Obesity and its many related health hazards have become a serious and growing problem worldwide. While environmental and lifestyle factors play a key role in the development of obesity, genetic variation may determine an individual's susceptibility to weight gain and to the rise of obesity-related health risks. Obesity increases the risk of cardiovascular diseases and diabetes especially when the extra fat is accumulated to central and intra-abdominal depots and when obesity is accompanied by an atherogenic dyslipidemia.
A Finnish team from the Finnish Twin Cohort, Helsinki University Central Hospital, and VTT Technical Research Centre of Finland performed a metabolomic analysis of lipids in 14 monozygous twins highly discordant for obesity, and 10 control pairs concordant for weight. They found that acquired obesity, independent of genetic influences, primarily relates to increases in lysophosphatidylcholines, constituents of an atherogenic lipid profile and decreases in ether phospholipids, lipids with anti-oxidative properties.
The origin of obesity and related dyslipidemias is multifactorial, involving complex genetic and environmental networks. Not all obese individuals develop dyslipidemia and not all dyslipidemic patients are obese. Cross-sectional studies comparing lipid profiles in obese vs. non-obese humans do not permit unequivocal distinction between genetic versus environmental and life-style effects. This can best be done by studying monozygotic (MZ) twins discordant for obesity. MZ twins are genetically identical at the sequence level and any differences between the co-twins are thus attributable to environmental factors. The co-twin design controls for age, gender, childhood socioeconomic background and other environmental experiences and exposures.
Serum patterns of small molecules such as lipids reflect the homeostasis of the organism. However, classical measurements of lipids in the clinical setting are unable to
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