Abstract
The causes of obesity in an individual may involve many factors, both genetic and environmental, including fat cell production and development, appetite and energy regulation. However, the excessive accumulation of triglyceride (triacylglycerol) that characterizes obesity and its effects on the use and storage of various fuels (glucose, fatty acids, and amino acids) are clearly the result of abnormalities in metabolism. The pathways of carbohydrate, protein, and fat metabolism and their interactions and regulatory mechanisms are described, including effects of insulin and counterregulatory hormones such as glucagon and epinephrine. Fructose, incorporated increasingly in the diet, has relatively unregulated metabolism compared with glucose and may thus promote obesity. New insights that have been obtained from studies of genetic models with oblation or modification of particular enzymes or hormone receptors often in a tissue-specific manner are presented, in particular the insulin receptor and the insulin-stimulated glucose transporter Glut4 of muscle and fat cells. The enzyme AMP-activated protein kinase (AMPK) is probably of central importance, as it has recently been identified as a cellular mediator of many events in intermediary metabolism and whose dysregulation may be a cause of disorders associated with the metabolic syndrome and a target for their therapy.
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Tornheim, K., Ruderman, N.B. (2011). Intermediary Metabolism of Carbohydrate, Protein, and Fat. In: Ahima, R. (eds) Metabolic Basis of Obesity. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-1607-5_2
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DOI: https://doi.org/10.1007/978-1-4419-1607-5_2
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