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1 2 weeks, while female KO mice had persistent glycosuria.
2 2 and in RPTCs of wild-type mice but induced glycosuria.
3 unced for neutral and polar amino acids, and glycosuria.
4  lower the blood glucose levels by promoting glycosuria.
5  knockout mice, we demonstrate that elevated glycosuria activates the hypothalamic-pituitary-adrenal
6 cative of Fanconi syndrome, characterized by glycosuria, aminoaciduria, calciuria, and albuminuria.
7 restingly, high dietary K(+) rapidly lowered glycosuria and gluconeogenesis, despite persistent reduc
8 t high risk of death and 2 new risk markers, glycosuria and hemoglobin decline.
9 , performed the best, was less influenced by glycosuria and identified culture positive pediatric (N
10 is the underlying mechanism for the observed glycosuria and improved glucose tolerance in ArcPOMC-def
11 s glucose production in response to elevated glycosuria and loss of glucose in urine is sensed as a b
12     The primary actions of SGLT2 inhibition, glycosuria and natriuresis, are pivotal in enhancing glu
13  (NFBC1986; 747/2991) using midwife-reported glycosuria and offspring genotype as a proxy for materna
14                         Associations between glycosuria and the primary composite end point from CRED
15  including low molecular weight proteinuria, glycosuria, and polyuria.
16                                              Glycosuria at some point during pregnancy has an estimat
17 revealed evidence for a consistent effect on glycosuria at the chromosome 16 locus.
18 intended to treat hyperglycemia by enhancing glycosuria but are met with a compensatory increase in e
19  normal-K(+) diet, mTORC2 KO mice had marked glycosuria despite normal blood glucose.
20                                     However, glycosuria disappeared in male KO mice at the age of 12
21 e and chronic empagliflozin treatment caused glycosuria during fasting (median, 7.8 [interquartile ra
22 ied a genetic association with self-reported glycosuria during pregnancy, with the lead SNP located 1
23 sts different genetic risk factors exist for glycosuria during pregnancy.
24                    Pharmacologically induced glycosuria elicits adaptive responses in glucose homeost
25 o pharmacologically induced acute or chronic glycosuria has not been investigated in human diabetes.
26 tio, 3.5; 95% confidence interval, 2.4-5.1); glycosuria (hazard ratio, 4.2; confidence interval, 1.3-
27  with type 2 diabetes, empagliflozin-induced glycosuria improved beta cell function and insulin sensi
28 e association study (GWAS) for self-reported glycosuria in pregnant mothers from the Avon Longitudina
29 e following: tubular proteinuria, euglycemic glycosuria, increased urinary phosphate, and uric acid e
30  effects could be attributed to the elevated glycosuria induced by these drugs.
31                               The pattern of glycosuria-induced changes was similar in subjects witho
32                                              Glycosuria is a condition where glucose is detected in u
33                    Loss of glucose in urine (glycosuria) is offset by an increase in endogenous gluco
34  canagliflozin, individuals with the highest glycosuria levels had the strongest protection against m
35 then validated using an obstetric measure of glycosuria measured in the same cohort (227/6639).
36                                          The glycosuria of ArcPOMC-deficient mice was due to decrease
37                                              Glycosuria or fructosuria was associated with increased
38 P = rs13337037; chromosome 16; odds ratio of glycosuria per effect allele: 1.42; 95% CI: 1.30, 1.56;
39 reased glucose effectiveness and exaggerated glycosuria relative to wild-type littermate controls at
40 m-glucose cotransporter-2 inhibitors promote glycosuria, resulting in possible effects on calcium, ph
41 s of carbohydrate into urine, SGLT2-mediated glycosuria results in a progressive shift in fuel utiliz
42 le dose of dapagliflozin to induce transient glycosuria showed increased activity of the WNK4-SPAK-NC
43 in the proximal tubule, these agents promote glycosuria, thereby reducing blood glucose concentration
44  role in the development of hypertension and glycosuria through modulation of renal Agt and Sglt2 exp
45 ecular weight proteinuria, aminoaciduria and glycosuria, together with rickets in some patients.
46 uced in the setting of hyperglycemia-induced glycosuria, were lower in black persons than in white pe
47 eversed alterations in glucose tolerance and glycosuria, whereas, conversely, administration of the a
48 nine ratio, tubulo-interstitial fibrosis and glycosuria without changes in blood glucose or glomerula