Scores of adults worldwide suffer from obesity, and most of these people are diagnosed with metabolic syndrome that includes symptoms like elevated blood cholesterol and blood pressure. Researchers say obesity is characterised by excess body fat, which for the most part is stored in the adipose tissue. Expansion of this tissue results in a failure to store lipid properly, enabling this excess lipid to accumulate in organs like the liver and muscle, and in turn triggering metabolic disease.
For their study, the researchers from Denmark, Finland, Poland and the United Kingdom identified the factors that lead to the malfunction of adipose tissue when it reaches its threshold of expansion. The approach was to use lipidomics to assess the fat tissue biopsies among various sets of monozygotic (identical) twins. The team points out that in each twin pair, one twin was obese but not morbidly obese and the other twin was lean. The researchers considered early upbringing and DNA (deoxyribonucleic acid) since identical twins share these factors. It should be noted that they did not consider adult diet and lifestyle choices.
The team discovered that obese twins had lower amounts of polyunsaturated fatty acids in their diets compared to their lean siblings. The types of lipids found in a body are contingent on the kinds of fats consumed by a person. What they didn't expect to find, but did, was that the obese twins had higher amounts of specific types of lipids containing polyunsaturated fatty acids in their adipose tissues.
'Using computer modelling, we show that 'lean' and 'obese' membrane lipid compositions have the same physical properties despite their different compositions,' the authors of the study write. 'We hypothesise that this represents allostasis —changes in lipid membrane composition in obesity occur to protect the physical properties of the membranes. However, protective changes cannot occur without a cost, and accordingly we demonstrate that switching to the 'obese' lipid composition is associated with higher levels of adipose tissue inflammation.'
The lipid-content changes in obese individuals could in fact be an adaptation that works to preserve membrane function as the cells expand, according to the researchers. This adaptation has limits and breaks down when individuals are morbidly obese.
The scientists also performed a statistical network analysis to identify the regulatory mechanisms supporting the changes. They discovered that Elovl6, the gene encoding the fatty acid elongase, could contribute to fatty acid remodelling in obese individuals. When Elovl6 expression was reduced in an adipocyte cell line, the researchers observed that the cells failed to maintain the right level of the adaptive lipids seen in obese twins.
While they should be validated by further studies, the findings could help researchers in their efforts to deal with the obesity issue.
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