Source-.news-medical.net
In a groundbreaking discovery reported in Cell, scientists have pinpointed a gene crucial for regulating both obesity and postnatal depression. The gene, known as the TRPC5 gene, was identified through a study involving two boys exhibiting severe obesity and behavioral issues, alongside their mothers who suffered from postnatal depression. This gene, located on the X chromosome, was found to be missing in both boys and inherited from their mothers, who also showed signs of obesity and postnatal depression.
Insights from Animal Models
To validate their findings, researchers utilized genetically engineered mice with a defective TRPC5 gene. Male mice with this mutation displayed symptoms akin to the boys, including weight gain, anxiety, and social aversion. Interestingly, female mice exhibited depressive behaviors particularly after becoming mothers, demonstrating impaired maternal care. This suggested a direct correlation between TRPC5 deficiency and the manifestation of depressive symptoms in the context of motherhood.
Dr. Yong Xu, from Baylor College of Medicine, remarked on the significance of their findings, stating, “Our observations in mice mirrored human conditions linked to TRPC5 deficiency, including maternal depression and caregiving challenges. This underscores the gene’s pivotal role in these behaviors.”
Mechanisms and Treatment Implications
Further investigations revealed that the TRPC5 gene operates within the hypothalamus, affecting pathways related to appetite regulation and mood control. Notably, the gene influences oxytocin-producing neurons, critical for emotional bonding and maternal behavior. Mice lacking TRPC5 in these neurons exhibited heightened anxiety and disrupted maternal care, which were alleviated upon gene restoration.
The implications extend beyond rare genetic conditions; analysis of genetic data from UK Biobank identified variants of TRPC5 associated with higher body mass index in a subset of individuals. This underscores the gene’s broader relevance in metabolic regulation.
Professor Farooqi emphasized the potential therapeutic implications, suggesting that oxytocin could be a promising treatment for individuals with TRPC5 deficiencies and possibly for mothers experiencing postnatal depression. She stated, “Our findings provide compelling evidence linking oxytocin deficiency to TRPC5-related conditions, paving the way for larger clinical trials.”
The study was supported by several research organizations, highlighting collaborative efforts in advancing understanding and treatment of complex genetic disorders.
This research not only sheds light on the biological underpinnings of obesity and postnatal depression but also underscores the potential for targeted treatments. By elucidating the role of TRPC5 gene and its impact on oxytocin pathways, scientists aim to revolutionize approaches to managing these prevalent health challenges. As Professor Farooqi noted, this work challenges assumptions about behavioral conditions and calls for greater compassion towards those affected.
Also Read: Genetic Variant Linked to Childhood Obesity Uncovered by CHOP Researchers
