期刊
ANNUAL REVIEW OF PHYSIOLOGY, VOL 83
卷 83, 期 -, 页码 503-528出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-physiol-031620-095920
关键词
SGLT2 inhibitor; diabetic nephropathy; heart failure; HFrEF; HFpEF; chronic kidney disease
类别
资金
- US National Institutes of Health (NIH) [R01DK112042, R01DK106102, R01HL139836, RF1AG061296]
- UAB/UCSD O'Brien Center of Acute Kidney Injury grant [NIH-P30DK079337]
- Department of Veterans Affairs
- Canadian Institutes of Health Research (CIHR)
- Heart and Stroke Foundation of Canada
SGLT2 inhibitors protect the kidneys and heart, prevent high and low blood sugar levels, and improve metabolic adaptations, leading to reduced fat mass.
SGLT2 inhibitors are antihyperglycemic drugs that protect kidneys and the heart of patients with or without type 2 diabetes and preserved or reduced kidney function from failing. The involved protective mechanisms include blood glucose-dependent and -independent mechanisms: SGLT2 inhibitors prevent both hyper- and hypoglycemia, with expectedly little net effect on HbA1C. Metabolic adaptations to induced urinary glucose loss include reduced fat mass and more ketone bodies as additional fuel. SGLT2 inhibitors lower glomerular capillary hypertension and hyperfiltration, thereby reducing the physical stress on the filtration barrier, albuminuria, and the oxygen demand for tubular reabsorption. This improves cortical oxygenation, which, together with lesser tubular gluco-toxicity, may preserve tubular function and glomerular filtration rate in the long term. SGLT2 inhibitors may mimic systemic hypoxia and stimulate erythropoiesis, which improves organ oxygen delivery. SGLT2 inhibitors are proximal tubule and osmotic diuretics that reduce volume retention and blood pressure and preserve heart function, potentially in part by overcoming the resistance to diuretics and atrial-natriuretic-peptide and inhibiting Na-H exchangers and sympathetic tone.
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