Researchers have found that burning energy through activation of brown adipose tissue (BAT) by the use of an extract from ginseng, a traditional Chinese medicinal herb, might be an alternative strategy for combating Obesity.
According to the study, published in the journal Gut, a ginseng extract can induce enterococcus faecalis, which can produce myristoleic acid (MA), an unsaturated long-chain fatty acid (LCFA).
“As a novel anti-obesity probiotic, enterococcus faecalis and myristoleic acid can reduce adiposity via BAT activation and beige fat formation,” said JIN Wanzhu, lead author of study, from the Chinese Academy of Sciences.
Overweight and obesity have become a severe public health issue around the world. Current anti-obesity strategies are mainly aimed at restricting calorie intake and absorption.
Previous studies have shown that brown adipose tissue facilitates weight control and generates a potent anti-obesity effect. Therefore, increasing BAT activity could be a novel and effective therapeutic approach for obesity and its related diseases, said JIN.
According to the study, it’s the first proof that the enterococcus faecalis LCFA (specifically myristoleic acid) axis can reduce obesity by increasing BAT activity and beige fat formation.
Shedding new light on why some people develop cancer while others do not, a new study has found that a person’s risk of developing cancer is affected by Genetic variations in regions of DNA that do not code for proteins, previously dismissed as “junk DNA”.
This study, published in the British Journal of Cancer, shows that inherited cancer risk is not only affected by mutations in key cancer genes, but that variations in the DNA that controls the expression of these genes can also drive the disease.
The researchers believe that understanding how non-coding DNA affects the development of this disease could one day improve genetic screening for cancer risk.
And in the future, this could lead to new prevention strategies, or help doctors diagnose the disease earlier, when it is more likely to be treated successfully.
“What we found surprised us as it had never been reported before — our results show that small genetic variations work collectively to subtly shift the activity of genes that drive cancer,” said lead researcher of the study John Quackenbush, Professor at Harvard T.H. Chan School of Public Health in the US.
“We hope that this approach could one day save lives by helping to identify people at risk of cancer, as well as other complex diseases,” Quackenbush said.
The researchers investigated 846 genetic changes within non-coding stretches of DNA, identified by previous studies as affecting cancer risk.
These Single Nucleotide Polymorphisms (SNPs) are particular positions in the human genome where a single letter of the genetic code varies between people.
Unlike mutations in coding DNA, such as BRCA, that are rare but significantly raise a person’s risk of developing cancer, non-coding SNPs are relatively common in the population but only slightly increase cancer risk.
The team analysed whether there was a correlation between the presence of a particular SNP and the expression of particular genes.
In total, they looked at over six million genetic variants across 13 different body tissues.
They found that variations in the regions that regulate the expression of oncogenes and tumour suppressor genes affect cancer risk.
The study also revealed that these cancer-risk SNPs tend to be specifically located in regions that regulate the immune system and tissue-specific processes — highlighting the importance of these cellular processes to the development of cancer.
“While minor genetic changes only have a small impact on cancer risk, the variations analysed in this study are numerous and common in the population,” said Emily Farthing, senior research information manager at British charity Cancer Research UK. (IANS)