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Do Endocannabinoids Regulate Glucose Reabsorption in the Kidney?

Do Endocannabinoids Regulate Glucose Reabsorption in the Kidney? Diabetic nephropathy (DN), a distinct manifestation of diabetic kidney disease, affects approximately 30% of patients with diabetes. While most attention has been focused on glomerular changes related to DN, there is growing evidence that tubulopathy is a key feature in the pathogenesis of this disease. The renal proximal tubule cells (RPTCs) are particularly sensitive to the deleterious effect of chronic hyperglycemia. However, the cellular changes that control the dysfunction of the RPTCs are not fully understood. Controlling glucose reabsorption in the proximal tubules via inhibition of glucose transporters (GLUT) has emerged as a promising therapeutic in ameliorating DN. Overactivation of the renal endocannabinoid (eCB) system via the cannabinoid-1 receptor (CB<sub>1</sub>R) contributes to the development of DN, and its blockade by globally acting or peripherally restricted CB<sub>1</sub>R antagonists has been shown to ameliorate renal dysfunction in different murine models for diabetes. Recently, we have utilized various pharmacological and genetic tools to show that the eCB/CB<sub>1</sub>R system contributes to the development of DN via regulating the expression, translocation, and activity of the facilitative GLUT2 located in the RPTCs. These findings have the potential to be translated into therapy, and support the rationale for the preclinical development of novel renal-specific CB<sub>1</sub>R and/or GLUT2 inhibitors for the treatment of DN. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nephron Karger

Do Endocannabinoids Regulate Glucose Reabsorption in the Kidney?

Hinden, Liad; Tam, Joseph
Nephron , Volume 143 (1): 4 – Sep 1, 2019
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Publisher
Karger
Copyright
© 2019 S. Karger AG, Basel
ISSN
1660-8151
eISSN
2235-3186
DOI
10.1159/000494512
Publisher site
See Article on Publisher Site

Abstract

Diabetic nephropathy (DN), a distinct manifestation of diabetic kidney disease, affects approximately 30% of patients with diabetes. While most attention has been focused on glomerular changes related to DN, there is growing evidence that tubulopathy is a key feature in the pathogenesis of this disease. The renal proximal tubule cells (RPTCs) are particularly sensitive to the deleterious effect of chronic hyperglycemia. However, the cellular changes that control the dysfunction of the RPTCs are not fully understood. Controlling glucose reabsorption in the proximal tubules via inhibition of glucose transporters (GLUT) has emerged as a promising therapeutic in ameliorating DN. Overactivation of the renal endocannabinoid (eCB) system via the cannabinoid-1 receptor (CB<sub>1</sub>R) contributes to the development of DN, and its blockade by globally acting or peripherally restricted CB<sub>1</sub>R antagonists has been shown to ameliorate renal dysfunction in different murine models for diabetes. Recently, we have utilized various pharmacological and genetic tools to show that the eCB/CB<sub>1</sub>R system contributes to the development of DN via regulating the expression, translocation, and activity of the facilitative GLUT2 located in the RPTCs. These findings have the potential to be translated into therapy, and support the rationale for the preclinical development of novel renal-specific CB<sub>1</sub>R and/or GLUT2 inhibitors for the treatment of DN.

Journal

Nephron – Karger

Published: Sep 1, 2019

Keywords: Renal proximal tubule cells; Cannabinoid-1 receptor ; Glucose transporters 2; Sodium-dependent glucose cotransporte 2

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