Hiperprolaktinemi ile kitotirozidaz ilişkisinin incelenmesi
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Date
2015
Authors
Tüysüz, Özlem
Journal Title
Journal ISSN
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Publisher
Uludağ Üniversitesi
Abstract
Kitotriozidaz (CHIT) aktive makrofajlardan salınan bir enzimdir ve Gaucher hastalığı, sarkoidoz, β-talasemi, malarya, diyabet, nörolojik hastalıklar ve atheroskleroz gibi birçok bozukluğun etyopatogenezinde rol oynadığı kabul edilmektedir. Kitotirozidaz aktivitesinin makrofaj aktivasyonun bir göstergesi olduğu öne sürülmüştür. Prolaktin üreme, gebelik ve laktasyon olaylarında önemli role sahip olmasının yanında büyüme-gelişme, metabolizma, immün regülasyon ve karsinogenez gibi birçok biyolojik süreçte de etkilidir. Prolaktinin immün sistem üzerinde önemli etkilerinin olduğu, gerek humoral gerekse hücresel immüniteyi uyardığı kabul edilmektedir. İn vitro olarak prolaktinin CHIT gen ekspresyonunu arttırdığı gözlenmiştir. CHIT ve prolaktinin her ikisinin de atherosklerotik fenotipe katkıda bulunduğu ve atherosklerotik lezyonlarda artmış olduğu gösterilmiştir. Bu çalışmada bir makrofaj aktivasyon belirteci olarak tanımlanan CHIT ile immün sistem üzerinde modülatör etkileri olan prolaktinin inflamatuvar bir süreç olan atheroskleroz oluşumu üzerine olası ilişkisinin incelenmesi amaçlandı. Çalışmada CHIT ve prolaktin düzeylerinin ilişkisinin incelenmesi amacıyla hiperprolaktinemik (H-PRL; 85 kadın, 36 erkek) ve makroprolaktinemik (M-PRL; 14 kadın, 5 erkek) hastalar kontrol grubu (37 kadın, 17 erkek) ile karşılaştırıldı. CHIT enzim aktivitesi florometrik yöntemle, CHIT kütle düzeyi ise ELISA ile tayin edildi. Ayrıca hiperprolaktinemide oksidan-antioksidan sistemleri araştırmak amacıyla lipit profili, lipit peroksidasyon belirteci olarak malondialdehit (MDA) ve total antioksidan kapasite (TAK) çalışıldı. Çalışmamızda H-PRL grubunda CHIT-kütle düzeyinin kontrol (p <0.01) ve M-PRL (p<0.05) gruplarından düşük olduğu bulundu. CHIT aktivitesinin gruplar arasında farklılık göstermediği saptandı. CHIT-kütle ile CHIT aktivitesi arasında kontrol ve M-PRL gruplarında istatistiksel olarak anlamlı pozitif ilişki saptandığı halde H-PRL grubunda bu ilişkinin olmadığı görüldü. CHIT-kütle ve aktivitesinin kontrol grubunda yaşla pozitif korelasyon gösterdiği ancak H-PRL ve M-PRL gruplarında bu korelasyonun bulunmadığı saptandı. Serum glukoz düzeyinin ve lipit parametrelerinin gruplar arasında farklı olmadığı görüldü. Serum prolaktin ve CHIT-kütle düzeyleri, CHIT aktivitesi ve lipid parametreleri arasında çalışma gruplarında anlamlı bir ilişki gözlenmedi. Serum TAK'nin H-PRL ve M-PRL gruplarında kontrol grubuna göre anlamlı şekilde daha yüksek olduğu saptandı. Serum MDA düzeyi gruplar arasında anlamlı farklılık göstermedi. Sonuç olarak bu çalışmada, in vitro şartlarda prolaktinin CHIT indüksiyonuna yol açtığı yönündeki verilerin aksine H-PRL grupta serum CHIT-kütle düzeyinin M-PRL ve kontrol gruplarından anlamlı olarak daha düşük olduğu bulundu. Hiperprolaktinemik gruplarda lipit parametrelerinin ve atherojenik indeksin kontrol grubuna göre farklı olmaması hiperprolaktineminin belirgin dislipidemi ile birlikte olmadığı bulgusunu destekler nitelikteydi.
Chitotriosidase (CHIT), an enzyme released from active macrophages, has been accepted to play role in the pathogenesis of several disorders, such as Gaucher disease, sarcoidosis, β-thalassemia, malaria, diabetes, neurological diseases and atherosclerosis. It is also suggested to be an indicator of macrophage activation. In addition to its pivotal role in fertility, maternity and lactation, prolactin effects many biological processes such as growth, metabolism, immune regulation and carcinogenesis. It is accepted that prolactin has a vital effects on immune system by stimulating both humoral and cellular immunity. It was observed that prolactin increased expression of CHIT genes. Moreover, it was suggested that both CHIT and prolactin contribute to expression of atherosclerotic phenotype and they were shown to be increased in atherosclerotic lesions. In this study, CHIT, identified as a macrophage activation indicator, and prolactin, an immune system modulator, were evaluated in order to investigate their possible association with atherogenesis which is an inflammatory process. In order to examine the relation between CHIT and prolactin levels, hyperprolactinemic (H-PRL) patients (85 female, 36 male; n: 121), macroprolactinemic (M-PRL) patients (14 female, 5 male; n: 19) and control group (37 female, 17 male; n: 54) were included in this study. CHIT enzyme activity and mass were determined by a fluorometric assay and ELISA, respectively. Moreover, lipid profile, malondialdehyde (MDA) a lipid peroxydation indicator, and total antioxidant capacity (TAC) were evaluated in order to investigate the oxidative and antioxidative systems in hyperprolactinemia. CHIT-mass level of the H-PRL group was significantly less than those of the control (p<0.01) and M-PRL (p<0.05) groups. It was observed that CHIT activity did not differ among the study groups. There was a significant positive correlation between the CHIT-mass and CHIT activity in both the control and M-PRL groups, but not in the H-PRL group. It is detected that both CHIT-mass and CHIT activity had a positive correlation with age in the control group; but not in the H-PRL and M-PRL groups. It was observed serum glucose and lipid profile parameters dwere not different between the study groups. There was not any significant correlation between the prolactin and CHIT-mass levels, CHIT activity and lipid profile parameters in any of the study groups. Serum TAC levels were significantly higher in both the H-PRL ve M-PRL groups compared with those of the control group. Serum MDA levels were not different among the study groups. In the present study, in contrast with the findings of in vitro studies which reported that prolactin induced CHIT expression, serum CHIT-mass concentration was significantly lower in H-PRL group compared with those of the M-PRL and control groups. Since serum lipid parameters and atherogenic index were not different between the study groups we conclude that hyperprolactinemia does not accompany with dyslipidaemia.
Chitotriosidase (CHIT), an enzyme released from active macrophages, has been accepted to play role in the pathogenesis of several disorders, such as Gaucher disease, sarcoidosis, β-thalassemia, malaria, diabetes, neurological diseases and atherosclerosis. It is also suggested to be an indicator of macrophage activation. In addition to its pivotal role in fertility, maternity and lactation, prolactin effects many biological processes such as growth, metabolism, immune regulation and carcinogenesis. It is accepted that prolactin has a vital effects on immune system by stimulating both humoral and cellular immunity. It was observed that prolactin increased expression of CHIT genes. Moreover, it was suggested that both CHIT and prolactin contribute to expression of atherosclerotic phenotype and they were shown to be increased in atherosclerotic lesions. In this study, CHIT, identified as a macrophage activation indicator, and prolactin, an immune system modulator, were evaluated in order to investigate their possible association with atherogenesis which is an inflammatory process. In order to examine the relation between CHIT and prolactin levels, hyperprolactinemic (H-PRL) patients (85 female, 36 male; n: 121), macroprolactinemic (M-PRL) patients (14 female, 5 male; n: 19) and control group (37 female, 17 male; n: 54) were included in this study. CHIT enzyme activity and mass were determined by a fluorometric assay and ELISA, respectively. Moreover, lipid profile, malondialdehyde (MDA) a lipid peroxydation indicator, and total antioxidant capacity (TAC) were evaluated in order to investigate the oxidative and antioxidative systems in hyperprolactinemia. CHIT-mass level of the H-PRL group was significantly less than those of the control (p<0.01) and M-PRL (p<0.05) groups. It was observed that CHIT activity did not differ among the study groups. There was a significant positive correlation between the CHIT-mass and CHIT activity in both the control and M-PRL groups, but not in the H-PRL group. It is detected that both CHIT-mass and CHIT activity had a positive correlation with age in the control group; but not in the H-PRL and M-PRL groups. It was observed serum glucose and lipid profile parameters dwere not different between the study groups. There was not any significant correlation between the prolactin and CHIT-mass levels, CHIT activity and lipid profile parameters in any of the study groups. Serum TAC levels were significantly higher in both the H-PRL ve M-PRL groups compared with those of the control group. Serum MDA levels were not different among the study groups. In the present study, in contrast with the findings of in vitro studies which reported that prolactin induced CHIT expression, serum CHIT-mass concentration was significantly lower in H-PRL group compared with those of the M-PRL and control groups. Since serum lipid parameters and atherogenic index were not different between the study groups we conclude that hyperprolactinemia does not accompany with dyslipidaemia.
Description
Keywords
Kitotriozidaz, Prolaktin, Makroprolaktin, Atheroskleroz, Oksidan-antioksidan sistem, Chitotriosidase, Prolactin, Macroprolactin, Atherosclerosis, Oxidative-antioxidative system
Citation
Tüysüz, Ö. (2015). Hiperprolaktinemi ile kitotirozidaz ilişkisinin incelenmesi. Yayınlanmamış uzmanlık tezi. Uludağ Üniversitesi Tıp Fakültesi.