ライフサイエンスコーパス: glucosuria

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1 cohort of 60 individuals with familial renal glucosuria.

2 eneral feature of patients with diabetes and glucosuria.

3 ar glucose transport, resulting in increased glucosuria.

4 nuria or proteinuria but was associated with glucosuria (1.00 glucosuria vs. 0.19 no glucosuria; P =

5 We investigated glucosuria and aminoaciduria in patients with HNF-1alpha

6 t mice exhibit a renal Fanconi syndrome with glucosuria and generalized aminoaciduria in addition to

7 Dapagliflozin treatment induced glucosuria and markedly lowered fasting plasma glucose.

8 e in urine output and a 500-fold increase in glucosuria, as well as compensatory increases in feeding

9 The HNF-1alpha patients had glucosuria at lower glycemic control (as shown by HbA1c)

10 ubjects with IFG and NFG produces comparable glucosuria but lowers the plasma glucose concentration a

11 SGLT2 (SLC5A2) associate with familial renal glucosuria, but the role of SGLT2 in the kidney is incom

12 ia and effectively normalized hyperglycemia, glucosuria, glucose intolerance, and insulin resistance

13 glycemic effect was associated with a robust glucosuria (> 8 g/dL) observed in nondiabetic mice.

14 t works specifically on the kidney to induce glucosuria improves muscle insulin sensitivity.

15 me with juvenile cataracts, microcornea, and glucosuria in a single family.

16 There was mild glucosuria in some animals.

17 However, glucosuria induction following SGLT2 inhibition is assoc

18 Thus, glucosuria is not part of the MCT12 mutation syndrome.

19 Empagliflozin caused 50 +/- 4 and 45 +/- 4 g glucosuria on day 2 in subjects with IFG and NFG, respec

20 with glucosuria (1.00 glucosuria vs. 0.19 no glucosuria; P = 0.002).

21 the eye phenotype, poor correlation with the glucosuria phenotype did not support a pathogenic role o

22 in the family that segregated with the renal glucosuria phenotype.

23 RC2 alone develop a Fanconi-like syndrome of glucosuria, phosphaturia, aminoaciduria, low molecular w

24 Sglt2(-/-) mice had glucosuria, polyuria, and increased food and fluid intak

25 drugs is entirely dependent on the amount of glucosuria produced, it is important to understand why S

26 Significant decrease in severe glucosuria, proteinuria, blood creatinine, urea and adva

27 ria but was associated with glucosuria (1.00 glucosuria vs. 0.19 no glucosuria; P = 0.002).

28 ects with IFG and NFG, respectively, and the glucosuria was maintained for 2 weeks in both groups.

29 showed significantly more aminoaciduria when glucosuria was present compared with when it was absent

30 Diabetic mice also had glucosuria, which may enhance bacterial replication in t

31 be ameliorated in animal models by inducing glucosuria with renal glucose transport inhibitors.

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