Metformina e AMPK: um antigo fármaco e uma nova enzima no contexto da síndrome metabólica
Open accessAbstract
A metformina é uma das drogas antidiabéticas orais mais prescritas mundialmente, entretanto seu mecanismo de ação permanece desconhecido. Os estudos do Diabetes Prevention Program Research Group demonstraram que tanto a administração de metformina como a mudança no estilo de vida (dieta e exercício físico) podem reduzir a incidência de diabetes melito tipo 2 (DM2). Uma possível conexão bioquímica entre essas duas terapias pode ser a proteína quinase ativada por AMP (AMPK). Essa enzima foi inicialmente descrita como um sensor energético celular, sendo ativada pelo exercício físico. Por outro lado, várias evidências experimentais indicam que a AMPK seja um alvo importante da ação da metformina. Este artigo discute as várias formas da regulação da AMPK, sugerindo um possível mecanismo para sua ativação pela metformina que envolve a formação de espécies reativas de nitrogênio. A ativação da AMPK determina ampla variedade de efeitos fisiológicos, incluindo o aumento da captação de glicose pelos músculos esqueléticos e aumento do catabolismo de lipídios, podendo ser interessante não apenas na prevenção e tratamento do DM2, mas também no contexto da síndrome metabólica. A descoberta da ativação da AMPK pela metformina faz dessa enzima importante alvo farmacológico.
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AMPK forms a molecular hub for cellular metabolic control.
“The activated protein kinase (AMPK) forms a molecular hub for cellular metabolic control [122].”
From Metformin: An Old But Still the Best Treatment for Type 2 Diabetes (2013) · cites this paper as [122]
AMPK is activated in the brain by metabolic stresses that inhibit ATP production, including ischemia, hypoxia, glucose deprivation, metabolic inhibitors such as metformin, and catabolic and ATP-consuming processes.
“AMPK is activated in the brain by metabolic stresses that inhibit ATP production such as ischemia, hypoxia, glucose deprivation, metabolic inhibitors (metformin), as well as catabolic and ATP consuming processes [122].”
From Metformin: An Old But Still the Best Treatment for Type 2 Diabetes (2013) · cites this paper as [122]
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References 28 · Cited by 33
Research works printed but not linked: 1
- Bailey CJ, Turner RC. Metformin. N Engl J Med. 1996;334:574-9.
- Authors
- Santomauro Jún, A. C., Ugolini, M. R., Santomauro, A. T., & Souto, R. P. D.
- Affiliations
- Faculdade de Medicina do ABC, Brasil
- Faculdade de Medicina do ABC (BR)
- Venue
- Arquivos Brasileiros de Endocrinologia & Metabologia
- Publisher
- FapUNIFESP (SciELO)
- Published
- 2008-02
- Volume
- 52
- Issue
- 1
- Pages
- 120-125
- ISSN
- 0004-2730 (ISSN-L)
- OpenAlex
- W2058623446
- Cited by
- 33
- References
- 28
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2022: 2 · 2021: 2 · 2020: 1 · 2019: 1 · 2018: 1 · 2017: 2 · 2016: 5 · 2015: 2 · 2014: 4 · 2013: 2 · 2012: 1
- FWCI
- 0.96
- Type
- journal article
- Language
- pt
- Open access
- diamond
- doi.org
- Licence
- cc-by-nc
- Locations
- Arquivos Brasileiros de Endocrinologia & Metabologia (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Natural Antidiabetic Agents Studies
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- metformin, AMPK, type 2 diabetes, metabolic syndrome, obesity, reactive nitrogen species, glucose uptake, skeletal muscle, lipid degradation, lifestyle intervention, therapeutic target
- MeSH terms
- Diabetes Mellitus, Type 2, Diet, Energy Metabolism, Glucose, Humans, Hypoglycemic Agents, Insulin, Metformin, Exercise, Metabolic Syndrome, Lipid Metabolism, AMP-Activated Protein Kinases
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