Obesity may not lie in the brainFebruary 5th, 2009 - 12:56 pm ICT by ANI
London, Feb 05 (ANI): A team of American researchers has identified a gene that when mutated causes obesity by dampening the body’’s ability to burn energy while leaving appetite unaffected.
Researchers at the University of North Carolina at Chapel Hill School of Medicine say that the new study could potentially lead to new pharmacologic approaches to treating obesity in humans that do not target the brain.
The findings also add new knowledge to the growing field of epigenetics, in which heritable changes in gene expression or physical appearance are caused by mechanisms besides changes in the underlying DNA.
The gene in question encodes for a specific epigenetic factor, an enzyme called Jhdm2a.
In 2006, studys senior author Yi Zhang, Ph.D. showed that Jhdm2a was able to demethylate, or remove, a methyl group from one of four histone proteins bound to all genes.
Because they are so intimately associated with DNA, even slight chemical alterations of histones can have profound effects on nearby genes.
The new study focused on a line of so-called “knockout” mice that lacked the Jhdm2a gene.
Zhang found impairment in two molecular signaling pathways important for normal function in brown fat tissue and muscle cells.
Both pathways exert a major influence on metabolism, the body’’s conversion of food to energy. Without the enzyme, the mice had reduced metabolisms, becoming visibly obese.
According to Zhang”, this is the first mouse model to exhibit obese traits that do not resulting from an alteration in appetite, which is largely a brain function.
“Given that this gene is not expressed in the brain, any drug that targets this gene would not have an effect on brain function. Therefore, we are really looking for a pure effect on metabolism,” Nature quoted him, as saying.
With that in mind, Zhang anticipates that the study could be of great interest to pharmaceutical companies eager to develop new anti-obesity drugs aimed at a novel, new molecular target expressed in non-brain tissues.
The study is published online February 4, 2009 in the journal Nature. (ANI)
- Key mechanism linked to cocaine addiction identified - Jan 08, 2010
- Mum's stress in pregnancy 'puts female offspring at obesity risk' - Apr 13, 2011
- Early life stress has lasting effects on gene vital to normal brain function - Sep 29, 2010
- New findings may lead to a novel treatment for obesity - Jan 12, 2011
- Human enzyme holds promise of weight loss - Nov 15, 2011
- Genome code for most common form of pediatric brain cancer cracked - Dec 17, 2010
- Key step for regulating embryonic development discovered - Apr 23, 2010
- Brain altering drug calms fears also - Jun 13, 2012
- Why some people become depressed when they are stressed - Jan 27, 2011
- Potential new target for diabetes, heart disease treatments identified - Nov 17, 2010
- New link shows mother's pregnancy diet influences child's chances of obesity - Apr 19, 2011
- Why fatty diets during pregnancy make kids obese - Nov 23, 2010
- Study offers potential new targets for novel anti-HIV drugs - Mar 26, 2011
- Liver's role vital in regulating body clock - May 04, 2012
- Molecular approach could be the key to understanding male infertility - Aug 25, 2010
Tags: american researchers, brain function, chapel hill school, gene expression, heritable changes, histone proteins, knockout mice, london feb, methyl group, mouse model, muscle cells, north carolina at chapel, north carolina at chapel hill, obesity drugs, physical appearance, profound effects, school of medicine, signaling pathways, university of north carolina, university of north carolina at chapel hill