Sodium glucose cotransporter 2 and the diabetic kidney : Current Opinion in Nephrology and Hypertension (original) (raw)
HORMONES, AUTACOIDS, NEUROTRANSMITTERS AND GROWTH FACTORS: Edited by Mark Cooper and Merlin Thomas
Komala, Muralikrishna Gangadharan; Panchapakesan, Usha; Pollock, Carol; Mather, Amanda
Renal laboratory, Kolling Institute of Medical Research, University of Sydney, Sydney, Australia
Correspondence to Dr Amanda Mather, Department of Medicine, Kolling Building, Royal North Shore Hospital, St Leonards, Sydney 2065, Australia. Tel: +61 2 9926 4652; e-mail: [email protected]
Abstract
Purpose of review
Reabsorption of glucose in the proximal tubule occurs predominantly via the sodium glucose cotransporter 2 (SGLT2). There has been intense interest in this transporter as a number of SGLT2 inhibitors have entered clinical development. SGLT2 inhibitors act to lower plasma glucose by promoting glycosuria and this review aims to outline the effect on the diabetic kidney of this hypoglycaemic agent.
Recent findings
This review provides an overview of recent findings in this area: the transcriptional control of SGLT2 expression in human proximal tubular cells implicates a number of cytokines in the alteration of SGLT2 expression; experimental data show that SGLT2 inhibition may correct early detrimental effects of diabetes by reducing proximal tubular sodium and glucose transport, suggesting a possible renoprotective effect independent of the glucose lowering effects of these agents; and the nonglycaemic effects of SGLT2 inhibitors may have an impact on renal outcomes.
Summary
The available clinical evidence shows consistent reduction in glycaemic parameters and some evidence suggests additional effects including weight loss and mild blood pressure reduction. There are some side effects that warrant further investigation and establishing whether SGLT2 inhibition provides a renal benefit relies on future long-term studies with specific renal end-points.
© 2013 Lippincott Williams & Wilkins, Inc.