Journals / Turkish Journal of Medical Sciences / 1998 / Cilt: 28 - Sayı: 4

Effects of gliclazide and insulin therapy on thromboxane B2 and 6-keta-PGF1alpha levels in type II diabetic patients

Pages
431–435
Publication Date
2022-11-05
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

According to the datas in our study, giiclazide therapy decreased TXB2 levels as well as 6-keto-PGF1a levels so that ratio of TXB.,/6-keto-PGF, did not change, which would 1a 3 mean that gliclazide has neutral effect on diabetic microvascular complications.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Diabetic patients show hemobiolo-gical abnormalities such as increased platelet adhesiveness, platelet hyperaggregability, decreased platelet half life, hemorheological abnormalities and altered fibrinolysis, perhaps contributing to a procoagulative state.
📊
Key Findings & Data:We studied thromboxane A metabolite; serum thomboxane B2 (TXB ] and the prostacyclin metabolite, 6-keto-PGF1 to assess the efficacy of gliclazide on these parameters.
💡
Conclusion & Impact:According to the datas in our study, giiclazide therapy decreased TXB2 levels as well as 6-keto-PGF1a levels so that ratio of TXB.,/6-keto-PGF, did not change, which would 1a 3 mean that gliclazide has neutral effect on diabetic microvascular complications.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Diabetic patients show hemobiolo-gical abnormalities such as increased platelet adhesiveness, platelet hyperaggregability, decreased platelet half life, hemorheological abnormalities and altered fibrinolysis, perhaps contributing to a procoagulative state. Gliclazide, a novel sulfonylurea in routine clinical use, was thought to have effects on prostanoid release and platelet function. We studied thromboxane A metabolite; serum thomboxane B2 (TXB ] and the prostacyclin metabolite, 6-keto-PGF1 to assess the efficacy of gliclazide on these parameters. Two groups of age and sex matched type Il diabetics were examined in the study. There were 16 subjects in each group (F: M= 10/6). The study period was 12 weeks. Gliclazide was given to the first group and insulin to the second. Following parameters were evaluated to see the effect of good control. HbAIc, cholesterol, triglycéride, HDL cholesterol, LDL cholesterol, serum TXB2,6-keto-PGF] levels were measured before and after 3 months of therapy. There was no significant change in TXB2 (2.24±0.2 to 2.08±0.4 nmol/L) and 6-keto-PGF] (2.53±0.2 to 2.15±0.1 nmol/L,) levels in patients treated with insulin despite the amelioration in the HbAIc levels. Therapy ' with gliclazide was followed by a significant decrease in both serum TXB levels (4.18±0.7 to 2.72±0.4, p=0.039] and 6-keto-PGF (2.97±0.3 to 2.03±0.1, p=0.0047)KTXB /6-keto-PGF] ratio did not change both after insulin (1.09±O.S to 1.06±0.8)and gliclazide (1.31±0.9 to 1.32±0.4) treatment. According to the datas in our study, giiclazide therapy decreased TXB2 levels as well as 6-keto-PGF1a levels so that ratio of TXB.,/6-keto-PGF, did not change, which would 1a 3 mean that gliclazide has neutral effect on diabetic microvascular complications.

🔖

Cite This Article

ÖZGEN, A. G., BAYINDIR, O., HAMULU, F., YILMAZ, C., ÇETİN, M., ÖZMEN, D. (2022). Effects of gliclazide and insulin therapy on thromboxane B2 and 6-keta-PGF1alpha levels in type II diabetic patients. Turkish Journal of Medical Sciences, Cilt: 28 - Sayı: 4, 431–435. https://ajindex.com/articles/612687

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (3)

  1. Jones DB, Carter RD, Haitas B, MannJI: Low phospholipid arachidonic acidvalues in diabetic patients. Br Med J286: 173-75, 1983. 2.Zigler O, Drovin P: Haemobiologicalactivity of gliclazide in diabetesmellitus. Diabetes Res Clin Pract 14-2P: 85-9, 1991. 3.Fitzpatrick FA: A radioimmunoassay forthromboxane B2. Methods-Enzymol86: 286-97, 1982. 4.Moncada S, Vane JR: Pharmacologyand endogenous roles of prostaglandinendoperoxides, thromboxane A2 andprostacyclin. Pharmac Rev 30: 292-331, 1979. 5.Hamberg M, Sevensson J, SamuelssonB: Thromboxanes: a new group ofbiologically active compounds derivedfrom prostaglandin endoperoxides.Proc Natl Acad Sci 72: 2294-2998,1975. 6.Larkins RG, Jerums G, Taft JL, GodfreyH, Smith IL, Martin TJ: Lack of effect ofgliclazide on platelet aggregation ininsulin treated and non insulin treateddiabetics. Diabetes Res Clin Pract 4:81-7, 1988. 7.Keskin A, Özgen AG, Sermez Y, YılmazC, Büyükkeçeci F. Platelet function intype II diabetes mellitus and the effectof glycemic control on plateletreactivity. Turk J Endoc 5: 179-185,1995. 8.Tsuboi T, Fujitani B, Maeda T, YashidaK, Shimizu M: Effect of gliclazide onprostaglandin and thromboxanesynthesis in guinea pig platelets.Thromb Res 21: 103-110, 1981. 9.Fujitani B, Maeda J, Tsuboi T,Kadokawa T, Shimizu M: Effect ofgliclazide on prostaglandin l2formation in normal and streptozotocininduced diabetic animals. Jpn JPharmacol 33:965-70, 1983. 10.Ziboh VA, Maruta H, Lord J, Cagle WD,Lucky W: Increased biosynthesis ofthromboxane A2 in diabetic platelets.Eur J Clin Invest 1979
  2. Legarde M, Budin M, Berclaud P, BlancM, Velardo B, Dechavanne M: Increaseof platelet Thromboxane A2 formationand of its plasmatic half life in diabetesmellitus. Thromb Res 1980
  3. Brunner D, Klinger J, Weisbort J, TuvalM, Nakash J, Rosenberg CH, Nissim S:Thromboxane, prostacyclin betathromboglobulin and diabetes mellitus.Clin Ther 6: 636-42, 1984. 13.DiMinno G, Silver MJ, Cerbone AM,Riccardi G, Rivellese A, Macini M,Thiagarajan P: Increased binding offibrinogen to platelets in diabetes therole of prostaglandin’s andthromboxane. Blood 65: 156-162,1985. 14.Silberbauer K, Schernthaner G,Sinzinger H, Piza Katzer H, Winer M:Decreased vascular prostacyclin injuvenile onset diabetes. N Eng J Med300: 306-7, 1979. 15.Davi G, Rini GB, Averna M, Novo S, DiFede G, Pinto A, Notarbartolo A, StranoA: Thromboxane B2 formation andplatelet sensitivity to prostacyclin ininsulin dependent and noninsulin-independent diabe