Naslov
Obesity and metabolic syndrome the targets for prevention

Autori
Štimac, Davor

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, neobjavljeni rad, znanstveni

Skup
EAGEN European postgraduate school in gastroenterology & nutrition

Mjesto i datum
Prag, Češka Republika, 13.04.2012. - 14.04.2012

Vrsta sudjelovanja
Pozvano predavanje

Vrsta recenzije
Nije recenziran

Ključne riječi
obesity; metabolic syndrome; ghrelin; leptin

Sažetak
In developed Western societies, cardiovascular and cancer-related mortality are tightly related to the rise of obesity and the metabolic syndrome. The same trend is perhaps even more pronounced in developing countries. An obese person is one whose BMI value exceeds 30 kg per square meter, which is a custom cut-off value determined mainly for middle-aged Caucasians. For Asians, the same values cannot be applied since they tend to have a higher risk of obesity-related complications for the same BMI value, and thus their cut-off value is set at 27 kg/m2. Similar differences are observed among various age groups, however, only children have age-defined BMI cut-off values, while the elderly have none. The metabolic syndrome, on the other hand, is a cluster of risk factors first described in cardiovascular diseases. Whether the accumulation of risk factors represents a clinical entity per se is still a major issue argued discussed at many formal gatherings. Today two generalized definitions of metabolic syndrome have been defined by the WHO and the IDF. Both obesity and metabolic syndrome have shown to increase the risk of GI cancer development. The strongest correlation has been found with the development of esophageal adenocarcinoma and colorectal carcinoma. Although the link between obesity and other GI malignancies is less obvious, there are specific situations that warrant our attention, such as non-cirrhotic hepatocellular carcinoma, which occurs more frequently in patients suffering from obesity and diabetes mellitus. The exact mechanisms by which obesity and metabolic syndrome contribute to the increased GI cancer risk are not clear, but it seems that hyperinsulinemia and the resulting mitogenic potential could be the cornerstone pathophysiological mechanism. Alternative possibilities, including adipocytokines, sex steroids and other intracellular signalling pathways, cannot be excluded either. Finally, the treatment of obesity and metabolic syndrome by pharmacological means has shown only limited effect on cancer risk reduction. Still, increased physical activity and diet modifications, the major contributors for achieving and retaining steady weight loss, do reduce the risk of cancer development.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti

POVEZANOST RADA