@article{RailaSchweigertKohn2014,
  author    = {Raila, Jens and Schweigert, Florian J. and Kohn, Barbara},
  title     = {Relationship between urinary Tamm-Horsfall protein excretion and renal function in dogs with naturally occurring renal disease},
  series = {Veterinary clinical pathology},
  volume    = {43},
  journal   = {Veterinary clinical pathology},
  number    = {2},
  publisher = {Wiley-Blackwell},
  address   = {Hoboken},
  issn      = {0275-6382},
  doi       = {10.1111/vcp.12143},
  pages     = {261 -- 265},
  year      = {2014},
  abstract  = {Background Tamm-Horsfall protein (THP) is physiologically excreted in urine, but little is known about the role of THP in the diagnosis of renal disease in dogs. Objective The aim of this study was to evaluate to which extent naturally occurring renal disease affects the urinary excretion of THP. Methods Dogs were divided into 5 groups according to plasma creatinine concentration, urinary protein-to-creatinine ratio (UP/UC), and exogenous plasma creatinine clearance (P-ClCr) rates: Group A (healthy control dogs; n=8), nonazotemic and nonproteinuric dogs, with P-ClCr rates > 90mL/min/m2; group B (n=25), nonazotemic and nonproteinuric dogs with reduced P-ClCr rates (51-89mL/min/m2); group C (n=7), nonazotemic but proteinuric dogs with P-ClCr rates 53-98mL/min/m2; group D (n=8), azotemic and borderline proteinuric dogs (P-ClCr rates: 22-45mL/min/m2); and group E (n=15), azotemic and proteinuric dogs (not tested for P-ClCr). THP was measured by quantitative Western blot analysis, and the ratio of THP-to-urinary creatinine (THP/UC) was calculated. Results The THP/UC concentrations were not different among dogs of groups A-D, but were reduced in dogs of group E (P<.001). THP/UC correlated negatively with serum creatinine (P<.01) and UP/UC (P<.01), but was not significantly associated with P-ClCr. Conclusions Decreased levels of THP/UC were present in moderately to severely azotemic and proteinuric dogs. This suggests tubular injury in these dogs and that THP might be useful as urinary marker to study the pathogenesis of renal disease.},
  language  = {en}
}
@article{NairHocherVerkaartetal.2012,
  author    = {Nair, Anil V. and Hocher, Berthold and Verkaart, Sjoerd and van Zeeland, Femke and Pfab, Thiemo and Slowinski, Torsten and Chen, You-Peng and Schlingmann, Karl Peter and Schaller, Andre and Gallati, Sabina and Bindels, Rene J. and Konrad, Martin and H{\"o}nderop, Joost G.},
  title     = {Loss of insulin-induced activation of TRPM6 magnesium channels results in impaired glucose tolerance during pregnancy},
  series = {Proceedings of the National Academy of Sciences of the United States of America},
  volume    = {109},
  journal   = {Proceedings of the National Academy of Sciences of the United States of America},
  number    = {28},
  publisher = {National Acad. of Sciences},
  address   = {Washington},
  issn      = {0027-8424},
  doi       = {10.1073/pnas.1113811109},
  pages     = {11324 -- 11329},
  year      = {2012},
  abstract  = {Hypomagnesemia affects insulin resistance and is a risk factor for diabetes mellitus type 2 (DM2) and gestational diabetes mellitus (GDM). Two single nucleotide polymorphisms (SNPs) in the epithelial magnesium channel TRPM6 ((VI)-I-1393, (KE)-E-1584) were predicted to confer susceptibility for DM2. Here, we show using patch clamp analysis and total internal reflection fluorescence microscopy, that insulin stimulates TRPM6 activity via a phosphoinositide 3-kinase and Rac1-mediated elevation of cell surface expression of TRPM6. Interestingly, insulin failed to activate the genetic variants TRPM6 ((VI)-I-1393) and TRPM6((KE)-E-1584), which is likely due to the inability of the insulin signaling pathway to phosphorylate TRPM6(T-1391) and TRPM6(S-1583). Moreover, by measuring total glycosylated hemoglobin (TGH) in 997 pregnant women as a measure of glucose control, we demonstrate that TRPM6((VI)-I-1393) and TRPM6((KE)-E-1584) are associated with higher TGH and confer a higher likelihood of developing GDM. The impaired response of TRPM6((VI)-I-1393) and TRPM6((KE)-E-1584) to insulin represents a unique molecular pathway leading to GDM where the defect is located in TRPM6.},
  language  = {en}
}