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Missing Gene Linked to Obesity and Postnatal Depression: Study

In what can be termed as a major development, scientists discovered a gene that, when missing or malfunctioning, can cause obesity, behavioural difficulties, and, in mothers, postnatal depression.

Today's publication in the journal Cell of this discovery could significantly impact the treatment of postnatal depression. A study with mice found that oxytocin, a hormone, may help alleviate symptoms.

Obesity and postnatal depression are significant global health concerns. More than one in every ten women experiences postnatal depression within a year of giving birth, and it is a primary cause of maternal mortality in developed countries. The World Health Organisation reports that obesity rates have more than doubled in adults and quadrupled in teenagers since 1990.

Researchers from the University of Cambridge in the United Kingdom and Baylor College of Medicine in the United States investigated two boys from separate families who suffered from significant obesity, anxiety, autism, and behavioural issues induced by sounds or scents. Researchers found that both boys lacked a single gene called TRPC5, located on the X chromosome.

Further analysis revealed that both boys received the missing gene from their moms, who were likewise obese and had postpartum depression.

To determine whether the TRPC5 gene was causing the problems, researchers bred mice with a defective form of the gene. Male mice with this faulty gene exhibited the same difficulties as boys, such as weight gain, anxiety, and aggressive behaviour.

“Previous studies had shown that disrupting gene Trpc5 in the brain causes obesity due to increased food intake and reduced energy expenditure in mice,” said co-corresponding author Dr. Yong Xu, professor of paediatrics – nutrition and associate director for basic sciences at the USDA/ARS Children’s Nutrition Research Center at Baylor College of Medicine.

Female mice with the faulty gene also exhibited these behaviours. When they became moms, they experienced despair and struggled to care for their newborns. Interestingly, male and female mice who were not mothers but had the defective gene did not exhibit depression-like behaviour.

"What we discovered in those mice was pretty astonishing. They displayed behaviours similar to those reported in adults who lack the TRPC5 gene, including indicators of despair and difficulty caring for their newborns. This demonstrates that the gene is causing these behaviours," Dr.  Xu, added.

TRPC5 belongs to a gene family that senses signals such as heat, taste, and touch. This gene affects a pathway in the hypothalamus area of the brain that is known to regulate hunger.


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