Tip 2 diyabetik hastalarda serum visfatin fetuin A ve eotaksin düzeylerinin incelenmesi
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Tarih
2016
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Erişim Hakkı
info:eu-repo/semantics/embargoedAccess
Özet
Yağ dokusu, adipokin olarak bilinen metabolik olarak aktif birçok molekül salgılar. Bunlardan bazıları obezite, insülin direnci ve tip 2 diyabetle ilişkili bulunmuştur. Tip 2 diyabet ile ilişkili olduğu belirtilen adipokinlerden biri özellikle viseral yağ dokusundan salgılanan visfatindir. Viseral yağ dokusunda bulunduğu belirtilen ve immün sistemin bazı hücreleri tarafından üretilen eotaksin, özellikle alerjik ve inflamatuar reaksiyonlarda rol oynayan bir proinflamatuar sitokin olarak tanımlanmıştır. Bununla birlikte, eotaksinin insülin direnci ve diyabetle ilişkili olabileceği ileri sürülmüştür. Obezite, insülin direnci ve tip 2 diyabetle ilişkili olabileceği ileri sürülen bir diğer molekül, başlıca karaciğerden salgılanan protein tabiatlı fetuin A dır. Ancak, şimdiye kadar yapılmış olan araştırmaların sonuçları visfatin, eotaksin ve fetuin A nın obezite, insülin direnci ve diyabetle ilişkisini tam olarak açıklamaya yeterli değildir. Üstelik bu konuda araştırma sonuçları birbirleriyle tam bir uyum göstermemektedir. Bu nedenle, yapmış olduğumuz çalışmada; obez ve obez olmayan medikal tedavi gören tip 2 diyabetik hastalarda serum visfatin, eotaksin ve fetuin A düzeylerini ölçtük ve bu parametrelerin hem diyabet ile hemde kendi aralarında olası ilişkilerini inceledik. Bu çalışmaya, yaşları 47-83 arasında değişen toplam 30 tip 2 diyabetik hasta ile yaş ve cinsiyet bakımından benzer toplam 20 sağlıklı ve gönüllü denek alındı. 30 hasta vücut kütle indeksine göre iki alt gruba ayrıldı. Obez olmayan diyabetik grup, BMI değeri 18.50 ile 24.99kg/m2 arasında olanlar (n=6), obez diyabetik grup ise BMI?25kg/m2 (n=24) olarak belirlendi. Yaklaşık 12 saatlik açlığı takiben alınan kan örneklerinde BUN, kreatinin, AST, ALT, açlık serum glukozu, HbA1c, açlık serum insülini, TG, total kolesterol, HDL-K, LDL-K düzeyleri uygun metotlarla ölçüldü. İnsülin direnci (HOMA-IR), açlık serum glukoz ve insülin değerleri kullanılarak formülden hesaplandı. Serum visfatin, eotaksin ve fetuin A düzeyleri ELİSA yöntemiyle ölçüldü. Elde edilen verilerin gruplar arasındaki karşılaştırmaları için Mann-Witney U testi, korelasyonlar için Spearman's analizi kullanıldı. Diyabetik hastalarda serum açlık glukoz düzeyi kontrollere kıyasla önemli ölçüde yüksek bulundu (P<0.001, P<0.05). Glikolize hemoglobin (HbA1c) değerleri de benzer şekilde yüksek bulundu (P<0.001). Serum açlık insülin düzeyi ve insülin dirençleri obez diyabetik hastalarda obez olmayan diyabetik hastalara göre önemli ölçüde yüksek bulundu (P<0.05). Total kolesterol ve LDL-K bakımından hasta ve kontrol grupları arasında önemli bir farklılık bulunmadı. Obez olmayan diyabetiklerde serum TG düzeyleri kontrollerine oranla yüksek bulundu (P<0.05). Her iki hasta grubunda da serum HDL-K düzeyi kontrollere ve referans değerlere göre düşük bulundu. Serum visfatin seviyeleri hem obez hem de obez olmayan diyabetik hastalarda kontrollerine göre yüksek olup, hasta ve kontrol grupları arasındaki farklılık istatistiksel olarak önemli bulundu (p<0.05). Kontrol grupları kendi aralarında karşılaştırıldığında obez kontrollerin serum visfatin seviyeleri obez olmayanlardan yüksek bulundu. Obez diyabetik hastalar ile bunların kontrollerinde serum visfatin düzeyi ile BMI arasında pozitif korelasyon (p<0.05, p<0.001) bulunurken, obez olmayan kontrollerde ise negatif korelasyon belirlendi (p<0.05). Obez kontrollerde visfatin düzeyi ile eotaksin düzeyi arasında doğrusal önemli bir ilişki belirlendi (p<0.05). Serum eotaksin düzeyleri, her iki diyabetik hasta grubunda da kontrollerine göre, önemli derecede yüksek bulundu (p<0.001, p<0.05). Obez kontrollerde serum eotaksin düzeyi ile serum visfatin düzeyi arasında pozitif önemli bir ilişki belirlendi (p<0.05). Serum fetuin A düzeyleri bakımından hasta ve kontrol grupları arasında önemli bir farklılık bulunmadı. Obez olmayan kontrollerde serum fetuin A düzeyi ile serum açlık insülin düzeyi ve insülin direnci arasında pozitif önemli korelasyon belirlendi (p<0.05). Sonuçlarımız visfatin, eotaksin ve fetuin A nın obezite ve tip 2 diyabet patogenezinde rol oynayabileceğini göstermektedir. Ancak, bunların hangi mekanizmalar aracılığıyla rol oynadığını açıklayabilmek için daha ileri ve kapsamlı çalışmalara ihtiyaç vardır. Anahtar kelimeler: Tip 2 diyabet, visfatin, eotaksin, fetuin A
Adipose tissue, secretes metabolically active many molecules that known as adipokin. Some of these have been found associated with obesity, insulin resistance and type 2 diabetes. Visfatin is the one of adipokines secreted by visceral adipose tissue especially and has been specified to be associated with type 2 diabetes. Eotaxin is located in visceral adipose tissue and produced by certain cells of the immune system that has a role involved particularly allergic and inflammatory reactions and it has been identified as a proinflammatory cytokin. In addition to this, it has been suggested that eotaxin to be associated with insulin resistance and diabetes. Fetuin A is another protein molecule secreted from the liver that it may be associated with obesity, insulin resistance and type 2 diabetes. However, the results of the research done so far are not enough to explain the relationship of obesity, insulin resistance and diabetes mellitus with visfatin, eotaxin and fetuin A. Moreover, the results of research on this subject does not present a complete harmony. Therefore, in this study; we measured serum levels of visfatin, eotaxin and fetuin A in obese and non-obese type 2 diabetic patients treated medically. And we examined the possible relationship these parameters both diabetes and between them. The study was carried out in 30 T2DM patients with varying ages between 47-83 and 20 sex and age matched healthy volunteers control subjects (n=20). According to the body mass index (BMI) 30 patients were divided into two subgroups; one group was non-obese diabetic patients with 18.50<BMI <24.99kg/m2 (n=6) and the other group was type 2 diabetic obese diabetic patients with BMI?25kg/m2 (n=24). In blood samples taken after fasting for about 12 hours BUN, creatinine, AST, ALT, fasting serum glucose, HbA1c, fasting serum insulin, TG, total cholesterol, HDL-C, LDL-C levels were measured by conventional methods. Insulin resistance (HOMA-IR) was calculated from the formula using the values of fasting serum glucose and insulin. Serum visfatin, eotaxin and fetuin A levels were measured by ELISA method. Mann-Witney U test obtained for comparisons between groups of data, Spearman's test were used for correlation analysis. Serum fasting glucose levels compared to controls in diabetic patients was significantly higher (P<0.001, P<0.05). Glycosylated hemoglobin (HbA1c) levels were likewise increased (P<0.001). Serum fasting insulin levels and insulin resistance in obese diabetic patients was significantly higher than non-obese diabetic patients (P <0.05). There were no significant differences between patient and control groups in terms of total cholesterol and LDL-C levels. Serum TG levels were higher in non-obese diabetic patients compared to their controls (P<0.05). Both groups of patients were had significantly lower serum HDL-C levels compared to controls and reference values. Serum visfatin levels are higher than controls in both obese and non-obese diabetic patients, the differences between the patient and control groups were statistically significant (p<0.05). The control groups were compared among themselves serum visfatin levels of obese controls were higher than non-obese controls. While a positive correlation was found between serum visfatin level and BMI in obese diabetic patients and their controls (p<0.05, p<0.001), negative correlations were determined In non-obese controls (p<0.05). A linear significant relationship were determined between visfatin and eotaxin levels in obese controls (p<0.05). Serum eotaxin levels in both diabetic groups were significantly higher than their controls (p<0.001, p<0.05). A significant positive correlation were determined between serum visfatin and eotaxin levels in obese controls (p <0.05). There were no significant differences between patient and control groups in terms of serum fetuin A levels. Serum fetuin A levels with serum fasting insulin levels and insulin resistance was observed a significant linear relationship in non-obese controls (p <0.05). Our results have showed that visfatin, eotaxin and fetuin A may play a role in pathogenesis of the obesity and type 2 diabetes. However, to explain the mechanism through which they act there is need for further and comprehensive study. Key words: Type 2 diabetes mellitus, visfatin, eotaxin, fetuin A
Adipose tissue, secretes metabolically active many molecules that known as adipokin. Some of these have been found associated with obesity, insulin resistance and type 2 diabetes. Visfatin is the one of adipokines secreted by visceral adipose tissue especially and has been specified to be associated with type 2 diabetes. Eotaxin is located in visceral adipose tissue and produced by certain cells of the immune system that has a role involved particularly allergic and inflammatory reactions and it has been identified as a proinflammatory cytokin. In addition to this, it has been suggested that eotaxin to be associated with insulin resistance and diabetes. Fetuin A is another protein molecule secreted from the liver that it may be associated with obesity, insulin resistance and type 2 diabetes. However, the results of the research done so far are not enough to explain the relationship of obesity, insulin resistance and diabetes mellitus with visfatin, eotaxin and fetuin A. Moreover, the results of research on this subject does not present a complete harmony. Therefore, in this study; we measured serum levels of visfatin, eotaxin and fetuin A in obese and non-obese type 2 diabetic patients treated medically. And we examined the possible relationship these parameters both diabetes and between them. The study was carried out in 30 T2DM patients with varying ages between 47-83 and 20 sex and age matched healthy volunteers control subjects (n=20). According to the body mass index (BMI) 30 patients were divided into two subgroups; one group was non-obese diabetic patients with 18.50<BMI <24.99kg/m2 (n=6) and the other group was type 2 diabetic obese diabetic patients with BMI?25kg/m2 (n=24). In blood samples taken after fasting for about 12 hours BUN, creatinine, AST, ALT, fasting serum glucose, HbA1c, fasting serum insulin, TG, total cholesterol, HDL-C, LDL-C levels were measured by conventional methods. Insulin resistance (HOMA-IR) was calculated from the formula using the values of fasting serum glucose and insulin. Serum visfatin, eotaxin and fetuin A levels were measured by ELISA method. Mann-Witney U test obtained for comparisons between groups of data, Spearman's test were used for correlation analysis. Serum fasting glucose levels compared to controls in diabetic patients was significantly higher (P<0.001, P<0.05). Glycosylated hemoglobin (HbA1c) levels were likewise increased (P<0.001). Serum fasting insulin levels and insulin resistance in obese diabetic patients was significantly higher than non-obese diabetic patients (P <0.05). There were no significant differences between patient and control groups in terms of total cholesterol and LDL-C levels. Serum TG levels were higher in non-obese diabetic patients compared to their controls (P<0.05). Both groups of patients were had significantly lower serum HDL-C levels compared to controls and reference values. Serum visfatin levels are higher than controls in both obese and non-obese diabetic patients, the differences between the patient and control groups were statistically significant (p<0.05). The control groups were compared among themselves serum visfatin levels of obese controls were higher than non-obese controls. While a positive correlation was found between serum visfatin level and BMI in obese diabetic patients and their controls (p<0.05, p<0.001), negative correlations were determined In non-obese controls (p<0.05). A linear significant relationship were determined between visfatin and eotaxin levels in obese controls (p<0.05). Serum eotaxin levels in both diabetic groups were significantly higher than their controls (p<0.001, p<0.05). A significant positive correlation were determined between serum visfatin and eotaxin levels in obese controls (p <0.05). There were no significant differences between patient and control groups in terms of serum fetuin A levels. Serum fetuin A levels with serum fasting insulin levels and insulin resistance was observed a significant linear relationship in non-obese controls (p <0.05). Our results have showed that visfatin, eotaxin and fetuin A may play a role in pathogenesis of the obesity and type 2 diabetes. However, to explain the mechanism through which they act there is need for further and comprehensive study. Key words: Type 2 diabetes mellitus, visfatin, eotaxin, fetuin A
Açıklama
Anahtar Kelimeler
Tip 2 diyabet, Type 2 diabetes mellitus, Visfatin, Eotaksin, Eotaxin, Fetuin A