Scientists from King’s College London found changes that occur in the body in response to an increase in belly fat. The finding offers new insight into the cause of metabolic disease.
The research is published in Genome Medicine and was conducted by Dr. Jordana Bell et al.
In the study, researchers looked at how epigenetic marks (measures of how the human body reads DNA to affect the way genes work) in fat tissue change as belly fat accumulates.
They used samples from 538 TwinsUK participants and combined genetic, gene function, diet, and health data.
The researchers examined epigenetic marks across the genome (the complete set of a person’s genetic material) and found nine genes that are highly relevant to metabolic disease risk.
Among these was a gene where the identified epigenetic changes were recognized as a potential mechanism through which diet can affect belly fat accumulation, as well as other epigenetic marks that translate genetic risk effects on metabolic health.
The findings also allowed the researchers to characterize the molecular changes that occur because of an increase in belly fat and the impact these changes have on gene function and insulin resistance.
Metabolic diseases—the most common of which is diabetes—disrupt normal metabolism or the process of converting food to energy on a cellular level.
While previous studies in this field have explored the role of epigenetic marks in overall obesity using body mass index (BMI), the build-up of belly fat deep within the abdomen is known to be a greater risk factor for metabolic disease than BMI alone.
The team says with rapidly rising rates of obesity worldwide, it is important that we understand how elevated body fat affects us at the molecular level and how this translates to metabolic disease risk.
Based on the results of the study, the researchers also developed an epigenetic predictor of insulin resistance, relating their findings to the clinical consequences of elevated belly fat.
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