| pubmed-article:18458706 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18458706 | lifeskim:mentions | umls-concept:C0028754 | lld:lifeskim |
| pubmed-article:18458706 | lifeskim:mentions | umls-concept:C0005477 | lld:lifeskim |
| pubmed-article:18458706 | lifeskim:mentions | umls-concept:C0205210 | lld:lifeskim |
| pubmed-article:18458706 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:18458706 | pubmed:dateCreated | 2008-5-6 | lld:pubmed |
| pubmed-article:18458706 | pubmed:abstractText | 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. | lld:pubmed |
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