Forcina, G., Gandolfo, L., Turner, D. S., McIntyre, N., Tutin, M., Rousselie, F., Rathery, M., Borna, H., Bour, H., Unger, R. H., Recant, L., McGavran, M., Siperstein, M. D., Vague, Ph., Depieds, R., Boeuf, G., Codaccioni, J. L., Vague, J., Vague, P., Vitelli, A., Segre, G., Martino, P., Saiani, A., Martini, P. F., Saisni, A., Martini, P. F., Vuletic, S., Wahl, P., Kettnaker, W., Walaas, W., Walaas, O., Wildenhoff, K. E., Dalsager, H., Schwartz, N., Böttcher, M., Sakomoto, N., Söling, H. D., Winand, J., Furnelle, J., Christophe, J., Woenckhaus, J. W., Günter, D., Yde, H., Young, D. A. B., Benson, B., Zahnd, G. R., Luyks, A., Zaragoza, N., and Felber, J. P.

Published
1966
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16. La estratigrafía de la Sierra de Neiba (República Dominicana)

Author

Hernáiz Huerta, P.P., Díaz de Neira, J.A., García-Senz, J., Deschamps, I., Lopera, E., Escuder Viruete, J., Ardévol Oró, Ll., Granados, L., Calvo Sorando, José Pedro, and Pérez-Estaún, A.

Subjects
Geología estratigráfica
Abstract

La reciente cartografía a escala 1:50.000 de los sectores centrales y meridionales, más desconocidos, de la Sierra de Neiba ha permitido establecer con mayor precisión su estratigrafía. Los materiales más antiguos corresponden a la Unidad de El Manguito, del Cretácico Superior. Son calizas y lutitas pizarrosas con intercalaciones de basaltos que afloran como un fragmento o bloque tectónico de interpretación estructural dudosa en el núcleo de un anticlinal. Por su edad, se considera que esta unidad debe constituir el sustrato de las series paleógenas de la Sierra de Neiba; la composición geoquímica de los basaltos (OIB-basaltos alcalinos intraplaca) sugiere su correlación con la meseta oceánica del Caribe. El registro estratigráfico más o menos continuo comienza en el Eoceno Inferior con el desarrollo de una extensa plataforma carbonatada, relativamente uniforme, que fue el medio de depósito de la Fm Neiba (sensu lato) y sus equivalentes, hasta el Mioceno Inferior. Durante buena parte del Eoceno, estos depósitos carbonatados coexistieron o fueron sustituidos por materiales volcánicos de signatura toleítica a alcalina (OIT a OIA) que se agrupan bajo la nueva denominación de Complejo Volcanosedimentario de El Aguacate de Neiba y se interpretan como generados en un contexto de intraplaca asociados al desarrollo de una pluma mantélica. La sedimentación de la Fm Sombrerito durante el Mioceno muestra los primeros signos de inestabilidad en la región: mientras que en los sectores septentrionales y centrales de la sierra sus facies más típicas se depositan en una cuenca turbidítica, en su extremo suroccidental afloran las calizas arrecifales de su Mb Barahona, propias de ambientes de plataforma somera, que se extienden con gran uniformidad hacia el sur hasta los dominios de la Sierra de Bahoruco. La Unidad de Cortadero, de nueva denominación y equivalente en edad a la Fm Sombrerito, con una posición intermedia entre ambos tipos de facies, puede representar el tránsito entre ellas.

Published
2007

19. Synthèse formelle du RO 67-8867, un antagoniste du récepteur NMDA 2B

Author

Deschamps, I., Gomez-Pardo, D., Karoyan, Ph, Synthèse, Structure et Fonction de Molécules Bioactives (SSFMB), and Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)

Published
2005

23. Complementation and maternal effect in insulin-dependent diabetes

Author

Françoise Clerget-Darpoux, Mc, Babron, Deschamps I, and Hors J

Subjects
Diabetes Mellitus, Type 1, HLA Antigens, Risk Factors, Genetic Complementation Test, Humans, Mothers, White People, Research Article
Abstract

The marker association segregation chi-square (MASC) method was applied to a sample of 416 Caucasians affected with insulin-dependent diabetes mellitus (IDDM), for which information on the parental and sibship status was available, as well as HLA typing. We show that the model which best explains all the observations assumes a cis or trans complementation of two tightly linked genes within the HLA region, an additional maternal effect, and other familial factors. The HLA molecule corresponding to the complementation of Arg52(+) and Asp57(-) has been recently proposed as explaining susceptibility to IDDM. However, this hypothesis does not account for the overall observations made on the HLA marker in IDDM patients and their relatives. The MASC method may also be applied to evaluate the risk for relatives of an affected individual (the "index"). For example, the risk for a sib depends not only on the parental status and on the number of HLA haplotypes he shares with the index, but also on which haplotype the index himself inherited from his mother and father.

Published
1991

27. Authors' Response

Author

Timsit, J., primary, Deschamps, I., additional, Boitard, C., additional, Robert, J. J., additional, and Assan, R., additional

Published
1995
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28. Genetic mapping of a susceptibility locus for insulin-dependent diabetes mellitus on chromosome llq

Author

Hashimoto, L., primary, Habita, C., additional, Beressi, J. P., additional, Delepine, M., additional, Basse, C., additional, Cambon-Thomsen, A., additional, Deschamps, I., additional, Rotter, J. I., additional, Djoulah, S., additional, James, M. R., additional, Froguel, P., additional, Weissenbach, J., additional, Lathrop, G. M., additional, and Julier, C., additional

Published
1994
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46. Effects of Diet on Insulin and Gastric Inhibitory Polypeptide Levels in Obese Children

Author

Deschamps, I, Heptner, W, Desjeux, J-F, Baltakse, V, Machinot, S, and Lestradet, H

Abstract

Summary: To improve understanding of the relationships between gastric inhibitory polypeptide (GIP) and insulin secretion and food intake in obesity, immunoreactive insulin and immunoreactive GIP were measured in 5 obese children during PO glucose tolerance test carried out before and after diet.Before diet, mean insulin levels were normal at fasting and rose after glucose ingestion. The mean fasting immunoreactive GIP level was very high (1235 ± 209 pg/ml) compared to that of 8 healthy adult controls (411 ± 44 pg/ml) and remained at this level throughout the test. There was only a short postabsorptive rise to 1515 ± 158 pg/ml at 30 min, which was not significantly different either from the patients' basal values or from the 30-min control values (1356 ± 67 pg/ml).After dieting for 3 to 7 months, immunoreactive insulin responses returned to normal ranges. Concomitantly, both basal and total GIP release diminished significantly (basal GIP, 343 ± 92 pg/ml; area under the GIP curve, 3820 and 1694 pg/ml/hr before and after diet, respectively). The postabsorptive GIP increment, however, rose significantly from 180 pg/ml/hr, before diet, to 665 pg/ml/hr afterwards.These results might be compatible with the hypothesis that in obesity, hyperinsulinemia, and overactivity of the GIP cells are associated phenomena caused by overeating and reversed by reduced food intake. However, several contradictory findings remain unexplained. The discrepancy between insignificant postabsorptive GIP increments and elevated insulin responses before diet casts doubts on the causal relationship between GIP and insulin secretion. The small GIP rise might be due to a limited secretory capacity of the GIP cells or to a diminished stimulatory capacity of glucose. The constantly high level of GIP might reflect chronic hypersecretion and/or some defect in basal regulation and feedback control of GIP release.The change caused by dietary measures in the GIP secretion pattern provides evidence that in obese children, basal GIP secretion is influenced by nutritional factors.Speculation: In spite of the small number of observations, the present findings illustrate the complexity of the mechanisms governing the regulation of gastric inhibitory polypeptide and insulin release in obesity. It seems likely that basal gastric inhibitory polypeptide secretion is influenced by food intake, but further studies will be necessary to confirm that gastric inhibitory polypeptide plays a causal role in the hyperinsulinemia of obesity in children.

Published
1980
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47. A systematic study of HLA class II-beta DNA restriction fragments in insulin-dependent diabetes mellitus.

Author

Cohen-Haguenauer, O, Robbins, E, Massart, C, Busson, M, Deschamps, I, Hors, J, Lalouel, J M, Dausset, J, and Cohen, D

Abstract

DNA restriction fragments of the genes encoding HLA class II-beta antigens were compared in 34 patients with insulin-dependent diabetes mellitus and 34 HLA-DR-matched healthy individuals. Ninety-three fragments, determined by six restriction enzymes (EcoRI, EcoRV, HindIII, BamHI, Pvu II, and Taq I), were analyzed: (i) A DR Taq I 12.7-kilobase-pair fragment might be a marker for the extended haplotype HLA-B8, DR3. (ii) In controls, DR4 haplotypes are associated with two distinct clusters of DQ restriction fragments (DQR4 and DQR5). Almost all (94%) DR4 patients belong to the DQR4 and not to the DQR5 cluster. This suggests that, among HLA-DR4 haplotypes, only DQR4 haplotypes are involved in susceptibility to insulin-dependent diabetes mellitus. (iii) A DR Taq I 14.5-kilobase-pair fragment was found to be strongly associated with DQR4, mainly in DR3/DR4 heterozygous patients (P = 5 X 10(-4). However, these results must be interpreted with caution, taking into account the high number of statistical tests performed.

Published
1985
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48. Effects of Diet and Weight Loss on Plasma Glucose Insulin and Free Fatty Acids in Obese Children

Author

DESCHAMPS, I., DESJEUX, J. F., MACHINOT, S., ROLLAND, F., and LESTRADET, H.

Abstract

In order to determine the relations between insulin and weight changes after diet, oral glucose tolerance tests (OGTT) were carried out before and after diet hi 37 obese children aged from 6–16 years, whose weights corrected for height exceeded by at least 2 SD the weights of normal children of the same age and sex.

Published
1978

49. Class II HLA-DC beta-chain DNA restriction fragments differentiate among HLA-DR2 individuals in insulin-dependent diabetes and multiple sclerosis.

Author

Cohen, D, Cohen, O, Marcadet, A, Massart, C, Lathrop, M, Deschamps, I, Hors, J, Schuller, E, and Dausset, J

Abstract

HLA-DR2 allele is negatively associated with insulin-dependent diabetes and positively associated with multiple sclerosis (MS). A 2.2-kilobase-pair EcoRI DNA restriction fragment detected with a beta-chain HLA-DC cDNA probe was found to be strongly correlated with HLA-DR2 in the normal population, but was absent in HLA-DR2 insulin-dependent diabetic patients. This fragment was found in HLA-DR2 multiple sclerosis patients with the same frequency as in controls. A beta-chain HLA-DC 12-kilobase-pair BamHI fragment might differentiate multiple sclerosis patients from healthy individuals.

Published
1984
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