Professionals worldwide are still on the lookout for a suitable obesity treatment as more clarity with respect to regulation of appetite in weight gain is required. Experts from The American Society for Cell Biology and the University of Alabama at Birmingham (UAB) have demonstrated that obesity could be due to ciliopathy.
The team of researchers believed that obesity may be a result of impairments in the process of liptin signaling and the working of the principal cilia. Leptin is a hormone that activates the hypothalamus of the brain to repress appetite. It would be considerably simple to just elevate the production of leptin by any means and combat obesity, but the situation is not as clear as it looks like.
Cilia are minute hairlike substances which expand outwardly from brain cells. Primary cilia have been linked to a variety of conditions such as rare kidney diseases after which defects arising due to them were termed as ciliopathies.
In this research, the team associated the aforesaid condition to morbid obesity. Moreover, weight gain is a symptom of a particular genetic disorder known as Bardet–Biedl syndrome (BBS), which appeared to be originated from primary cilia. The scientists found that mice prototypes of BBS became obese, as they could not control their feeding behavior.
These BBS mice specimens were used to examine the link between obesity, liptin signaling and cilia. Seemingly, the liptin signaling process did not function in the aforesaid mice which could be a consequence of obesity and not a causal variable.
This researchers are searching for other possible appetite-regulating avenues that could pave the path to treating obesity. They also affirmed the contribution of primary cilia in weight gain.
The research is being presented at the 51st Annual Meeting of the American Society for Cell Biology.