Renal Handling of Ketones in Response to Sodium–Glucose Cotransporter 2 Inhibition in Patients With Type 2 Diabetes
| Autor: | Silvia Frascerra, Simona Baldi, Elza Muscelli, Ele Ferrannini, E. Barsotti, Aldo Clerico, Brenno Astiarraga |
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| Rok vydání: | 2017 |
| Předmět: |
Blood Glucose
Male Glycosuria medicine.medical_specialty Endocrinology Diabetes and Metabolism medicine.medical_treatment Natriuresis 030209 endocrinology & metabolism 030204 cardiovascular system & hematology Kidney Glucagon Body Mass Index 03 medical and health sciences 0302 clinical medicine Glucosides Sodium-Glucose Transporter 2 Internal medicine Natriuretic Peptide Brain Internal Medicine medicine Empagliflozin Humans Hypoglycemic Agents Glucose homeostasis Lactic Acid Benzhydryl Compounds Erythropoietin Sodium-Glucose Transporter 2 Inhibitors Advanced and Specialized Nursing 3-Hydroxybutyric Acid Renal sodium reabsorption business.industry Insulin Sodium Ketones Middle Aged Peptide Fragments Endocrinology Diabetes Mellitus Type 2 Sodium/Glucose Cotransporter 2 Female medicine.symptom business Glomerular Filtration Rate |
| Zdroj: | Diabetes Care. 40:771-776 |
| ISSN: | 1935-5548 0149-5992 |
| Popis: | OBJECTIVE Pharmacologically induced glycosuria elicits adaptive responses in glucose homeostasis and hormone release, including decrements in plasma glucose and insulin levels, increments in glucagon release, enhanced lipolysis, and stimulation of ketogenesis, resulting in an increase in ketonemia. We aimed at assessing the renal response to these changes. RESEARCH DESIGN AND METHODS We measured fasting and postmeal urinary excretion of glucose, β-hydroxybutyrate (β-HB), lactate, and sodium in 66 previously reported patients with type 2 diabetes and preserved renal function (estimated glomerular filtration rate ≥60 mL · min−1 · 1.73 m−2) and in control subjects without diabetes at baseline and following empagliflozin treatment. RESULTS With chronic (4 weeks) sodium–glucose cotransporter 2 inhibition, baseline fractional glucose excretion ( CONCLUSIONS We conclude that the sodium–glucose cotransporter 2 inhibitor–induced increase in β-HB is not because of reduced renal clearance but because of overproduction. The increased lactate excretion contributes to lower plasma lactate levels, whereas the increased natriuresis may help in normalizing the exchangeable sodium pool. Taken together, glucose loss through joint inhibition of glucose and sodium reabsorption in the proximal tubule induces multiple changes in renal metabolism. |
| Databáze: | OpenAIRE |
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