What exactly is metabolism?

 

Here's what you need to know about the connection between metabolism and weight — and how exercise helps. Metabolism is defined as the bodily processes needed to maintain life. But when you hear the word "metabolism" used today, it's usually in reference to weight issues. You may hear someone say, "I can't lose weight because I have a slow metabolism." While there's some truth to this, other factors — such as how much you eat and exercise — play a much bigger role in your weight than your metabolism does. And while it's true that how much lean body mass you have can affect how many calories you burn at rest, its effect is limited — in part, because you can build only so much lean muscle by strength training. Here are some other facts about metabolism. What it is Though the process of metabolism, your body turns the food you eat into the energy it needs. It's a vital process for all living things, not just humans. What can affect your metabolism Some medications can affect your metabolism — either dangerously speeding it up or slowing it down. Eating breakfast every day can jump-start your metabolism. Weight loss — especially when it's rapid — actually slows your metabolism because it takes less energy for your body to function at a lower weight. So, as you lose weight, you need to take in fewer calories or get more physical activity to burn more calories to keep losing pounds. Age can slow your metabolism. In general, as you age, you gain fat and lose muscle. Some people also become less active. However, you can do the opposite and take on more physical activity to make up for your slower metabolism. The bottom line You can help your metabolism — and your odds of weight-loss success — by changing your energy balance, or the balance between what you consume and what you burn off, through a healthy diet and regular physical activity. http://diet.mayoclinic.org/diet/move/what-is-metabolism?xid=nl_MayoClinicDiet_20150910

Cold improved longevity for some

Mon, 06/01/2015 - 8:13am

Laura Williams, Univ. of Michigan

 

Microscope image of a C. elegans roundworm by HoPo via Wikimedia Commons.

Century-old wisdom holds that cold-blooded creatures—flies, worms, fish—live longer in colder environments. And more recent studies have found it's true for mammals as well: Dropping the core body temperatures of mice by less than one degree Fahrenheit can extend their lives by 20%. But new research on roundworms from the Univ. of Michigan Life Sciences Institute and collaborators from Huazhong Univ. of Science and Technology in China adds a new layer of complexity to the existing models, showing that colder temperatures are not beneficial in all circumstances.
For many years, the effect was thought to be a simple matter of chemical reactions inside the organism slowing down at lower temperatures, and therefore slowing the rate of aging.
In the last few years, studies have shown genes also play an active role. In 2013, researchers at the LSI reported that the sensation of cold triggers a genetic program that promotes longevity in C. elegans worms.

The new research, published online in Cell Reports, shows for the first time that the law does not apply equally to adults and developing young. The same temperature-sensitive channel whose signaling extends the longevity of adult worms actually shortens the lifespan of larvae. Larvae raised in warmer temperatures lived about 20% longer.

"These findings show that temperature's impact on longevity is more complex than was previously thought," said study senior author Shawn Xu, the Bernard W. Agranoff Collegiate Professor in the Life Sciences at the U-M Medical School and faculty member of the LSI, where his lab is located. "It also reveals that temperature experience in early life can have a long-lasting effect in later years."

Does this mean parents shouldn't let their kids play outside in the snow? "There's no need to worry," Xu said. "People are a lot different than worms—orders of magnitude more robust and complex—but it's important to understand how these fundamental mechanisms work in much simpler organisms if we want to better understand factors that impact longevity in people."

These differences were seen at temperatures that were neither frigid nor broiling: the worms were kept between 59 and 77 F.
The process works like this: Cold air activates a receptor in the worms known as the TRPA1 channel, which is found in nerve and fat cells. This initiates a chain of biochemical signals that ultimately activates a gene known as DAF-16/FOXO, which has been associated with longevity in worms.

The current study found that the same pathway triggers the opposite effect in larvae as it does in adult worms, though it's not clear why, Xu said. The research also uncovered a critical window during larval development that had the greatest impact on longevity.
Since mammals share much of the same genetic programs, it raises the possibility that exposure to cold—or pharmacological stimulation of the cold-sensitive genetic program—could also affect longevity in humans, Xu noted.

Source: University of Michigan

How a wound closes

Epithelial cells move collectively out of their original shape (left) into the environment (right). Localisation of Merlin is shown in green, the cell nuclei in red. For wounds to close, cells need to move collectively in one direction in a coordinated fashion. Until now the central molecular mechanism that allows cells to coordinate these movements over larger distances has been unclear. Now researchers from Heidelberg University and the Max Planck Institute for Intelligent Systems in Stuttgart have succeeded in decoding it. Collective cell migration is not only important in wound healing, but also in the development of the embryo and even of cancer. The results of their research, published in the journal "Nature Cell Biology," have tremendous implications for all three of these areas. "The collective migration of cells and biological systems is one of the most important natural phenomena and occurs in nature at different levels and length scales. We have now identified the key molecular player and the related mechanism that controls the collective migration of epithelial cells, that is the covering layer of skin cells," explains Prof. Dr. Joachim Spatz of the Institute for Physical Chemistry at Heidelberg University and the Max Planck Institute for Intelligent Systems. In their investigation, the researchers introduce a complete molecular mechanism that focuses on the protein called Merlin. The results link intercellular mechanical forces to collective cell movements and also demonstrate how local interactions give rise to collective dynamics at the multicellular level. "They create an analogy with what we already know about collective movements observable in both the biological and physical world," explains Prof. Spatz. The researcher compares the process of cell migration to running a marathon. "At the level of the organism, an individual in a collective consciously tries to align its movements with those of its neighbours, which involves orchestrated sensing and action." Within a cellular collective, these two processes are linked via signal transduction pathways. There is a lead cell in the collective, similar to the leader in a marathon. It is mechanically connected to its follower cells by cell-to-cell contacts. The forward motion of the lead cell puts mechanical tension on the follower cells, according to Spatz. The merlin protein senses this mechanical tension and initiates spatially polarised following movement. This transmits the mechanical tension among the follower cells from one cell to the next. The follower cells respond by forming 'leg-like' protrusions directed at the lead cell in order to move forward. "Until now it has been unclear what molecular link connects these two events, sensing and action," says Joachim Spatz. "Our study now shows how the mechanosensitive Merlin protein converts cellular forces to collective cell motions by acting as a mechanochemical transducer. What's truly astonishing is that Merlin is the only protein in the responsible signal network that conveys this property to cellular collectives -- that there are no replacement mechanisms. If Merlin fails, the cells lose their ability to move collectively and trigger the related medically relevant, pathophysiological properties in the organism." The major player in the study, Merlin, is also a known tumour suppressor that is responsible for several types of cancer. Merlin is also a regulator of the Hippo pathway, an important signal pathway in biology that controls cell proliferation and organ size. It has been preserved in evolution since the emergence of primitive multicellular organisms. "It's exciting to see a connection between these seemingly disparate fields, linked by a Merlin-mediated signalling mechanism," says the researcher. Story Source: The above story is based on materials provided by Heidelberg, Universität. Note: Materials may be edited for content and length. Journal Reference: Tamal Das, Kai Safferling, Sebastian Rausch, Niels Grabe, Heike Boehm, Joachim P. Spatz. A molecular mechanotransduction pathway regulates collective migration of epithelial cells. Nature Cell Biology, 2015; DOI: 10.1038/ncb3115 Cite This Page:

'Paradigm shift' in understanding of potassium channels

 

---

A new discovery relating to one of the most common processes in human cells is being described as a 'paradigm shift' in understanding.

Researchers at the University of Dundee, the Max Planck Institute for Biophysical Chemistry, the University of Göttingen and the University of Oxford have observed ion permeation in potassium channels which does not follow previously predicted pathways.

They have published the results of their research in the journal Science.

Potassium channels are tiny pores that stud the surface of almost all cell types in the human body, playing a role in the transmission of signals between brain cells and also helping control the frequency of our heartbeat. When they are not working properly they are implicated in a range of diseases, including neurodegenerative conditions and heart disease.

The channels allow the passage of potassium ions in an extremely rapid-fire opening and closing of the channel, acting as highly efficient filters.

The previous theory in this field was part of a project which led to the award of the 2003 Nobel Prize in Chemistry to the American biochemist Roderick MacKinnon. His work proposed that the ions were separated by water as they passed through the channel and that ion-to-ion contact was unlikely due to high electrostatic repulsion.

The research team working on the new project have found a completely different scenario, using advances in technology to reveal the fundamental physical principles that facilitate the channels' operation.

Previous work examining the activity of potassium channels was only possible from looking at static or `closed-state' crystal structures. Advances in computing have allowed researchers to now look at the channels 'in action'which have provided much more detail and revealed the workings of the channels.

Using computer simulations at the atomistic scale and including a transmembrane voltage, they found that water is not co-transported through the channels with ions and is not needed to separate the potassium ions. They found that pairs of potassium ions were stably formed and then passed through the channel, with electrostatic repulsion driving the startling efficiency of the process.

"Our findings explain how potassium flux is able to happen at the maximum physically attainable speed, which is vital for the fast response of neurons," said Dr Ulrich Zachariae, Reader in Computational Biophysics and Drug Discovery at the University of Dundee.

"This is a paradigm shift in the field. It changes our understanding of how these hugely important channels work. These channels are tremendously important as they are active in all cells so it is vital that we understand how they work."

---

Story Source:

The above story is based on materials provided by University of Dundee. Note: Materials may be edited for content and length.

---

Journal Reference:

1. D. A. Kopfer, C. Song, T. Gruene, G. M. Sheldrick, U. Zachariae, B. L. de Groot. Ion permeation in K channels occurs by direct Coulomb knock-on. Science, 2014; 346 (6207): 352 DOI: 10.1126/science.1254840

3-D model of filaments during contraction of muscle

 

A 3-D computer model of filaments of myosin (in red) reaching out and tugging along filaments of actin (in blue, looking like stands of pearls twined together) during the contraction of a muscle. The model, created by C. David Williams as part of his research into force regulation and the length-tension relationship in muscle, enables researchers to consider the geometry and physics at work on the filaments when a muscle bulges. Williams earned his doctorate at the University of Washington (UW) while conducting this research and is currently a postdoctorate at Harvard University.
This visualization let's researchers see how the individual motor proteins generating force interact with each other to regulate the overall level of force the system develops. The 3-D nature of such models also allows researchers to investigate how the spatial arrangement of a muscles contractile filaments alter the force generated as the muscle goes from very long to very short lengths.
The work was supported by the National Institutes of Health and the National Science Foundation (grant IOS 10-22471, awarded to T.L. Daniel and T.I. Irving to support non-modeling aspects of this research) and with cloud computer access provided by an Amazon.com grant for research.
To learn more, see the UW news story Biceps bulge, calves curve, 50-year-old assumptions muscled aside. (Date of Image: May 2013)