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5. [Polymorphisms of the UDP-glucuronosyltransferase 1-A1 gene in Tunisian population]

Author

Chaouch**, L., Mahjoubi**, I., Louati, I., Mrad, R., Douzi, K., Ghanem, A., Abbes, S., Laboratoire d'hématologie moléculaire et cellulaire (LR11IPT07), Institut Pasteur de Tunis, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP), Université de Tunis El Manar (UTM), Service de pédiatrie [Grombalia, Tunisie], Hôpital Grombalia, Service de Biochimie [Grombalia, Tunisia], Service de biochimie, Centre de traumatologie et des grands brulés de Ben Arous [Hôpital Mohamed-Bouazizi, Tunisie], and Cet article a fait l’objet du soutien financier du ministère de l’enseignement supérieur et de la recherche scientifique de Tunisie (LR 05 SP 04)

Subjects
Male, Tunisia, Crigler Najjar’s syndrome, Gilbert’s syndrome, MESH: Glucuronosyltransferase, polymorphisme A(TA)n TAA, Young Adult, structure haplotypique, MESH: Polymorphism, Genetic, Humans, Glucuronosyltransferase, glucuronoconjugaison, syndrome de Gilbert, MESH: Humans, Polymorphism, Genetic, glucuronidation, [SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/Hematology, polymorphism G211A, UDP-glucuronosyltransferase 1A1, polymorphism A(TA)n TAA, polymorphisme G211A, MESH: Male, bilirubine, syndrome de Crigler Najjar, MESH: Young Adult, haplotype structure, UDP-glucuronosyltransférase 1A1, Female, bilirubin, MESH: Tunisia, MESH: Female
Abstract

equal contribution; International audience; The UDP-glucuronosyltransferase 1A1 gene that encode the enzyme UGT1A1 responsible for glucuronidation undergoes several variations that may affect the enzymatic activity or expression and which are the cause of metabolic disorders related to the glucuronidation of bilirubin, such as Gilbert's syndrome and Crigler Najjar's syndrome. Among the most common variations, there is the repeat polymorphism A (TA) n TAA in TATA box and biallelic mutation G211A in exon 1. We consider in this work to determine their frequencies in a healthy population. The polymorphism A (TA) n TAA showed that genotype [TA7/TA7] was described as being associated with Gilbert's syndrome and was encountered in 11% of the population studied. This percentage is close to the value described in the Caucasian population, estimated at 10%. Concerning the polymorphism G211A, our results show that the mutated allele is encountered in 15.7% of our study population. This frequency differs greatly from that reported for Caucasians and Afro-Americans but it is similar to that perceived at the Japanese. All these results suggest that the Tunisian population appears to be heterogeneous view UGT1A1 gene mutation status. Regarding the origins and distribution of such polymorphisms in our population, the study reveals a high haplotypic haplotype (TA) 6-G considered ancestral. The comparison of the haplotype structure generally leads to the development of a hypothetical tree of the origin and spread of different haplotypes.; Le gène UDP-glucuronosyltransferase 1A1 qui code pour l’enzyme de glucuroconjugaison, UGT1A1 est le siège de plusieurs variations qui peuvent affecter l’activité ou l’expression enzymatique. Ces dernières sont à l’origine de troubles métaboliques liés à la glucuronoconjugaison de la bilirubine tels que le syndrome de Gilbert et le syndrome de Crigler Najjar. Parmi les variations les plus étudiées, on note le polymorphisme de répétition A(TA)n TAA situé dans la boite TATA au niveau du promoteur et la mutation biallélique G211A au niveau de l’exon 1. Vue l’importance de ces deux mutations, nous envisageons dans ce travail de déterminer leurs fréquences dans une population saine. Le polymorphisme A(TA)n TAA montre que le génotype [TA7/TA7] qui a été décrit comme associé à la maladie de Gilbert était rencontré chez 11% de la population étudiée. Ce pourcentage est proche de la valeur décrite dans la population Caucasienne, estimée à 10%. Concernant le polymorphisme G211A, nos résultats montrent que l’allèle muté est rencontré chez 15.7% de notre population. Cette fréquence s’écarte beaucoup de celle rapportée pour les Caucasiens et les Afro-américains mais elle est similaire à celle rapportée pour les Japonais. L’ensemble de ces résultats suggère que la population Tunisienne semble être hétérogène du point de vue statut mutationnel du gène UGT1A1. En ce qui concerne les origines et la répartition de tels polymorphismes dans notre population, l’étude haplotypique révèle une grande hétérogénéité et une émergence particulière de l’haplotype (TA)6-G considéré comme ances-tral. La comparaison de la structure haplotypique générale conduit à l’élaboration d’un arbre hypothétique concernant l’origine et la propagation des différents haplotypes

Published
2013

6. [Polymorphisms of the UDP-glucuronosyltransferase 1-A1 gene in Tunisian population]

Author

Chaouch**, L., Mahjoubi**, I., Louati, I., Mrad, R., Douzi, K., Ghanem, A., Abbes, S., Laboratoire d'hématologie moléculaire et cellulaire (LR11IPT07), Institut Pasteur de Tunis, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP), Université de Tunis El Manar (UTM), Service de pédiatrie [Grombalia, Tunisie], Hôpital Grombalia, Service de Biochimie [Grombalia, Tunisia], Service de biochimie, Centre de traumatologie et des grands brulés de Ben Arous [Hôpital Mohamed-Bouazizi, Tunisie], and Cet article a fait l’objet du soutien financier du ministère de l’enseignement supérieur et de la recherche scientifique de Tunisie (LR 05 SP 04)

Subjects
MESH: Humans, Crigler Najjar’s syndrome, glucuronidation, [SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/Hematology, Gilbert’s syndrome, polymorphism G211A, UDP-glucuronosyltransferase 1A1, polymorphism A(TA)n TAA, MESH: Glucuronosyltransferase, polymorphisme G211A, MESH: Male, polymorphisme A(TA)n TAA, bilirubine, syndrome de Crigler Najjar, MESH: Young Adult, structure haplotypique, MESH: Polymorphism, Genetic, haplotype structure, UDP-glucuronosyltransférase 1A1, bilirubin, MESH: Tunisia, MESH: Female, glucuronoconjugaison, syndrome de Gilbert
Abstract

equal contribution; International audience; The UDP-glucuronosyltransferase 1A1 gene that encode the enzyme UGT1A1 responsible for glucuronidation undergoes several variations that may affect the enzymatic activity or expression and which are the cause of metabolic disorders related to the glucuronidation of bilirubin, such as Gilbert's syndrome and Crigler Najjar's syndrome. Among the most common variations, there is the repeat polymorphism A (TA) n TAA in TATA box and biallelic mutation G211A in exon 1. We consider in this work to determine their frequencies in a healthy population. The polymorphism A (TA) n TAA showed that genotype [TA7/TA7] was described as being associated with Gilbert's syndrome and was encountered in 11% of the population studied. This percentage is close to the value described in the Caucasian population, estimated at 10%. Concerning the polymorphism G211A, our results show that the mutated allele is encountered in 15.7% of our study population. This frequency differs greatly from that reported for Caucasians and Afro-Americans but it is similar to that perceived at the Japanese. All these results suggest that the Tunisian population appears to be heterogeneous view UGT1A1 gene mutation status. Regarding the origins and distribution of such polymorphisms in our population, the study reveals a high haplotypic haplotype (TA) 6-G considered ancestral. The comparison of the haplotype structure generally leads to the development of a hypothetical tree of the origin and spread of different haplotypes.; Le gène UDP-glucuronosyltransferase 1A1 qui code pour l’enzyme de glucuroconjugaison, UGT1A1 est le siège de plusieurs variations qui peuvent affecter l’activité ou l’expression enzymatique. Ces dernières sont à l’origine de troubles métaboliques liés à la glucuronoconjugaison de la bilirubine tels que le syndrome de Gilbert et le syndrome de Crigler Najjar. Parmi les variations les plus étudiées, on note le polymorphisme de répétition A(TA)n TAA situé dans la boite TATA au niveau du promoteur et la mutation biallélique G211A au niveau de l’exon 1. Vue l’importance de ces deux mutations, nous envisageons dans ce travail de déterminer leurs fréquences dans une population saine. Le polymorphisme A(TA)n TAA montre que le génotype [TA7/TA7] qui a été décrit comme associé à la maladie de Gilbert était rencontré chez 11% de la population étudiée. Ce pourcentage est proche de la valeur décrite dans la population Caucasienne, estimée à 10%. Concernant le polymorphisme G211A, nos résultats montrent que l’allèle muté est rencontré chez 15.7% de notre population. Cette fréquence s’écarte beaucoup de celle rapportée pour les Caucasiens et les Afro-américains mais elle est similaire à celle rapportée pour les Japonais. L’ensemble de ces résultats suggère que la population Tunisienne semble être hétérogène du point de vue statut mutationnel du gène UGT1A1. En ce qui concerne les origines et la répartition de tels polymorphismes dans notre population, l’étude haplotypique révèle une grande hétérogénéité et une émergence particulière de l’haplotype (TA)6-G considéré comme ances-tral. La comparaison de la structure haplotypique générale conduit à l’élaboration d’un arbre hypothétique concernant l’origine et la propagation des différents haplotypes

Published
2011

10. 46th Medical Maghrebian Congress. November 9-10, 2018. Tunis

Author

Alami Aroussi, A., Fouad, A., Omrane, A., Razzak, A., Aissa, A., Akkad, A., Amraoui, A., Aouam, A., Arfaoui, A., Belkouchi, A., Ben Chaaben, A., Ben Cheikh, A., Ben Khélifa, A., Ben Mabrouk, A., Benhima, A., Bezza, A., Bezzine, A., Bourrahouat, A., Chaieb, A., Chakib, A., Chetoui, A., Daoudi, A., Ech-Chenbouli, A., Gaaliche, A., Hassani, A., Kassimi, A., Khachane, A., Labidi, A., Lalaoui, A., Masrar, A., Mchachi, A., Nakhli, A., Ouakaa, A., Siati, A., Toumi, A., Zaouali, A., Condé, A. Y., Haggui, A., Belaguid, A., abdelkader jalil el hangouche, Gharbi, A., Mahfoudh, A., Bouzouita, A., Aissaoui, A., Ben Hamouda, A., Hedhli, A., Ammous, A., Bahlous, A., Ben Halima, A., Belhadj, A., Blel, A., Brahem, A., Banasr, A., Meherzi, A., Saadi, A., Sellami, A., Turki, A., Ben Miled, A., Ben Slama, A., Daib, A., Zommiti, A., Chadly, A., Jmaa, A., Mtiraoui, A., Ksentini, A., Methnani, A., Zehani, A., Kessantini, A., Farah, A., Mankai, A., Mellouli, A., Touil, A., Hssine, A., Ben Safta, A., Derouiche, A., Jmal, A., Ferjani, A., Djobbi, A., Dridi, A., Aridhi, A., Bahdoudi, A., Ben Amara, A., Benzarti, A., Ben Slama, A. Y., Oueslati, A., Soltani, A., Chadli, A., Aloui, A., Belghuith Sriha, A., Bouden, A., Laabidi, A., Mensi, A., Sabbek, A., Zribi, A., Green, A., Ben Nasr, A., Azaiez, A., Yeades, A., Belhaj, A., Mediouni, A., Sammoud, A., Slim, A., Amine, B., Chelly, B., Jatik, B., Lmimouni, B., Daouahi, B., Ben Khelifa, B., Louzir, B., Dorra, A., Dhahri, B., Ben Nasrallah, C., Chefchaouni, C., Konzi, C., Loussaief, C., Makni, C., Dziri, C., Bouguerra, C., Kays, C., Zedini, C., Dhouha, C., Mohamed, C., Aichaouia, C., Dhieb, C., Fofana, D., Gargouri, D., Chebil, D., Issaoui, D., Gouiaa, D., Brahim, D., Essid, D., Jarraya, D., Trad, D., Ben Hmida, E., Sboui, E., Ben Brahim, E., Baati, E., Talbi, E., Chaari, E., Hammami, E., Ghazouani, E., Ayari, F., Ben Hariz, F., Bennaoui, F., Chebbi, F., Chigr, F., Guemira, F., Harrar, F., Benmoula, F. Z., Ouali, F. Z., Maoulainine, F. M. R., Bouden, F., Fdhila, F., Améziani, F., Bouhaouala, F., Charfi, F., Chermiti Ben Abdallah, F., Hammemi, F., Jarraya, F., Khanchel, F., Ourda, F., Sellami, F., Trabelsi, F., Yangui, F., Fekih Romdhane, F., Mellouli, F., Nacef Jomli, F., Mghaieth, F., Draiss, G., Elamine, G., Kablouti, G., Touzani, G., Manzeki, G. B., Garali, G., Drissi, G., Besbes, G., Abaza, H., Azzouz, H., Said Latiri, H., Rejeb, H., Ben Ammar, H., Ben Brahim, H., Ben Jeddi, H., Ben Mahjouba, H., Besbes, H., Dabbebi, H., Douik, H., El Haoury, H., Elannaz, H., Elloumi, H., Hachim, H., Iraqi, H., Kalboussi, H., Khadhraoui, H., Khouni, H., Mamad, H., Metjaouel, H., Naoui, H., Zargouni, H., Elmalki, H. O., Feki, H., Haouala, H., Jaafoura, H., Drissa, H., Mizouni, H., Kamoun, H., Ouerda, H., Zaibi, H., Chiha, H., Saibi, H., Skhiri, H., Boussaffa, H., Majed, H., Blibech, H., Daami, H., Harzallah, H., Rkain, H., Ben Massoud, H., Jaziri, H., Ben Said, H., Ayed, H., Harrabi, H., Chaabouni, H., Ladida Debbache, H., Harbi, H., Yacoub, H., Abroug, H., Ghali, H., Kchir, H., Msaad, H., Manai, H., Riahi, H., Bousselmi, H., Limem, H., Aouina, H., Jerraya, H., Ben Ayed, H., Chahed, H., Snéne, H., Lahlou Amine, I., Nouiser, I., Ait Sab, I., Chelly, I., Elboukhani, I., Ghanmi, I., Kallala, I., Kooli, I., Bouasker, I., Fetni, I., Bachouch, I., Bouguecha, I., Chaabani, I., Gazzeh, I., Samaali, I., Youssef, I., Zemni, I., Bachouche, I., Bouannene, I., Kasraoui, I., Laouini, I., Mahjoubi, I., Maoudoud, I., Riahi, I., Selmi, I., Tka, I., Hadj Khalifa, I., Mejri, I., Béjia, I., Bellagha, J., Boubaker, J., Daghfous, J., Dammak, J., Hleli, J., Ben Amar, J., Jedidi, J., Marrakchi, J., Kaoutar, K., Arjouni, K., Ben Helel, K., Benouhoud, K., Rjeb, K., Imene, K., Samoud, K., El Jeri, K., Abid, K., Chaker, K., Bouzghaîa, K., Kamoun, K., Zitouna, K., Oughlani, K., Lassoued, K., Letaif, K., Hakim, K., Cherif Alami, L., Benhmidoune, L., Boumhil, L., Bouzgarrou, L., Dhidah, L., Ifrine, L., Kallel, L., Merzougui, L., Errguig, L., Mouelhi, L., Sahli, L., Maoua, M., Rejeb, M., Ben Rejeb, M., Bouchrik, M., Bouhoula, M., Bourrous, M., Bouskraoui, M., El Belhadji, M., Essakhi, M., Essid, M., Gharbaoui, M., Haboub, M., Iken, M., Krifa, M., Lagrine, M., Leboyer, M., Najimi, M., Rahoui, M., Sabbah, M., Sbihi, M., Zouine, M., Chefchaouni, M. C., Gharbi, M. H., El Fakiri, M. M., Tagajdid, M. R., Shimi, M., Touaibia, M., Jguirim, M., Barsaoui, M., Belghith, M., Ben Jmaa, M., Koubaa, M., Tbini, M., Boughdir, M., Ben Salah, M., Ben Fraj, M., Ben Halima, M., Ben Khalifa, M., Bousleh, M., Limam, M., Mabrouk, M., Mallouli, M., Rebeii, M., Ayari, M., Belhadj, M., Ben Hmida, M., Boughattas, M., Drissa, M., El Ghardallou, M., Fejjeri, M., Hamza, M., Jaidane, M., Jrad, M., Kacem, M., Mersni, M., Mjid, M., Serghini, M., Triki, M., Ben Abbes, M., Boussaid, M., Gharbi, M., Hafi, M., Slama, M., Trigui, M., Taoueb, M., Chakroun, M., Ben Cheikh, M., Chebbi, M., Hadj Taieb, M., Ben Khelil, M., Hammami, M., Khalfallah, M., Ksiaa, M., Mechri, M., Mrad, M., Sboui, M., Bani, M., Hajri, M., Mellouli, M., Allouche, M., Mesrati, M. A., Mseddi, M. A., Amri, M., Bejaoui, M., Bellali, M., Ben Amor, M., Ben Dhieb, M., Ben Moussa, M., Chebil, M., Cherif, M., Fourati, M., Kahloul, M., Khaled, M., Machghoul, M., Mansour, M., Abdesslem, M. M., Ben Chehida, M. A., Chaouch, M. A., Essid, M. A., Meddeb, M. A., Gharbi, M. C., Elleuch, M. H., Loueslati, M. H., Sboui, M. M., Mhiri, M. N., Kilani, M. O., Ben Slama, M. R., Charfi, M. R., Nakhli, M. S., Mourali, M. S., El Asli, M. S., Lamouchi, M. T., Cherti, M., Khadhraoui, M., Bibi, M., Hamdoun, M., Kassis, M., Touzi, M., Ben Khaled, M., Fekih, M., Khemiri, M., Ouederni, M., Hchicha, M., Ben Attia, M., Yahyaoui, M., Ben Azaiez, M., Bousnina, M., Ben Jemaa, M., Ben Yahia, M., Daghfous, M., Haj Slimen, M., Assidi, M., Belhadj, N., Ben Mustapha, N., El Idrissislitine, N., Hikki, N., Kchir, N., Mars, N., Meddeb, N., Ouni, N., Rada, N., Rezg, N., Trabelsi, N., Bouafia, N., Haloui, N., Benfenatki, N., Bergaoui, N., Yomn, N., Maamouri, N., Mehiri, N., Siala, N., Beltaief, N., Aridhi, N., Sidaoui, N., Walid, N., Mechergui, N., Mnif, N., Ben Chekaya, N., Bellil, N., Dhouib, N., Achour, N., Kaabar, N., Mrizak, N., Chaouech, N., Hasni, N., Issaoui, N., Ati, N., Balloumi, N., Haj Salem, N., Ladhari, N., Akif, N., Liani, N., Hajji, N., Trad, N., Elleuch, N., Marzouki, N. E. H., Larbi, N., M Barek, N., Rebai, N., Bibani, N., Ben Salah, N., Belmaachi, O., Elmaalel, O., Jlassi, O., Mihoub, O., Ben Zaid, O., Bouallègue, O., Bousnina, O., Bouyahia, O., El Maalel, O., Fendri, O., Azzabi, O., Borgi, O., Ghdes, O., Ben Rejeb, O., Rachid, R., Abi, R., Bahiri, R., Boulma, R., Elkhayat, R., Habbal, R., Tamouza, R., Jomli, R., Ben Abdallah, R., Smaoui, R., Debbeche, R., Fakhfakh, R., El Kamel, R., Gargouri, R., Jouini, R., Nouira, R., Fessi, R., Bannour, R., Ben Rabeh, R., Kacem, R., Khmakhem, R., Ben Younes, R., Karray, R., Cheikh, R., Ben Malek, R., Ben Slama, R., Kouki, R., Baati, R., Bechraoui, R., Fradi, R., Lahiani, R., Ridha, R., Zainine, R., Kallel, R., Rostom, S., Ben Abdallah, S., Ben Hammamia, S., Benchérifa, S., Benkirane, S., Chatti, S., El Guedri, S., El Oussaoui, S., Elkochri, S., Elmoussaoui, S., Enbili, S., Gara, S., Haouet, S., Khammeri, S., Khefecha, S., Khtrouche, S., Macheghoul, S., Mallouli, S., Rharrit, S., Skouri, S., Helali, S., Boulehmi, S., Abid, S., Naouar, S., Zelfani, S., Ben Amar, S., Ajmi, S., Braiek, S., Yahiaoui, S., Ghezaiel, S., Ben Toumia, S., Thabeti, S., Daboussi, S., Ben Abderahman, S., Rhaiem, S., Ben Rhouma, S., Rekaya, S., Haddad, S., Kammoun, S., Merai, S., Mhamdi, S., Ben Ali, R., Gaaloul, S., Ouali, S., Taleb, S., Zrour, S., Hamdi, S., Zaghdoudi, S., Ammari, S., Ben Abderrahim, S., Karaa, S., Maazaoui, S., Saidani, S., Stambouli, S., Mokadem, S., Boudiche, S., Zaghbib, S., Ayedi, S., Jardek, S., Bouselmi, S., Chtourou, S., Manoubi, S., Bahri, S., Halioui, S., Jrad, S., Mazigh, S., Ouerghi, S., Toujani, S., Fenniche, S., Aboudrar, S., Meriem Amari, S., Karouia, S., Bourgou, S., Halayem, S., Rammeh, S., Yaïch, S., Ben Nasrallah, S., Chouchane, S., Ftini, S., Makni, S., Miri, S., Saadi, S., Manoubi, S. A., Khalfallah, T., Mechergui, T., Dakka, T., Barhoumi, T., M Rad, T. E. B., Ajmi, T., Dorra, T., Ouali, U., Hannachi, W., Ferjaoui, W., Aissi, W., Dahmani, W., Dhouib, W., Koubaa, W., Zhir, W., Gheriani, W., Arfa, W., Dougaz, W., Sahnoun, W., Naija, W., Sami, Y., Bouteraa, Y., Elhamdaoui, Y., Hama, Y., Ouahchi, Y., Guebsi, Y., Nouira, Y., Daly, Y., Mahjoubi, Y., Mejdoub, Y., Mosbahi, Y., Said, Y., Zaimi, Y., Zgueb, Y., Dridi, Y., Mesbahi, Y., Gharbi, Y., Hellal, Y., Hechmi, Z., Zid, Z., Elmouatassim, Z., Ghorbel, Z., Habbadi, Z., Marrakchi, Z., Hidouri, Z., Abbes, Z., Ouhachi, Z., Khessairi, Z., Khlayfia, Z., Mahjoubi, Z., and Moatemri, Z.

11. 46th Medical Maghrebian Congress. November 9-10, 2018. Tunis.

Author

Alami Aroussi A, Fouad A, Omrane A, Razzak A, Aissa A, Akkad A, Amraoui A, Aouam A, Arfaoui A, Belkouchi A, Ben Chaaben A, Ben Cheikh A, Ben Khélifa A, Ben Mabrouk A, Benhima A, Bezza A, Bezzine A, Bourrahouat A, Chaieb A, Chakib A, Chetoui A, Daoudi A, Ech-Chenbouli A, Gaaliche A, Hassani A, Kassimi A, Khachane A, Labidi A, Lalaoui A, Masrar A, McHachi A, Nakhli A, Ouakaa A, Siati A, Toumi A, Zaouali A, Condé AY, Haggui A, Belaguid A, El Hangouche AJ, Gharbi A, Mahfoudh A, Bouzouita A, Aissaoui A, Ben Hamouda A, Hedhli A, Ammous A, Bahlous A, Ben Halima A, Belhadj A, Bezzine A, Blel A, Brahem A, Banasr A, Meherzi A, Saadi A, Sellami A, Turki A, Ben Miled A, Ben Slama A, Daib A, Zommiti A, Chadly A, Jmaa A, Mtiraoui A, Ksentini A, Methnani A, Zehani A, Kessantini A, Farah A, Mankai A, Mellouli A, Zaouali A, Touil A, Hssine A, Ben Safta A, Derouiche A, Jmal A, Ferjani A, Djobbi A, Dridi A, Aridhi A, Bahdoudi A, Ben Amara A, Benzarti A, Ben Slama AY, Oueslati A, Soltani A, Chadli A, Aloui A, Belghuith Sriha A, Bouden A, Laabidi A, Mensi A, Ouakaa A, Sabbek A, Zribi A, Green A, Ben Nasr A, Azaiez A, Yeades A, Belhaj A, Mediouni A, Sammoud A, Slim A, Amine B, Chelly B, Jatik B, Lmimouni B, Daouahi B, Ben Khelifa B, Louzir B, Dorra A, Dhahri B, Ben Nasrallah C, Chefchaouni C, Konzi C, Loussaief C, Makni C, Dziri C, Bouguerra C, Kays C, Zedini C, Dhouha C, Mohamed C, Aichaouia C, Dhieb C, Fofana D, Gargouri D, Chebil D, Issaoui D, Gouiaa D, Brahim D, Essid D, Jarraya D, Trad D, Ben Hmida E, Sboui E, Ben Brahim E, Baati E, Talbi E, Chaari E, Hammami E, Ghazouani E, Ayari F, Ben Hariz F, Bennaoui F, Chebbi F, Chigr F, Guemira F, Harrar F, Benmoula FZ, Ouali FZ, Maoulainine FMR, Bouden F, Fdhila F, Améziani F, Bouhaouala F, Charfi F, Chermiti Ben Abdallah F, Hammemi F, Jarraya F, Khanchel F, Ourda F, Sellami F, Trabelsi F, Yangui F, Fekih Romdhane F, Mellouli F, Nacef Jomli F, Mghaieth F, Draiss G, Elamine G, Kablouti G, Touzani G, Manzeki GB, Garali G, Drissi G, Besbes G, Abaza H, Azzouz H, Said Latiri H, Rejeb H, Ben Ammar H, Ben Brahim H, Ben Jeddi H, Ben Mahjouba H, Besbes H, Dabbebi H, Douik H, El Haoury H, Elannaz H, Elloumi H, Hachim H, Iraqi H, Kalboussi H, Khadhraoui H, Khouni H, Mamad H, Metjaouel H, Naoui H, Zargouni H, Elmalki HO, Feki H, Haouala H, Jaafoura H, Drissa H, Mizouni H, Kamoun H, Ouerda H, Zaibi H, Chiha H, Kamoun H, Saibi H, Skhiri H, Boussaffa H, Majed H, Blibech H, Daami H, Harzallah H, Rkain H, Ben Massoud H, Jaziri H, Ben Said H, Ayed H, Harrabi H, Chaabouni H, Ladida Debbache H, Harbi H, Yacoub H, Abroug H, Ghali H, Kchir H, Msaad H, Ghali H, Manai H, Riahi H, Bousselmi H, Limem H, Aouina H, Jerraya H, Ben Ayed H, Chahed H, Snéne H, Lahlou Amine I, Nouiser I, Ait Sab I, Chelly I, Elboukhani I, Ghanmi I, Kallala I, Kooli I, Bouasker I, Fetni I, Bachouch I, Bouguecha I, Chaabani I, Gazzeh I, Samaali I, Youssef I, Zemni I, Bachouche I, Youssef I, Bouannene I, Kasraoui I, Laouini I, Mahjoubi I, Maoudoud I, Riahi I, Selmi I, Tka I, Hadj Khalifa I, Mejri I, Béjia I, Bellagha J, Boubaker J, Daghfous J, Dammak J, Hleli J, Ben Amar J, Jedidi J, Marrakchi J, Kaoutar K, Arjouni K, Ben Helel K, Benouhoud K, Rjeb K, Imene K, Samoud K, El Jeri K, Abid K, Chaker K, Abid K, Bouzghaîa K, Kamoun K, Zitouna K, Oughlani K, Lassoued K, Letaif K, Hakim K, Cherif Alami L, Benhmidoune L, Boumhil L, Bouzgarrou L, Dhidah L, Ifrine L, Kallel L, Merzougui L, Errguig L, Mouelhi L, Sahli L, Maoua M, Rejeb M, Ben Rejeb M, Bouchrik M, Bouhoula M, Bourrous M, Bouskraoui M, El Belhadji M, El Belhadji M, Essakhi M, Essid M, Gharbaoui M, Haboub M, Iken M, Krifa M, Lagrine M, Leboyer M, Najimi M, Rahoui M, Sabbah M, Sbihi M, Zouine M, Chefchaouni MC, Gharbi MH, El Fakiri MM, Tagajdid MR, Shimi M, Touaibia M, Jguirim M, Barsaoui M, Belghith M, Ben Jmaa M, Koubaa M, Tbini M, Boughdir M, Ben Salah M, Ben Fraj M, Ben Halima M, Ben Khalifa M, Bousleh M, Limam M, Mabrouk M, Mallouli M, Rebeii M, Ayari M, Belhadj M, Ben Hmida M, Boughattas M, Drissa M, El Ghardallou M, Fejjeri M, Hamza M, Jaidane M, Jrad M, Kacem M, Mersni M, Mjid M, Sabbah M, Serghini M, Triki M, Ben Abbes M, Boussaid M, Gharbi M, Hafi M, Slama M, Trigui M, Taoueb M, Chakroun M, Ben Cheikh M, Chebbi M, Hadj Taieb M, Kacem M, Ben Khelil M, Hammami M, Khalfallah M, Ksiaa M, Mechri M, Mrad M, Sboui M, Bani M, Hajri M, Mellouli M, Allouche M, Mesrati MA, Mseddi MA, Amri M, Bejaoui M, Bellali M, Ben Amor M, Ben Dhieb M, Ben Moussa M, Chebil M, Cherif M, Fourati M, Kahloul M, Khaled M, Machghoul M, Mansour M, Abdesslem MM, Ben Chehida MA, Chaouch MA, Essid MA, Meddeb MA, Gharbi MC, Elleuch MH, Loueslati MH, Sboui MM, Mhiri MN, Kilani MO, Ben Slama MR, Charfi MR, Nakhli MS, Mourali MS, El Asli MS, Lamouchi MT, Cherti M, Khadhraoui M, Bibi M, Hamdoun M, Kassis M, Touzi M, Ben Khaled M, Fekih M, Khemiri M, Ouederni M, Hchicha M, Kassis M, Ben Attia M, Yahyaoui M, Ben Azaiez M, Bousnina M, Ben Jemaa M, Ben Yahia M, Daghfous M, Haj Slimen M, Assidi M, Belhadj N, Ben Mustapha N, El Idrissislitine N, Hikki N, Kchir N, Mars N, Meddeb N, Ouni N, Rada N, Rezg N, Trabelsi N, Bouafia N, Haloui N, Benfenatki N, Bergaoui N, Yomn N, Ben Mustapha N, Maamouri N, Mehiri N, Siala N, Beltaief N, Aridhi N, Sidaoui N, Walid N, Mechergui N, Mnif N, Ben Chekaya N, Bellil N, Dhouib N, Achour N, Kaabar N, Mrizak N, Mnif N, Chaouech N, Hasni N, Issaoui N, Ati N, Balloumi N, Haj Salem N, Ladhari N, Akif N, Liani N, Hajji N, Trad N, Elleuch N, Marzouki NEH, Larbi N, M'barek N, Rebai N, Bibani N, Ben Salah N, Belmaachi O, Elmaalel O, Jlassi O, Mihoub O, Ben Zaid O, Bouallègue O, Bousnina O, Bouyahia O, El Maalel O, Fendri O, Azzabi O, Borgi O, Ghdes O, Ben Rejeb O, Rachid R, Abi R, Bahiri R, Boulma R, Elkhayat R, Habbal R, Rachid R, Tamouza R, Jomli R, Ben Abdallah R, Smaoui R, Debbeche R, Fakhfakh R, El Kamel R, Gargouri R, Jouini R, Nouira R, Fessi R, Bannour R, Ben Rabeh R, Kacem R, Khmakhem R, Ben Younes R, Karray R, Cheikh R, Ben Malek R, Ben Slama R, Kouki R, Baati R, Bechraoui R, Fakhfakh R, Fradi R, Lahiani R, Ridha R, Zainine R, Kallel R, Rostom S, Ben Abdallah S, Ben Hammamia S, Benchérifa S, Benkirane S, Chatti S, El Guedri S, El Oussaoui S, Elkochri S, Elmoussaoui S, Enbili S, Gara S, Haouet S, Khammeri S, Khefecha S, Khtrouche S, Macheghoul S, Mallouli S, Rharrit S, Skouri S, Helali S, Boulehmi S, Abid S, Naouar S, Zelfani S, Ben Amar S, Ajmi S, Braiek S, Yahiaoui S, Ghezaiel S, Ben Toumia S, Thabeti S, Daboussi S, Ben Abderahman S, Rhaiem S, Ben Rhouma S, Rekaya S, Haddad S, Kammoun S, Merai S, Mhamdi S, Ben Ali R, Gaaloul S, Ouali S, Taleb S, Zrour S, Hamdi S, Zaghdoudi S, Ammari S, Ben Abderrahim S, Karaa S, Maazaoui S, Saidani S, Stambouli S, Mokadem S, Boudiche S, Zaghbib S, Ayedi S, Jardek S, Bouselmi S, Chtourou S, Manoubi S, Bahri S, Halioui S, Jrad S, Mazigh S, Ouerghi S, Toujani S, Fenniche S, Aboudrar S, Meriem Amari S, Karouia S, Bourgou S, Halayem S, Rammeh S, Yaïch S, Ben Nasrallah S, Chouchane S, Ftini S, Makni S, Manoubi S, Miri S, Saadi S, Manoubi SA, Khalfallah T, Mechergui T, Dakka T, Barhoumi T, M'rad TEB, Ajmi T, Dorra T, Ouali U, Hannachi W, Ferjaoui W, Aissi W, Dahmani W, Dhouib W, Koubaa W, Zhir W, Gheriani W, Arfa W, Dougaz W, Sahnoun W, Naija W, Sami Y, Bouteraa Y, Elhamdaoui Y, Hama Y, Ouahchi Y, Guebsi Y, Nouira Y, Daly Y, Mahjoubi Y, Mejdoub Y, Mosbahi Y, Said Y, Zaimi Y, Zgueb Y, Dridi Y, Mesbahi Y, Gharbi Y, Hellal Y, Hechmi Z, Zid Z, Elmouatassim Z, Ghorbel Z, Habbadi Z, Marrakchi Z, Hidouri Z, Abbes Z, Ouhachi Z, Khessairi Z, Khlayfia Z, Mahjoubi Z, and Moatemri Z

Subjects
Africa, Northern epidemiology, Anatomy education, Education, Medical history, Education, Medical methods, Education, Medical organization & administration, History, 21st Century, Humans, Internship and Residency standards, Internship and Residency trends, Job Satisfaction, Pathology, Clinical education, Tunisia epidemiology, Education, Medical trends, Medicine methods, Medicine organization & administration, Medicine trends
Published
2019

12. Association of MTHFR C677T, MTHFR A1298C, and MTRR A66G Polymorphisms with Neural Tube Defects in Tunisian Parents.

Author

Nasri K, Midani F, Kallel A, Ben Jemaa N, Aloui M, Boulares M, Lassoued M, Ben Halima M, Ben Wafi S, Soussi M, Mahjoubi I, Baara A, Ben Fradj MK, Omar S, Feki M, Jemaa R, Gaigi SS, and Marrakchi R

Subjects
Alleles, Fathers, Female, Folic Acid metabolism, Genotype, Homocysteine metabolism, Homocystinuria genetics, Humans, Male, Methylenetetrahydrofolate Reductase (NADPH2) deficiency, Mothers, Muscle Spasticity genetics, Neural Tube Defects physiopathology, Polymorphism, Restriction Fragment Length, Pregnancy, Psychotic Disorders genetics, Tunisia, Ferredoxin-NADP Reductase genetics, Genetic Predisposition to Disease, Methylenetetrahydrofolate Reductase (NADPH2) genetics, Neural Tube Defects genetics, Polymorphism, Single Nucleotide
Abstract

Objective: This study aims to investigate the association of 5,10-methylenetetrahydrofolate reductase (MTHFR C677T and A1298C) and methionine synthase reductase (MTRR A66G) gene polymorphisms with neural tube defects (NTDs) in a Tunisian population., Methods: Genotyping was performed by polymerase chain reaction with restriction fragment length polymorphisms (PCR-RFLPs) using the restriction enzymes. Allele and genotype frequencies were compared between mothers and fathers of fetuses with NTDs with matched controls based on an association analysis using SPSS software., Results: MTHFR (C677T, A1298C) and MTRR A66G polymorphisms were found to be protector factors for NTD fetuses in the mother group. In addition, a combination of the three wild-type alleles C677/A1298/A66 has increased four-fold the incidence of NTDs (p = 0.004, OR = 3.96, 95% CI: 1.53-10.23). In the father group, MTHFR C677T was a risk factor for NTDs. However, no association was found between MTHFR A1298C, MTRR A66G, and the occurrence of this anomaly. The analysis of MTHFR C677T and MTRR A66G polymorphisms has demonstrated a significant difference in vitamin B12 levels between recessive and dominant genotypes in case mothers (p < 0.05)., Conclusion: Additional studies are required to better understand the roles of parental gene polymorphisms related to folate-homocysteine metabolism in the pathogenesis of NTD., (© 2019 S. Karger AG, Basel.)

Published
2019
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13. Lack of association between FokI polymorphism in vitamin D receptor gene ( VDR ) & type 2 diabetes mellitus in the Tunisian population.

Author

Mahjoubi I, Kallel A, Sbaï MH, Ftouhi B, Ben Halima M, Jemaa Z, Feki M, Slimane H, Jemaa R, and Kaabachi N

Subjects
Adult, Diabetes Mellitus, Type 2 pathology, Female, Gene Frequency genetics, Genetic Predisposition to Disease, Genotype, Humans, Male, Middle Aged, Polymorphism, Single Nucleotide, Tunisia, Diabetes Mellitus, Type 2 genetics, Genetic Association Studies, Receptors, Calcitriol genetics
Abstract

Background & Objectives: The impact of several environmental and genetic factors on diabetes is well documented. Though the association between the vitamin D receptor (VDR) gene polymorphisms and type 2 diabetes mellitus (T2DM) has been analyzed in different ethnic groups, the results have been inconsistent. The aim of this study was to evaluate the possible association between VDR FokI polymorphism and genetic susceptibility to T2DM in Tunisian population., Methods: A total of 439 unrelated patients with T2DM and 302 healthy controls were included in the study. Genomic DNA was extracted from blood and genotyped for the single nucleotide polymorphism (SNP) of FokI (T/C: (rs2228570) by polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP) analysis., Results: The genotype distribution and the relative allelic frequencies for the FokI polymorphism were not significantly different between T2DM and controls: in T2DM patients the frequencies of the CC, CT, and TT genotypes were 52.6, 41.0, and 6.1 per cent, respectively, and in controls the genotype frequencies were 55.6, 38.7, and 5.6 per cent, respectively. In our study, the TT genotype of the FokI polymorphism was not associated with T2DM (OR =1.19, 95% CI 0.63 - 2.25, P=0.577)., Interpretation & Conclusions: Our study showed no significant association of the FokI polymorphism in the vitamin D receptor gene with type 2 diabetes mellitus in Tunisian population., Competing Interests: None.

Published
2016
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14. The Gly482Ser polymorphism of the peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) is associated with type 2 diabetes in Tunisian population.

Author

Jemaa Z, Kallel A, Sleimi C, Mahjoubi I, Feki M, Ftouhi B, Slimane H, Jemaa R, and Kaabachi N

Subjects
Adult, Case-Control Studies, Female, Follow-Up Studies, Genotype, Humans, Male, Middle Aged, Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Polymerase Chain Reaction, Polymorphism, Restriction Fragment Length, Prognosis, Risk Factors, Tunisia epidemiology, Biomarkers metabolism, Diabetes Mellitus, Type 2 epidemiology, Diabetes Mellitus, Type 2 genetics, Polymorphism, Single Nucleotide genetics, Transcription Factors genetics
Abstract

Background and Aims: Peroxisome proliferator-activated receptor-γ co-activator-1α (PGC-1α) is a transcriptional co-activator involved in adaptive thermogenesis, skeletal muscle metabolism, fatty acid oxidation, and gluconeogenesis. Several studies have suggested that the common PGC-1α polymorphism Gly482Ser (rs8192678) may be associated with risk of type 2 diabetes (T2D), with conflicting results. The aim of this study was to analyze whether the Gly482Ser variant is a risk factor for development of T2D in Tunisian population., Methods: In a case-control study 487 unrelated patients with type 2 diabetes and 402 apparently healthy controls were recruited from January 2008 to August 2010. The Gly482Ser polymorphism was determined by PCR-RFLP analysis., Results: A significant difference in genotypes distribution was observed between patients (Gly/Gly: 34.1%; Gly/Ser: 47.1%; Ser/Ser: 18.5%) and controls (Gly/Gly: 43.8%; Gly/Ser: 42.3%; Ser/Ser: 13.9%) (χ(2)=9.44, p=0.009). The T2D patient group showed a significant higher frequency of the Ser allele compared to the controls (43% vs. 34%; OR: 1.35, 95% [CI]: 1.11-1.65, p=0.002). The association between the Gly482Ser polymorphism and T2D remained significant after adjustment for other well-established cardiovascular risk factors., Conclusions: In the current study, a significant and independent association between the Gly482Ser polymorphism (rs8192678) of the PGC-1α gene and T2D in the Tunisian population was found., (Copyright © 2013 Diabetes India. Published by Elsevier Ltd. All rights reserved.)

Published
2015
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15. Tumor necrosis factor-α (TNF-α) -863C/A promoter polymorphism is associated with type 2 diabetes in Tunisian population.

Author

Kallel A, Ftouhi B, Jemaa Z, Mahjoubi I, Feki M, Slimane H, Jemaa R, and Kaabachi N

Subjects
Adult, Aged, Case-Control Studies, Diabetes Mellitus, Type 2 epidemiology, Female, Gene Frequency, Genotype, Humans, Insulin Resistance genetics, Logistic Models, Male, Middle Aged, Polymerase Chain Reaction, Polymorphism, Restriction Fragment Length, Tumor Necrosis Factor-alpha metabolism, Tunisia epidemiology, Diabetes Mellitus, Type 2 genetics, Polymorphism, Genetic, Promoter Regions, Genetic genetics, Tumor Necrosis Factor-alpha genetics
Abstract

Aims: Tumor necrosis factor α (TNFα) plays a key role in orchestrating the complex events involved in inflammation and immunity. Accordingly, TNF α has been implicated in a wide range of autoimmune and infectious diseases, but also in conditions such as obesity and insulin resistance. The aim of the present study was to investigate the association between the -863C/A polymorphism in the promoter of the TNFα gene and type 2 diabetes in the Tunisian population., Methods: The polymorphism -863C/A in the TNFα gene was determined in 211 type 2 diabetes patients and 345 healthy controls using the Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) analysis., Results: A significant difference in genotype distribution and allele frequency was observed between patients and controls. Patients with type 2 diabetes had significantly higher frequency of the CA+AA genotypes compared to controls [35.5% vs. 22.3%; OR (95%CI), 1.91 (1.31-2.8); p=0.001]. The type 2 diabetes patient group showed a significant higher frequency of the A allele compared to the controls (0.19 vs. 0.11; p=0.001). After adjustment by a stepwise logistic regression method, hypertension, dyslipidemia, and CA+AA genotype were found to be significantly associated with T2D., Conclusion: The present study showed a significant and independent association between the -863C/A polymorphism of the TNFα gene and type 2 diabetes in the Tunisian population., (Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.)

Published
2013
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16. Implication of genetic variation at the promoter and exon1 of UGT1A1 in occurrence of cholelithiasis in Tunisia.

Author

Chaouch L, Said Y, Moumni I, Mahjoubi I, Chaabene AB, Darragi I, Ghanem A, and Abbes S

Subjects
Algorithms, Alleles, Case-Control Studies, Female, Genetic Variation genetics, Humans, Male, Polymerase Chain Reaction, Tunisia, Cholelithiasis genetics, Exons, Glucuronosyltransferase genetics, Polymorphism, Single Nucleotide, Promoter Regions, Genetic genetics
Abstract

Bilirubin is conjugated with glucoronic acid in the liver by UDP-glucuronosyltransferase 1A1 (UGT1A1). Polymorphisms at the promoter region or exon1 of UGT1A1 gene result in unconjugated hyperbilirubinemia and could be at the origin of gallstone formation. The purpose of this study is to determine whether polymorphisms in the promoter area and exon 1 of UGT1A1 can be considered as a risk factor for lithogenesis. Our study involved 76 patients with cholelithiasis as well as 141 unaffected subjects. For each subject an analysis of the bilirubin parameters was performed. We screened genetic variation in the promoter and exon1 UGT1A1 namely the A (TA) nTAA and the six following SNPs: 44T>G, 101C>A, 115C>G, 145C>T, 211G>A and 222 C>A by PCR/sequencing. Our findings show that subjects with (TA)(7) or (TA)(8) variant in their genotypes are associated with high bilirubin level. Furthermore, the comparison between patients and controls according to A(TA)nTAA variation demonstrated that (TA)(6)/(TA)(7) and (TA)(7)/(TA)(7) genotype and (TA)(7) and (TA)(8) alleles were significantly associated with an increased risk of gallstone diseases p=0.0017, p= 6.1 10(-6), p=1.5 10(-6) and p=0.025 respectively. However, polymorphisms in exon1 were normal in all studied subjects except for the 211G>A which appears to be associated with a protective effect p=7.910(-9); OR=0.03, CI95% (0.001-0.158).

Published
2012
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17. [Polymorphisms of the UDP-glucuronosyltransferase 1-A1 gene in Tunisian population].

Author

Chaouch L, Mahjoubi I, Louati I, Mrad R, Douzi K, Ghanem A, and Abbes S

Subjects
Female, Humans, Male, Tunisia, Young Adult, Glucuronosyltransferase genetics, Polymorphism, Genetic
Abstract

The UDP-glucuronosyltransferase 1A1 gene that encode the enzyme UGT1A1 responsible for glucuronidation undergoes several variations that may affect the enzymatic activity or expression and which are the cause of metabolic disorders related to the glucuronidation of bilirubin, such as Gilbert's syndrome and Crigler Najjar's syndrome. Among the most common variations, there is the repeat polymorphism A (TA) n TAA in TATA box and biallelic mutation G211A in exon 1. We consider in this work to determine their frequencies in a healthy population. The polymorphism A (TA) n TAA showed that genotype [TA7/TA7] was described as being associated with Gilbert's syndrome and was encountered in 11% of the population studied. This percentage is close to the value described in the Caucasian population, estimated at 10%. Concerning the polymorphism G211A, our results show that the mutated allele is encountered in 15.7% of our study population. This frequency differs greatly from that reported for Caucasians and Afro-Americans but it is similar to that perceived at the Japanese. All these results suggest that the Tunisian population appears to be heterogeneous view UGT1A1 gene mutation status. Regarding the origins and distribution of such polymorphisms in our population, the study reveals a high haplotypic haplotype (TA) 6-G considered ancestral. The comparison of the haplotype structure generally leads to the development of a hypothetical tree of the origin and spread of different haplotypes.

Published
2011

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