Maybe it’s not just the cheese puffs.

Reporting in the online journal BMC Genetics, researchers from the Monell Center have for the first time attempted to count the number of genes that contribute to obesity and body weight.

The findings suggest that over 6,000 genes – about 25 percent of the genome – help determine an individual’s body weight.

“Reports describing the discovery of a new ‘obesity gene’ have become common in the scientific literature and also the popular press,” notes Monell behavioral geneticist Michael G. Tordoff, PhD, an author on the study.

“Our results suggest that each newly discovered gene is just one of the many thousands that influence body weight, so a quick fix to the obesity problem is unlikely.”

To obtain an estimate of how many genes contribute to body weight, the Monell researchers surveyed the Jackson Laboratory Mouse Genome Database for information on body weights of knockout mouse strains.

Knockout mice have had a specific gene inactivated, or “knocked out.” By studying how the knockout mice differ from normal mice, researchers obtain information about that gene’s function and how it might contribute to disease. Mice can provide valuable information on human disease because they share many genes with humans.

The knockout approach is so useful that the inventors of the technology were awarded the 2007 Nobel Prize in Medicine. Knockout mice are now standard tools in all mouse models of behavior and disease.

In 60% of strains, knocking out a gene produces mice that are nonviable; that is, the mouse cannot survive without the knocked out gene.

The Monell survey revealed that body weight was altered in over a third of the viable knockout stains; 31 percent weighed less than controls (indicating that the missing genes contribute to heavier body weight), while another 3 percent weighed more (contributing to lighter weight).

Extrapolating from the total number of genes in the mouse genome, this implies that over 6,000 genes could potentially contribute to the body weight of a mouse.

Tordoff comments, “It is interesting that there are 10 times more genes that increase body weight than decrease it, which might help explain why it is easier to gain weight than lose it.”

Because body weight plays a role in many diseases, including hypertension, diabetes, and heart disease, the implications of the findings extend beyond studies of obesity and body weight. Gene knockouts reported to affect these diseases and others could potentially be due to a general effect to lower body weight.

This cat might need some genes “knocked out.”

The findings also hold clinical relevance, according to lead author Danielle R. Reed, PhD, a Monell geneticist. “Clinicians and other professionals concerned with the development of personalized medicine need to expand their ideas of genetics to recognize that many genes act together to determine disease susceptibility.”

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Maureen P. Lawler also contributed to the study.

The Monell Chemical Senses Center is a nonprofit basic research institute based in Philadelphia, Pennsylvania. For 40 years, Monell has been the nation’s leading research center focused on understanding the senses of smell, taste and chemical irritation: how they function and affect lives from before birth through old age. Using a multidisciplinary approach, scientists collaborate in the areas of: sensation and perception, neuroscience and molecular biology, environmental and occupational health, nutrition and appetite, health and well being, and chemical ecology and communication. Monell: Making Sense of Taste and Smell for 40 Years. For more information, visit www.monell.org.

Hopefully they didn’t use gummies for the study.

The roundworm C. elegans, a staple of laboratory research, may be key in unlocking one of the central biological mysteries: why we sleep. Researchers at the University of Pennsylvania School of Medicine report in this week’s advanced online edition of Nature that the round worm has a sleep-like state, joining most of the animal kingdom in displaying this physiology. This research has implications for explaining the evolution and purpose of sleep and sleep-like states in animals.

In addition, genetic work associated with the study provides new prospects for the use of C. elegans to identify sleep-regulatory genes and drug targets for sleep disorders.

First author David M. Raizen, MD, PhD, Assistant Professor of Neurology, in collaboration with other researchers at the Penn Center for Sleep, showed that there is a period of behavioral quiescence during the worm’s development called lethargus that has sleep-like properties. “Just as humans are less responsive during sleep, so is the worm during lethargus,” explains Raizen. “And, just as humans fall asleep faster and sleep deeper following sleep deprivation, so does the worm.”

By demonstrating that worms sleep, Raizen and colleagues have not only demonstrated the ubiquity of sleep in nature, but also propose a compelling hypothesis for the purpose for sleep.

Because the time of lethargus coincides with a time in the round worms’ life cycle when synaptic changes occur in the nervous system, they propose that sleep is a state required for nervous system plasticity. In other words, in order for the nervous system to grow and change, there must be down time of active behavior. Other researchers at Penn have shown that, in mammals, synaptic changes occur during sleep and that deprivation of sleep results in a disruption of these synaptic changes.

In addition, the research team used C. elegans as a model system to identify a gene that regulates sleep. This gene, which encodes a protein kinase and is regulated by a small molecule called cyclic GMP, has been previously studied but not suspected to play a role in sleep regulation. The findings suggest a potential role for this gene in regulating human sleep and may provide an avenue for developing new drugs for sleep disorders.

“It opens up an entire new line of inquiry into the functions of sleep,” notes Penn Center for Sleep Director and co-author Allan I. Pack, MB, Chb, PhD.

Scientists at LS9, Inc. hard at work

A recent recent article on The Washington Post went into detail about how the idea creating artificial life forms through artificial DNA may be soon turned reality. Up until recently, even the most advanced laboratories couldn’t really do much more than add a few extra genes to something like a corn plant to make it more resistant to drought.

“Scientists in Maryland have already built the world’s first entirely handcrafted chromosome — a large looping strand of DNA made from scratch in a laboratory, containing all the instructions a microbe needs to live and reproduce.

In the coming year, they hope to transplant it into a cell, where it is expected to “boot itself up,” like software downloaded from the Internet, and cajole the waiting cell to do its bidding. And while the first synthetic chromosome is a plagiarized version of a natural one, others that code for life forms that have never existed before are already under construction.”

It seems big corporations are already trying to patent these DNA creation technologies in hopes of monopolizing this potentially huge industry. You can’t help but make the comparison to the early days of computer programming. Pretty scary that a rogue DNA programmer might be able to create a malicious virus with this, except instead of infecting computers, it infects you.

This orangutan could probably use some

Coffee drinkers everywhere, rejoice! A nasal spray containing the naturally occurring hormone known as “orexin A” appears to reverse the effects of sleep deprivation in monkeys. These sleep deprived monkeys performed similarly to well-rested monkeys on cognitive tests, researchers said.

“Orexin A is a promising candidate to become a “sleep replacement” drug. For decades, stimulants have been used to combat sleepiness, but they can be addictive and often have side effects, including raising blood pressure or causing mood swings. The military, for example, administers amphetamines to pilots flying long distances, and has funded research into new drugs like the stimulant modafinil and orexin A in an effort to help troops stay awake with the fewest side effects. The monkeys were deprived of sleep for 30 to 36 hours and then given either orexin A or a saline placebo before taking standard cognitive tests. The monkeys given orexin A in a nasal spray scored about the same as alert monkeys, while the saline-control group was severely impaired.

The study, published in the Dec. 26 edition of The Journal of Neuroscience, found orexin A not only restored monkeys’ cognitive abilities but made their brains look “awake” in PET scans.”

So where can you get your hands on some of this stuff, you may be wondering? Hold your horses, because any commercial use of this treatment will have to be approved by the FDA, which could take over 10 years.