Research about Faulty Genes Linked to Obesity:
A recent study sheds insight on new molecular mechanisms causing obesity by demonstrating how three genes with problematic variations have been connected to obesity-related disorders while having no effect on men.
John Perry, a geneticist and professor at the University of Cambridge in the UK, is the study’s senior author. “There are a million and one reasons why we should be thinking about sex, age, and other specific mechanisms rather than just lumping everyone together and assuming that disease mechanism works the same way for everyone,” he said.
The research group sequenced the exome, or protein-coding portion of the genome, of over 4,14,000 adults from the UK Biobank study and examined variations, or mutations, within genes linked to body mass index (BMI), for both men and women. In the journal Cell Genomics, they have made their research public.
In contrast to men, women with defective versions of the three genes DIDO1, PTPRG, and SLC12A5 had higher BMIs.
Women with DIDO1 variants had stronger associations with higher testosterone levels and a larger waist-to-hip ratio, both of which are risk factors for obesity-related complications like diabetes and heart disease. However, SLC12A5 variant carriers were found to have a higher risk of type 2 diabetes.
In an effort to identify age-specific factors impacting obesity, Perry and his team then went through the process again. Using the participants’ memories as a guide, they looked for gene variations connected to childhood body size.
They discovered the OBSCN and MADD genes, which had not previously been connected to childhood body growth and obesity.
According to the researchers, carriers of the MADD variant were linked to smaller body sizes, but carriers of the OBSCN variant had a higher likelihood of having a heavier weight as a child.
Furthermore, it was discovered that the genetic variations affecting MADD had no association with adult obesity risk, showing age-specific impacts on body size.
What’s extremely unexpected, according to Perry, is that several of these genes we uncovered are obviously involved in DNA damage response and cell death.
“A scientific paradigm that explains how the reaction to DNA damage could affect body size does not yet exist. These studies have provided us with evidence that suggests that variations in this crucial biological process may contribute to the genesis of obesity, according to Perry.
The research team intends to repeat the study on a bigger, more varied group after that.
Perry added, “We hope the study can uncover new biological pathways that might one day open the door to new drug discovery for obesity.”
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