Origins of metabolic complications in obesity: adipose tissue and free fatty acid trafficking

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Purpose of review

Obesity is associated with a number of serious medical complications that are risk factors for cardiovascular disease (e.g., insulin resistance, dyslipidemia, and liver fat accumulation). Alterations in fatty acid trafficking, both between tissues and within cells, represent a key feature in the pathophysiology of the metabolic complications in obese patients. The ways by which fatty acid ‘re-routing’ may affect metabolic function are summarized in this article.

Recent findings

Ectopic fat accumulation (i.e., fat accumulation in nonadipose tissues) appears to be a key feature distinguishing metabolically healthy from metabolically abnormal patients. This observation has led to the belief that an imbalance in fatty acid trafficking away from adipose tissue toward nonadipose tissues is a primary cause for the development of metabolic alterations in obese patients. More recently, however, it has become apparent that fatty acid trafficking within nonadipose tissues cells (i.e., toward storage – in the form of triglycerides – and oxidation) may be equally important in determining a person's risk for development of metabolic disease.


The pathophysiology of the metabolic alterations associated with obesity is probably multifactorial within a complex network of coordinated physiological responses. Only through the integration of multiple concepts, will it be possible to further our understanding in this area and to help prevent the metabolic alterations associated with obesity.

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