Obesity rates are increasing and it is important to understand how elevated body fat affects and translates to metabolic disease risk.
Belly fat increases the risk of metabolic disease. Read on to learn how the belly fat leads to increased risk, reveals a study from TwinsUK. The study, led by King’s College London //researchers Dr. Jordana Bell and Colette Christiansen and published in the medical journal Genome Medicine, 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.
‘Belly fat deep within the abdomen is known to be a greater risk factor for metabolic disease than just body mass index (BMI) alone.’
Details of the Study
Using samples from 538 TwinsUK participants and combining 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.
“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,” said Dr. Jordana Bell, Reader in Epigenomics in the School of Life Course and Population Sciences.
Metabolic diseases – the most common of which is diabetes – disrupt normal metabolism, or the process of converting food to energy on a cellular level.
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“Our study brings us one step closer to this goal by identifying an epigenetic signature of excess belly fat, understanding its genetic and dietary triggers, and characterizing its functional impacts and clinical consequences for insulin resistance,” added Dr. Bell.
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Colette Christiansen, a Ph.D. researcher in the School of Life Course and Population Sciences said: “It is exciting to see that when we combine many different layers of biological information, we can start to unravel the mechanisms which drive the state of our biological health.”
Source-Eurekalert