Key regions of our DNA, that control when genes are switched on and off, have been altered by around 140,000 naturally-occurring mutations over the last six million years, the researchers found.

This has left modern humans with sloppy ™ gene control mechanisms which can make us susceptible to diseases, or directly cause genetic diseases.

The researchers suggest that most of the mildly harmful ™ mutations occurred at a time when there was only a small population (10,000) of early Hominids, the two legged primates that were to later evolve into both humans and chimpanzees.

Had there been more early Hominids, and hence a greater choice of mates, most of these mutations would have been overridden by natural selection from a larger pool of available DNA.

This contrasts dramatically with rats and mice which, because of their larger ancestral population, have been able to maintain the integrity of their regulatory sections of DNA.

The researchers, from the Universities of Bath, Edinburgh and Sussex, made the finding after comparing control regions in human, rat, mouse and chimpanzee DNA.

After unwinding ™ evolution using statistical techniques, they found that the way our genes are switched on and off is much less carefully controlled in humans and chimpanzees compared to other animals.

We are used to viewing us as the pinnacle of evolution but seeing that rodents control their genes much more precisely is somewhat sobering, said Dr Martin Lercher from the University of Bath.

As a species we have become used to the benefits of ever-increasing health care and nutrition, but if what we found is still ongoing, then these improvements might at some point be offset by the deterioration of our gene control regions.

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Osmotin is a stable protein that is resistant to heat, acidity and enzymes, meaning it could circulate through the body without being broken down by digestion, he said.

Whether osmotin plays any role in the health benefits attributed to diets high in fruits and vegetables is a tantalizing possibility, and this research opens the door to that question, Bressan said.

"We know that osmotin is an active protein in many of the plants we eat," he said. "We control and label nutrients like fats, carbohydrates and protein - but the really active materials in the foods we eat are the ones we know the least about and don't label in our foods."

Both adiponectin and osmotin jump-start a process called "AMP kinase phosphorylation," which increases both sugar and fat use by muscle cells.

"By binding to the adiponectin receptor, osmotin, like adiponectin, can control the energy status of muscle cells, " said Meena Narsimhan, research scientist at Purdue's Bindley Bioscience Center and a study co-author.

Curiously, adiponectin also can kill some types of mammalian cells, Narsimhan said.

"Other research has shown a strong correlation between low levels of adiponectin and increased risk of breast cancer," she said.

Whether osmotin also has a similarly lethal effect on any types of mammalian cells remains to be seen; however, osmotin, when bound to its receptor on yeast cells, does kill those cells, Narsimhan said.

"What's interesting about this research is that is raises so many questions," she said.

Collaborating researchers in this study include Maria A. Coca, who first isolated the yeast receptor gene, at the Instituto de Biologia Molecular, Barcelona, Spain; Dae-Jin Yun of the Environmental Biotechnology National Core Research Center at Gyeongsang National University, Korea; Jingo Jin, Barbara Damsz and Paul Hasegawa at Purdue's Center for Plant Environmental Stress Physiology; Toshimasa Yamauchi, Yusuke Ito and Takashi Kadowaki at the University of Tokyo Graduate School of Medicine and CREST, Japan Society and Technology Corporation; Jose Pardo with the Instituto de Recuersos Naturales y Agrobioloia in Seville, Spain; and Kyeong Kyu Kim with the Sungkyunkwan University School of Medicine, Suwon, Korea.

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