ISLAMABAD – A British study said that researchers have found a genetic clue of why women generally outlive men through studying fruit flies.
The research, published in the journal Current Biology and conducted by Lancaster University in Britain reported that a set of DNA inherited only from the mother can be harmful to males and speed up male aging.
After carrying experiments with fruit flies, researchers said the results point to numerous mutations within mitochondrial DNA that affect how long males live, and the speed at which they age.
Mitochondrial DNA, which is found in many species including human, is inherited through the mother only. So there is no evolution pressure from the male side to sieve out those mutations that are just harmful to male, and the unaffected females will continue to pass on those mutations to their sons.
The accumulation of those mutations could eventually lead to the difference of longevity between male and female. That theory was named “Mother’s Curse” by some researchers.
“We show that Mother’s Curse is much broader in its effects on male life history than previously envisaged, resulting in the build-up of mutations that cause males to age faster, and live shorter lives than females,” said Dr David Clancy of Lancaster University.
He said these findings offer a new and compelling explanation to one of life’s greatest puzzles - why the female of many species, including humans, live longer than the males.
Generally women outlive men by about five to six years. By age 85 there are roughly six women to every four men and by age 100 the ration is more than two to one.
Researchers find potential target for treating diabetes, obesity
US researchers at Washington University School of Medicine in St. Louis have identified a potential target for treating diabetes and obesity, according to a study published online on Thursday in the journal Cell Metabolism.
Studying mice, the researchers found that when the target protein was disabled, the animals became more sensitive to insulin and were less likely to get fat even when they ate a high-fat diet that caused their littermates to become obese.
They studied how the body manufactures fat from dietary sources such as carbohydrates. That process requires an enzyme called fatty acid synthase (FAS). Mice engineered so that they don’t make FAS in their fat cells can eat a high-fat diet without becoming obese.
“Mice without FAS were significantly more resistant to obesity than their wild-type littermates,” said first author Irfan Lodhi. “And it wasn’t because they ate less. The mice ate just as much fatty food, but they metabolised more of the fat and released it as heat.”
To understand why that happened, the researchers analyzed the mice’s fat cells. Mice have two types of fat: white fat and brown fat. White fat stores excess calories and contributes to obesity. Brown fat helps burn calories and protects against obesity.
In mice genetically blocked from making fatty acid synthase in fat cells, the researchers noticed that the animals’ white fat was transformed into tissue that resembled brown fat.
Scientists identify gene causing congenital blindness
An international research team has found a new gene that can cause congenital blindness.
Congenital blindness is a kind of autosomal recessive inherited retinal degenerative disease. About 70 percent of the cases are caused by the mutation of one of the 17 disease-causing genes, which have already been discovered, while the causes of the rest 30 percent have not been found yet.
After studying cases where the cause of disease was still unknown, the researchers, led by Qi Ming, a professor with Zhejiang University, concluded that a gene called “NMNAT1” is a disease-causing gene for the congenital eye disease.
The research team is made up of scientists from countries including China, the United States, Brazil, Canada and Australia.
The NMNAT1 gene can protect the light receptor cells in the retina and is also of great importance for the nerve cells and the heart, kidney and liver tissue in human body.
The mutation of the gene can cause a kind of congenital blindness called the Leber congenital amaurosis (LCA), Qi said, adding that the mutation of NMNAT1 also harms the patients’ nerves and some organs.
Gu Yangshun, an expert with the First Affiliated Hospital of Zhejiang University, said that there are over 600 kinds of hereditary eye diseases, which are hard to diagnose, and genetic testing is a key measure to diagnose the diseases.
Besides Qi Ming’s team, three other teams led by Chen Rui from Baylor College of Medicine in Houston, Josseline Kaplan and Jean-Michel Rozet from France and Eric Pierce from Massachusetts Eye and Ear Infirmary in Boston have also found that particular disease-causing gene, and their essays were published together in the Nature Genetics on July 29.
Experts said identifying of the gene had provided a way to treat the disease, since the rapid development of molecular biology has made it possible to prevent and treat the hereditary diseases from the core via the technology of genetic diagnose and genetic treatment.
Qi said that in the US and Europe, some scientists have mastered the technology to identify the location of the disease-causing gene in the patients’ eyes and inject good genes there to promote the healthy development of the organs.
Within three years, China will be able to use this kind of treatment as well to treat the congenital eye diseases and the identifying of the NMNAT1 gene will be of great significance for the kind of treatment, Qi said.