White fat or brown fat?

A recent study, published in the journal Cell Metabolism, defines a mechanism that controls if a precursor fat cell matures into a brown fat or white fat cell. Why would this matter?

Most people are undergoing a constant battle to get rid of fat. But, fat cells aren't all the same. Two forms of fat cells exist; white fat and brown fat. White fat is the stuff that stores the excess calories and energy that we taken in, making sure we have enough reserves for lean times when food is scarce. White fat accumulates around the mid-section of our body, along the butt and thighs, and elsewhere. Brown fat is quite different. Brown fat generates heat and burns energy. These cells are filled with energy producing iron-filled mitochondria, hence the brown color, and generates heat for the organism. Brown fat, found mostly in infants (along the spine and shoulders of the back) and hibernating mammals. It's main function is to provide heat to avoid hypothermia in mammals that don't shiver. In adult humans, the amount of brown fat is quite low.

Dr Seale and colleagues have now shown that a protein called early B cell factor-2 or Ebf2 acts like a switch during fat cell development that controls which type of fat cell emerges, a brown fat or white fat cell. It turns out that Ebf2 binds to the promoter of genes involved in brown fat development. This results in the recruitment and binding of another protein, PPAR, and the subsequent expression of these genes. This study also showed that overexpression of Ebf2 in white fat cells converts into brown fat cells. Understanding how these cells develop may help develop new ways to control the amount of white fat cells in the body to help fight obesity.

http://www.alnmag.com/news/how-brown-fat-cells-develop-mice?et_cid=3143363&et_rid=454985655&linkid=http%3a%2f%2fwww.alnmag.com%2fnews%2fhow-brown-fat-cells-develop-mice

New gene controls obesity

The search for an (the) obesity gene has been a long and arduous one that has implicated many candidate genes during this quest. Although these genes that have had important roles in regulating weight, the common thread linking them together has been that have had some role in metabolism and regulating the cell's ability to use energy.

Researchers at the University of Colorado and Tufts Medical School have recently identified another potential regulator of obesity, Plin2. Like previous candidate genes, Plin2 may play a key role in regulating cellular metabolism. Further, the deletion of this gene in mice prevented weight gain, even when the animal was fed a high fat diet. Surprisingly, researchers found that lack of expression of this gene prevented the onset of other obesity associated outcomes -- like high triglycerides and increased inflammation that are seen along with obesity. Even the adipose (fat) cells in these mice were smaller than their paired control mice that faithfully expressed Plin2.

Work is ongoing to learn more about Plin2 and how this gene controls metabolism and weight gain. http://www.scienceomega.com/article/863/removing-gene-stops-obesity-in-mice

Salt activates different receptors depending on concentration

Do you like lots of salt? You may not be alone -- many people love salt. But, even for these salt-lovers, high concentrations of salt taste transitions from delectable to disgusting. How does this happen? We have taste receptors that recognize the sweet, savory, salty, bitter and sour tastes in the foods we ingest. This is an evolutionary adaptation that prevents us from eating potentially deadly or toxic foods. Sweet and savory foods activate one set of receptors and one pathway. On the other hand, sour and bitter foods stimulate a different set of receptors and pathways. This makes sense; different pathways informs us if a food is acceptable or potentially toxic and shouldn't be eaten.

But what about salt? A new paper published in Nature magazine, by Dr. Y. Oka and colleagues (ePub February 13, 2013, print 494: 472), provides new insight into how salty tastes transition from good to bad. At low concentrations, salt activates the savory and sweet pathways, but switches to the bitter and sour pathways at higher levels. Researchers have begun to identify specific receptors that a involved and have shown how blocking these receptors changes the reaction to salt concentrations. This research opens the door to understanding how and why we like salt at times, but not when there is too much of it.

Where have all the postdocs gone, part 2.

Did you "step away from the bench"? What are you doing now and how did you get there?

In recent weeks, I have talked to many scientists about their career tracks away from bench research. We are an intersting bunch. So many have come up with creative ways to use their science background. It really strkes home that having a solid scientific education is very valuable, even if you are not participating directly in science any more.

In a few weeks, I will be talking to science students about careers in science - within academia and outside of it. It would be good to hear how other "alternative career scientists" spend their time. Let me know what you do and how you got there.

Where have all the postdocs gone (aka "alternative careers")?

I heard an interesting statistic that I am not sure is true, but it emphasizes a point. Today at the AAAS annual scientific meeting in Boston, a speaker stated that almost 90% of scientific postdocs are (or will be) looking for alternative careers. Even if that statistic isn't quite accurate, that is a huge number. Where have all the postdocs gone? What are these "alternative careers"? Why are they "alternative" if so many seek them out and pursue them?

I began my own journey to an alternative science career about 2 years ago. Well, in reality it was longer than that, but in earnest, it started two years ago. It has been a great decision and I don't plan on going back, but I don't think the career tracks should be mutually exclusive. Over the coming weeks, I will talk about my journey from academic scientist (as a tenure-track assistant professor) to science policy analyst (for now at least).

Before I start, it's probably good to discuss these "alternative careers" a bit. When I was in graduate school and postdoc training, my colleagues joked that there was only 1 true path for a scientist. Everyone was (and still is to a great extent) expected to follow in the footsteps of their mentor and become an academic researcher. This is a great career and one I pursued for several years. Many aspects of it are incredibly rewarding. For anyone who didn't want to become a professional researcher in medical school or research intensive university, there was little help or guidance provided. To be fair, there are some great mentors that do help their students find a good career option, but the overwhelming advice doled out, however, is that you could work in "industry", whatever that means. Anything that was not a research position with a research lab to run was considered less desirable. All other choices were labeled "alternative" careers in science. Young (and not so young) scientists interested in other career options were cast adrift to explore for themselves. No guidance was available (and sometimes you even dropped of the radar of your mentor as a scientist in their lab - or worse, asked to leave).

The good news is that there are so-called "alternative" careers. There are many of them and many of opportunities. Having a science degree is very beneficial, even if you aren't actively involved in any scientific field or in a way that you imagined when you started to become a scientist. If 90% of postdocs are pursuing alternatives, there are plenty of people out there to tell their story and give advice.

I hope this spurs on some genuine discussion and sharing of success stories. There is a big life away from the bench. I'd like to hear more of them!

Does when you eat matter?

Everyone has an internal clock, called the circadian rhythm, that controls wake/sleep cycles, body temperatures, brain activity, and changes in hormone levels throughout the day.  Disruption in these circadian rhythms can alter metabolism.  In the latest issue of Cell Metabolism (epub ahead of print June  2012 DOI 10.1016/j.cmet.2012.04.019), Dr. Megumi Hatori and colleagues investigated how feeding patterns, in particular time restrictions to eating, can alter metabolism and the expression of genes that control the circadian rhythm.  

Mice were divided into four groups as follows:

1. Normal calorie diet, freely accessible all day
2. Normal calorie diet, limited access
3. High fat diet, freely accessible all day
4. High fat diet, limited access

Mice are nocturnal and were placed on a 12 hour light/dark cycle.  For groups 2 and 4, food was available from 1 hour after lights off (waking) until 3 hours before lights on (sleeping).  

Their data were intriguing.  Mice in both high fat diet groups consumed equivalent numbers of calories over a 24 hour period.  Those with free access appeared to eat all day with no spike in intake at any regular time period, while those with limited access consumed their calories only during the 8 hour period.  

As expected, mice with unlimited access to the high fat diet gained significant weight compared with either of the normal calorie diet groups.  Conversely, the mice on the high fat diet with limited access did not have the same weight gain as the unlimited access group.  Indeed, mice in the time restricted groups were lower weight than those with unlimited access.  When comparing the high fat diet groups, the mice with limited food access did not become obese as did the unlimited access mice. In fact, their weight was only slightly higher than the normal calorie diet groups.  In addition, the time restricted high fat diet group also retained sensitivity to insulin and did not exhibit liver problems as seen in the unlimited high fat diet group.

This very interesting study suggests that circadian rhythms control metabolism and restricting food intake to regimented periods during the day can help to keep the metabolism strong and avoid excessive weight gain.  This is a small study in mice, but could have implications in human dieting and the control of weight gain.

Science for the public

by Jasper Manning, Ph.D.

Each day large amounts of scientific information is disseminated from mass media to the general public. This includes healthy-related studies and novel scientific breakthroughs with the aim of educating, informing and improving the quality of life. Much of this information comes from pundits and medical reporters who support their ideas with well researched facts. However, in some instances, facts are misconstrued in order to support a specific agenda(s) of a political lobby or industry i.e. global warming or endangered species lists. In addition, the summary of published information by medical writers sometimes is erroneous due to lack of available print space and/or time set aside for an article or misinterpreted perhaps due to a lack of knowledge about a topic. In the end, an article that is unable to convey to laypersons the benefits or detriments of a study defeats the intended purpose of the article. Howy Jacobs, a distinguished professor of molecular biology at the Institute of Medical Technology (IMT), University of Tampere and senior editor at EMBO Reports recently suggested that a miseducation of the masses through mass media is due to the misconnection between science and the media (Jacobs, 2012) and believes that the responsibility of educating medical writers falls on scientists. Once this can occur, the reader, has a better chance of receiving complete and concise information. 

Jacobs illustrates the lack of clearly presented information to the general population by relating a recent conversation that he had with a southern Alaskan Bed and Breakfast owner. The owner espoused that climate change was not a reality and had no affect on wildlife specifically in the case of the polar bear. Jacobs notes that after some fact-checking, he found published data of comparative mitochondrial DNA sequence of polar bears and brown bears that supported that environmental stress (Edwards, et al, 2011) may have influenced a recent introgression between the two species. Dr. Jacobs chose not to challenge the beliefs of the owner (perhaps many scientist choose to sit out these arguments), but realized that the scientific data is available although public awareness is lacking. This is a plus for lobbying groups and others since a uninformed public can be easily influenced by those who have a vested interest in exploiting the environment. He astutely points out that science should not support political argument/agenda, nor “prove” a hypothesis but accumulate, interpret data and form a predictive model based on the interpretation. In his opinion, the media should explain this process used by scientists and report the findings legibly or risk painting a picture of science as a confusing and perhaps dishonest profession as in the case of global warming.

 All in all, the take home message of the Jacob's editorial is that scientists must be able to better convey scientific results to the media in a clear and comprehensible way. On the other side of the coin, the media has a responsibility to become more knowledgeable in basic science and the aspects of the scientific method. He believes that miscommunication is the primary problem and scientist must learn to better explain interpreted data to the world and correct poorly presented interpretations that are published in the media.

 It is refreshing that scientists such as Howy Jacobs understands that scientist are the key to explaining the latest breakthroughs and correcting errors in summarized studies that are published in the public domain. Blogs such as N3science communications is a good starting point as well. Take a read and pass it along. Scientists are trying to educate, now it is your turn to read and understand what is happening with science around you.

 REFERENCES Howy Jacobs EMBO reports (2012) 13, 471;doi:10.1038/embor.2012.56 Edwards CJ et al 2011) Curr Biol 21:1251-1258