Journal article

Novel mechanisms of Na retention in obesity: phosphorylation of NKCC2 and regulation of SPAK/OSR1 by AMPK

Matthew Davies, Scott A Fraser, Sandra Galic, Suet-Wan Choy, Marina Katerelos, Kurt Gleich, Bruce E Kemp, Peter F Mount, David A Power

American Journal of Physiology: Renal Physiology | AMER PHYSIOLOGICAL SOC | Published : 2014

Abstract

Enhanced tubular reabsorption of salt is important in the pathogenesis of obesity-related hypertension, but the mechanisms remain poorly defined. To identify changes in the regulation of salt transporters in the kidney, C57BL/6 mice were fed a 40% fat diet [high-fat diet (HFD)] or a 12% fat diet (control diet) for 14 wk. Compared with control diet-fed mice, HFD-fed mice had significantly greater elevations in weight, blood pressure, and serum insulin and leptin levels. When we examined Na(+) transporter expression, Na(+)-K(+)-2Cl(-) cotransporter (NKCC2) was unchanged in whole kidney and reduced in the cortex, Na(+)-Cl(-) cotransporter (NCC) and α-epithelial Na(+) channel (ENaC) and γ-ENaC w..

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Grants

Funding Acknowledgements

This work was supported by project grants from the Australian National Health and Medical Research Council (to B. E. Kemp and D. A. Power) and supported in part by the Victorian Government's Operational Infrastructure Support Program (to B. E. Kemp). M. R. P. Davies was supported by a Medical Postgraduate Scholarship from the Australian National Health and Medical Research Council. The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.