The clinical biochemistry of obesity
- PMID: 18458706
- PMCID: PMC1880830
The clinical biochemistry of obesity
Abstract
Obesity is essentially an excessive accumulation of triacylglycerols in fatty tissue that is the net result of excessive energy intake compared to energy usage. Severe forms of the disease are most likely to have a predominantly genetic basis and this is probably polygenic. The 'thrifty gene' hypothesis also describes the disturbance that a modern environment, including higher energy intake and decreased physical activity, has on otherwise advantageous genetic variations. While the physical consequences of obesity, such as arthritis, are debilitating and costly, the metabolic consequences are the drivers behind the modern epidemics of insulin resistance, diabetes, fatty liver disease, coronary artery disease, hypertension and polycystic ovary syndrome. The pathophysiological mechanisms behind these diseases are probably a combination of the toxic metabolic effects of free fatty acids and adipokines - the numerous messengers that adipose tissue has been discovered to produce.
References
-
- Gray DS. Diagnosis and prevalence of obesity. Med Clin North Am. 1989;73:1–13. - PubMed
-
- Ferreira IM, Verreschi IT, Nery LE, et al. The influence of 6 months of oral anabolic steroids on body mass and respiratory muscles in undernourished COPD patients. Chest. 1998;114:19–28. - PubMed
-
- Bjorntorp P. Metabolic implications of body fat distribution. Diabetes Care. 1991;14:1132–43. - PubMed
-
- Kershaw EE, Flier JS. Adipose tissue as an endocrine organ. J Clin Endocrinol Metab. 2004;89:2548–56. - PubMed
-
- Prins JB. Adipose tissue as an endocrine organ. Best Pract Res Clin Endocrinol Metab. 2002;16:639–51. - PubMed
LinkOut - more resources
Full Text Sources