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Glycosuria-mediated urinary uric acid excretion in patients with uncomplicated type 1 diabetes mellitus

机译:糖尿病患者患有简单的1型糖尿病患者的尿尿酸排泄物

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Plasma uric acid (PUA) is associated with metabolic, cardiovascular, and renal abnormalities in patients with type 2 diabetes but is less well understood in type 1 diabetes (T1D). Our aim was to compare PUA levels and fractional uric acid excretion (FE_(UA)) in patients with T1D vs. healthy controls (HC) during euglycemia and hyperglycemia. PUA, FEua, blood pressure (BP), glomerular filtration rate (GFR-inulin), and effective renal plasma flow (ERPF-paraaminohippurate) were evaluated in patients with T1D (n = 66) during clamped euglycemia (glucose 4-6 mmol/l) and hyperglycemia (9-11 mmol/l), and in HC (n = 41) during euglycemia. To separate the effects of hyperglycemia vs. increased glycosuria, parameters were evaluated during clamped euglycemia in a subset of T1D patients before and after sodium glucose cotransporter 2 (SGLT2) inhibition for 8 wk. PUA was lower in T1D vs. HC (228 ± 62 vs. 305 ± 75 mumol/l, P < 0.0001). In T1D, hyperglycemia further decreased PUA (228 ± 62 to 199 ± 65 mumol/l, P < 0.0001), which was accompanied by an increase in FEua (7.3 ± 3.8 to 11.6 ± 6.7, P < 0.0001). In T1D, PUA levels correlated positively with SBP (P = 0.029) and negatively with ERPF (P = 0.031) and GFR (P = 0.028). After induction of glycosuria with SGLT2 inhibition while maintaining clamped euglycemia, PUA decreased (P < 0.0001) and FE_(UA) increased (P < 0.0001). PUA is lower in T1D vs. HC and positively correlates with SBP and negatively with GFR and ERPF in T1D. Glycosuria rather than hyperglycemia increases uricosuria in T1D. Future studies examining the effect of uric acid-lowering therapies should account for the impact of ambient glycemia, which causes an important uricosuric effect.
机译:血浆尿酸(PUA)与2型糖尿病患者的代谢,心血管和肾异常有关,但在1型糖尿病(T1D)中较小地理解。我们的目的是将Pua水平和分数尿酸排泄(Fe_(ua))(Fe_(ua))在晚期血症和高血糖期间的T1D对照(HC)中的患者。 PUA,Feua,血压(BP),肾小球过滤速率(GFR-菊粉)和有效的肾脏等离子体流动(ERPF-PARAAMINAPHUPESPURE)在夹紧Eugneycemia期间(葡萄糖4-6mmol / l)和高血糖(9-11mmol / L),在晚期期间的HC(n = 41)。为了分离高血糖对糖尿的影响,在葡萄糖Cotorangerporter 2(SGLT2)抑制8周之前和之后,在T1D患者的血栓抑制期间在T1D患者的子集中进行参数。 PUA在T1D与HC中较低(228±62 vs.305±75 mumol / L,P <0.0001)。在T1D中,高血糖进一步降低PUA(228±62至199±65 mumol / L,P <0.0001),伴随着Feua的增加(7.3±3.8至11.6±6.7,P <0.0001)。在T1D中,PUA水平与SBP(P = 0.029)正面相关,并与ERPF(P = 0.031)和GFR负相关(P = 0.028)。在用SGLT2抑制诱导糖尿针的同时保持夹紧的Euglycemia,PUA降低(P <0.0001)和Fe_(UA)增加(P <0.0001)。 PUA在T1D与HC中较低,与SBP呈正相关,与GFR和T1D中的ERPF负相关。 Glycosuria而不是高血糖在T1D中增加了尿囊尿。检查尿酸酸性疗法的效果的未来研究应考虑到环境糖血症的影响,这导致了重要的尿道疗效。

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