AMPK/Mitochondria in Metabolic Diseases.
The obtaining of nutrients is the most important task in our lives. Energy is central to life's evolutions; this was one of the aspect that induced the selection of the more adaptable and more energetically profitable species. Nowadays things have changed in our modern society. A high proportion of people has access to plenty amount of food and the obesity appear as one of the pathological characteristics of our society. Energy is obtained essentially in the mitochondria with the transfer of protons across the inner membrane that produce ATP. The exactly regulation of the synthesis and degradation of ATP (ATP ↔ ADP + phosphate) is essential to all form of life. This task is performed by the 5' adenosine monophosphate-activated protein kinase (AMPK). mtDNA is highly exposed to oxidative damage and could play a central role in human health and disease. This high potential rate of abnormalities is controlled by one of the most complex mechanism: the autophagy. AMPK appears to be the key cellular energy sensor involved in multiple cellular mechanisms and is essential to have a good metabolic homeostasis to face all the aggression and start the inflammatory reaction. Therefore its disturbances have been related with multiple diseases. Recent findings support the role of AMPK in inflammation and immunity such as Metabolic Syndrome, Obesity and Diabetes. All these Metabolic Disorders are considered pandemics and they need an adequate control and prevention. One important way to achieve it is deepen in the pathogenic mechanisms. Mitochondria and AMPK are the key elements through which it happen, their knowledge and research allow us to a better management. The discovery and use of drugs that can modulate them is imperative to improve our way of manage the metabolic disorders.
Department of Oral Medicine and Periodontology, Dental School, University of Seville, C/Avicena s/n, Seville, 41009, Spain. pbullon@us.es.
Pedro
P
Bullon
Departament of Oral Medicine and Periodontology, Ministry of Education, Culture and Sport, c/Avicena s/n, Seville, 41009, Spain.
Fabiola
F
Marin-Aguilar
Departament of Oral Medicine and Periodontology, University of Seville, c/Avicena s/n, Seville, 41009, Spain.
Lourdes
L
Roman-Malo
D055372:AMP-Activated Protein Kinases / Q000235:genetics* / Q000378:metabolism; D001343:Autophagy / Q000235:genetics; D003920:Diabetes Mellitus / Q000188:drug therapy / Q000201:enzymology / Q000235:genetics* / Q000473:pathology; D004734:Energy Metabolism / Q000235:genetics; D005786:Gene Expression Regulation; D006706:Homeostasis / Q000235:genetics; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007249:Inflammation; D007333:Insulin Resistance / Q000235:genetics; D024821:Metabolic Syndrome / Q000188:drug therapy / Q000201:enzymology / Q000235:genetics* / Q000473:pathology; D008687:Metformin / Q000627:therapeutic use; D008928:Mitochondria / Q000201:enzymology* / Q000473:pathology; D009765:Obesity / Q000188:drug therapy / Q000201:enzymology / Q000235:genetics* / Q000473:pathology; D021122:Protein Subunits / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D045162:Thiazolidinediones / Q000627:therapeutic use
D007004:Hypoglycemic Agents; D021122:Protein Subunits; D045162:Thiazolidinediones; D008687:Metformin; D055372:AMP-Activated Protein Kinases
AMPK; Diabetes; Inflammation; Inflammation treatment; Metabolic Diseases; Metabolic Syndrome; Mitochondria; Obesity; mtDNA