NCTimes.com Blogs

A master switch that controls hunger and reproduction has been discovered —- in mice.
The switch for these primordial animal instincts likely also is present in humans, said Mark Montminy, a professor at the Salk Institute, in a telephone interview last week.
Further research could lead to new obesity and infertility treatments, said Montminy, who took part in a study identifying the molecular switch. The study was published Sunday in the online edition of the journal Nature Medicine.
The study examined what happens to mice when the gene that makes the master switch is disabled. These mice appeared normal at birth, but began to put on weight about eight weeks later. They also became resistant to insulin, a critical hormone that controls blood sugar.
Moreover, both male and female mice lacking the switch were found to be infertile.
Insulin resistance and obesity are characteristic of Type II diabetes, the most common form of the disease. Potential complications include heart disease, blindness, nerve and kidney damage.
Obesity and Type II diabetes are linked. As obesity has ballooned in the United States, so has the incidence of Type II diabetes. So any effective treatment that cures or prevents the disease would not only provide a major health benefit, it could be a huge money-maker.
About 18 million Americans have diabetes, according to the American Diabetes Association, and about 90 percent of those people have Type II diabetes.
Millions more are obese and in danger of developing diabetes. Controlling weight has been proven effective in reducing the severity of Type II diabetes.
Montminy said the master switch, which occurs in brain cells, gives the brain information that helps it regulate food intake and energy expenditure.
“The brain is the central processing unit for the organism, and it needs a way to know what’s going on outside the brain, like how much food you’re taking in and how much exercise you’re doing,” Montminy said. “It puts that all together and makes certain decisions, like will you be able to reproduce, or whether you can grow.”
Lack of food is known to inhibit female reproduction, Montminy said. The organism conserves energy for survival, because it doesn’t have enough to sustain itself and produce healthy offspring.
But in some cases, the brain receives incorrect information from the signals, Montminy said. He likened the miscommunication to a game of “telephone,” in which a message relayed from person to person is progressively distorted. In such cases, drug therapy could help overweight or infertile people.
The master switch, called TORC1, is regulated by leptin, a hormone that tells the brain enough food has been consumed. Leptin is made from adipose, or fat cells. Mice lacking leptin became overweight, according a 1995 study that caused great excitement in the scientific community.
Biotech giant Amgen Inc. of Thousand Oaks licensed the discovery for $20 million from Rockefeller University, and tested a leptin-derived drug as an obesity treatment. However, the leptin drug had a relatively minor effect in humans, so Amgen discontinued testing.
It’s since been discovered that leptin is part of a complex set of regulatory mechanisms that govern appetite and obesity. So researchers think any one drug alone is not going to be sufficient to regulate weight and appetite.
San Diego-based Amylin Pharmaceuticals says it has made progress in understanding how the appetite and metabolic mechanisms work together. Amylin licensed the rights to the leptin drug from Amgen, and is now testing it in human clinical trials in combination with pramlintide, a drug it developed on its own.
Pramlintide is derived from amylin, a hormone that acts with insulin to control blood sugar and weight control. Pramlintide and leptin given together to rats produce greater weight loss than would be expected from the combination of their individual effects, according to a paper by Amylin researchers published in the July 31 issue of the journal Endocrinology.

A conference on reproductive technologies will take place Oct. 2-3 at the San Diego Marriott La Jolla. It’s called “Emerging Technologies for the Assessment of Gametes and Embryos: The ‘Omics.’”

The conference is intended for reproductive technologies specialists, including infertility doctors and researchers, embryologists and stem cell scientists, and others interested in reproductive medicine.

From the conference’s Web site:

The aim of this two-day symposium is to provide the Assisted Reproduction Technologies (ART) community an overview of fast-approaching technologies that may allow us to improve our assessment of the reproductive potential of gametes and embryos.

These emerging technologies will allow clinicians and scientists in the IVF laboratory to assess gametes and embryos at the four basic levels of cell biology: DNA, RNA, proteins and metabolites. A variety of technologies, that will soon be available or are currently available to laboratories today, based on the “omics” – genomics, transcriptomics, proteomics and metabolomics – will be discussed by internationally recognized experts.

The symposium will culminate in the faculty engaging participants in a debate regarding the merits of invasive vs. non-invasive embryo assessment.

While other scientists are discovering the secrets of sonic hedgehog or stellar evolution or the platypus genome, Caltech’s Michael Dickenson has focused on something we can all relate to: Why are flies so hard to swat?

Planning.

The fly’s fly-brain takes information from its compound eyes, air currents brushing its hairs and other clues and uses this to calculate the best way to escape the threat. Then, the fly-brain orients the body for this escape route by placing its legs for the calculated takeoff.

From the press release:

For example, the videos showed that if the descending swatter–actually, a 14-centimeter-diameter black disk, dropping at a 50-degree angle toward a fly standing at the center of a small platform–comes from in front of the fly, the fly moves its middle legs forward and leans back, then raises and extends its legs to push off backward. . .

With all that information, Dickinson suggests a way for our human brains, with our superior ability to anticipate events through the miracle of consciousness, to defeat the pesky fly: Aim a bit into the future. Bring down the swatter where the fly is likely to go, not where it is.

It can be done. A friend of mine has the uncanny ability of catching flies in his bare hand. What do you do with such flies? My friend feeds them to his Venus fly-traps.

Battered Amylin stock up about 5 percent as of this writing (8:36 a.m. PDT) after the terrible beating it took yesterday. The stock is at $21.52, up $1.04 so far for the day. Earlier, Amylin briefly climbed over $22 per share.

If the 6 deaths from patients who took Amylin’s diabetes drug, Byetta, were not caused by the drug, Amylin shares will slowly begin to recover as investors regain confidence. In my story about the Byetta debacle, I talked with a prominent diabetes doctor who says there is no linkage, and continues to prescribe the drug.

Amylin is doing (sorry for the buzzwords) cutting-edge research in metabolism, and its discoveries of how other hormones work with insulin to control blood sugar is fascinating. It is also working with leptin, the much-hyped weight-regulating hormone, leptin, previously found not to work well. Amylin is tweaking how leptin is administered, based on a more sophisticated understanding of how the various metabolic regulatory centers are coordinated.

So this heart-stopping episode may be just a hiccup for Amylin.