Metformin benefits: Another example for alternative energy substrate mechanism?
| Autor: | Anna Solini, Stefano Del Prato, Andrea Giaccari, Simona Frontoni |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
endocrine system diseases
Endocrinology Diabetes and Metabolism 030209 endocrinology & metabolism Type 2 diabetes Pharmacology personalized medecine 03 medical and health sciences Perspectives in Care Settore MED/13 0302 clinical medicine Diabetes mellitus Internal Medicine Diabetes Mellitus Medicine Humans Hypoglycemic Agents Glycolysis 030212 general & internal medicine Prospective Studies Advanced and Specialized Nursing business.industry Mechanism (biology) Lactic diabetic nephropathy Acidosis Lactic Diabetes Mellitus Type 2 Metformin lactic acid Settore MED/13 - ENDOCRINOLOGIA medicine.disease Increased lactate Mechanism of action Lactic acidosis medicine.symptom business Acidosis Type 2 medicine.drug |
| Zdroj: | Diabetes Care |
| Popis: | Since the UK Prospective Diabetes Study (UKPDS), metformin has been considered the first-line medication for patients with newly diagnosed type 2 diabetes. Though direct evidence from specific trials is still lacking, several studies have suggested that metformin may protect from diabetes- and nondiabetes-related comorbidities, including cardiovascular, renal, neurological, and neoplastic diseases. In the past few decades, several mechanisms of action have been proposed to explain metformin’s protective effects, none being final. It is certain, however, that metformin increases lactate production, concentration, and, possibly, oxidation. Once considered a mere waste product of exercising skeletal muscle or anaerobiosis, lactate is now known to act as a major energy shuttle, redistributed from production sites to where it is needed. Through the direct uptake and oxidation of lactate produced elsewhere, all end organs can be rapidly supplied with fundamental energy, skipping glycolysis and its possible byproducts. Increased lactate production (and consequent oxidation) could therefore be considered a positive mechanism of action of metformin, except when, under specific circumstances, metformin and lactate become excessive, increasing the risk of lactic acidosis. We are proposing that, rather than considering metformin-induced lactate production as dangerous, it could be considered a mechanism through which metformin exerts its possible protective effect on the heart, kidneys, and brain and, to some extent, its antineoplastic action. |
| Databáze: | OpenAIRE |
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