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PPARδ: a link between sodium and glucose homeostasis

Nature Reviews Nephrology volume 12, page 313 (2016)Cite this article

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High sodium intake is a risk factor for hypertension, which increases the risk of adverse cardiovascular outcomes and mortality in patients with diabetes, but whether sodium and glucose homeostasis share common regulatory mechanisms is not clear. New findings show that the peroxisome proliferator-activated receptor PPARδ regulates natriuresis and glucose homeostasis by inducing the inhibition of the renal sodium–glucose cotransporter 2 (SGLT2) by adiponectin. “We reveal that high sodium intake promotes urinary sodium excretion and glycosuria by increasing plasma adiponectin levels through the upregulation of PPARδ in adipose tissue,” explains researcher Zhiming Zhu. “Adiponectin downregulates renal SGLT2, which in turn reduces the reabsorption of sodium and glucose; however, this mechanism is dampened by hyperglycaemia in diabetes.”

Using mice fed a high sodium diet (HSD) the researchers found that sodium intake increased sodium excretion and upregulated the expression of PPARδ in perirenal fat. Adipose-specific deletion of PPARδ attenuated the effect of a HSD on sodium excretion and exacerbated sodium-induced elevations in blood pressure. Adipose-specific PPARδ-knockout mice also had higher fasting blood glucose levels in response to a HSD than did control mice, indicating a role for PPARδ in the regulation of glucose homeostasis and natriuresis in response to high sodium levels.

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References

  1. Zhao, Y. et al. Sodium intake regulates glucose homeostasis through the PPARδ/adiponectin-mediated SGLT2 pathway. Cell Metab. http://dx.doi.org/10.1016/j.cmet.2016.02.019

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  1. Susan J. Allison
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Allison, S. PPARδ: a link between sodium and glucose homeostasis. Nat Rev Nephrol 12, 313 (2016). https://doi.org/10.1038/nrneph.2016.49

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  • DOI: https://doi.org/10.1038/nrneph.2016.49

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