AP Biology class blog for discussing current research in Biology

Tag: mitochondria

Can Obesity Be Cured Through Thermogenesis by Brown and Beige Fat Cells?

In an attempt to find methods for treating obesity and diabetes, researchers recently discovered a new cellular pathway that triggers thermogenesis, the process by which fat cells (called adipocytes) create heat by burning energy. 

The human body has white adipocytes in which energy is stored in the shape of a single, large oily droplet. It also has brown adipocytes which contain a mixture of many, small oily droplets and dark-colored mitochondria (which create the brown color of these fat cells). The mitochondria in the brown adipocytes act as engines that turn the oily droplets into heat and energy. Some people also have “beige” adipocytes consisting of brown-like cells found within white adipocytes which can be triggered to burn energy. 

Brown fat cell

Adipose tissue, otherwise known as fat tissue, can be composed of either white adipocytes or brown adipocytes. The white tissue is primarily used for triglyceride storage while brown tissue functions to expend energy, potentially counteracting obesity. BMP7 is the protein that causes the adipogenesis (formation) of brown fat cells. It was found in a study that mice lacking the gene BMP7 did not have any brown fat and subsequently had a more difficult time losing weight. The protein BMP7 causes an increase in energy expenditure and reduction in weight gain. 

In order to create energy, the human body converts carbohydrates into glucose (much like the mice described above), a type of sugar used as fuel for cells. Excess glucose is stored in the white adipocytes of muscles and the liver for later use by the body to stabilize blood sugar levels and create energy as needed. By contrast, in adipocytes, glycogen not only stores energy but also sends a signal to the uncoupling protein to “uncouple” ATP, the molecule providing energy for fueling cellular processes. This process, which is completed using Uncoupling Protein 1 (UCP1), ensures that only the adipocytes with sufficient energy to provide fuel for heat are triggered to generate heat and balance energy needed by the body. 

The uncoupling protein, formally known as Uncoupling Protein 1 (UCP1), is a unique protein, located in the inner membrane of mitochondria. UCP1 is devoted to adaptive thermogenesis, a special function performed by brown adipocytes. The protein itself is located near the multi-enzymatic complex called the respiratory chain where, by reducing coenzymes, electrons are driven towards oxygen in a process called oxido-reduction. Through oxido-reduction, an electrochemical gradient of protons is generated across the inner membrane of the mitochondria.

This electrochemical gradient is normally consumed by ATP-synthase, which occurs from the phosphorylation of ADP. UCP1 simultaneously transports proteins passively, in what is known as a futile cycle. Named after its lack of perceived utility, the futile cycle was thought to be a quirk of metabolism when initially discovered. In reality, the futile cycle generates heat by dissipating energy through two separate metabolic pathways. Playing an integral role in regulating metabolism, the futile cycle maintains thermal homeostasis within brown adipocytes.

In the future, it is possible that the injection of brown fat cells into white fat cells will become a common method of inducing fat burn in individuals struggling with obesity.

Throughout my life, I’ve personally struggled to maintain an appropriate weight. It always seemed to me that even though I didn’t eat as much as others, I somehow seemed to gain weight more easily than many people who ate more than I did and yet remained skinny. This new understanding by researchers of how glycogen works in fat cells to promote fat burning and better metabolism has implications for obese people who may someday be injected with more brown fat cells to help increase their metabolism and thus decrease their weight gain. Hurray!!

Sea Otters: Tiny and Toasty

Weighing in at anywhere from 30 to just under 100 lbs, sea otters are the smallest ocean mammal. Scientists have long wondered how such small animals can withstand the cold waters in which they live. Unlike other sea mammals like whales who can have hundreds of pounds of blubber to insulate themselves, sea otters have rather trim, muscular builds. Although their fur is the densest out of any creature on the planet, scientists have concluded that their fur alone is not enough to insulate their bodies from harsh coastal climates. Scientists were puzzled for years as to how these petite mammals could endure water temperatures approaching and below 0 degrees Celsius. Finally, in the summer of 2021, a group of scientists revealed they found the answer to how sea otters stay warm: mitochondrial leaking.

On July 9 2021, Traver Wright and his colleagues at Texas A&M University published their research that solved the long standing mystery of sea otter survival. For their research, the team took muscular tissue samples from 21 different otters, varying in age and habitat. The team chose to study muscle tissue as this is predominantly where metabolic reactions occur in mammals. Utilizing a tool called a respirator, the researchers measured the oxygen flow and respiratory capacity of the otters’ cells as an indicator for the amount of heat their cells are producing.

The mitochondria is an organelle found in all living cells. Often cited as “the powerhouse of the cell”, the mitochondria is responsible for many important processes within a cell, most notably the generation of ATP through the process known as the Krebs Cycle. The mitochondria also has a special process of generating heat. Peter Mitchell’s 1961 chemiosmotic theory explains how electrons being passed through the mitochondrial electron transport chain creates a proton gradient, or gradual change in concentration within an area, that drives the production of ATP. Sometimes, the protons escape the mitochondria’s inner membrane, leading to energy being released as heat. This process is called “non-shivering thermogenesis” and it is precisely what happens in the muscles of sea otters.

Because a lot of energy is lost in this process of generating heat, sea otters have a high metabolism and need to consume a lot of food to maintain homeostasis. This explains the studies of oxygen flow in and out of the otters’ muscles! The research shows that over 40 percent of the cell respiratory capacity is due to these proton leaks, showing the major significance of this phenomenon on the metabolisms of otters and how hard their bodies work to keep them warm.

The scientists’ next steps are to find whether otters are born with such traits or if they develop them when they live in cold water as a means to survive. While baby otters don’t generate heat well due to their low muscle mass, the study showed that proton leak was still heavily occurring in the babies’ cells. While the Texas A&M team made significant contributions to our scientific understanding of otters, they have also opened the door to a many new research opportunities to further our understanding and answer the new questions that their research posed.

Small But Mighty: Sea Otters And Their Leaky Mitochondria

Sea otters: they bob up and down in the water, hold hands when they are sleeping, poop together at social events, stay warm by their fur and leaky mitochondria… wait, what?

Let’s rewind.

Sea-otter-morro-bay 13

A Cute Sea Otter Floating On Its Back

Warm-blooded marine mammals have a thick layer of fat and oils, known as blubber, as their skin layer to insulate their body. In cold waters, blubber helps retain heat and maintain homeostasis.

But what if warm-blooded marine mammals lack blubber? Sea otters are a prime example (and the only example) of a marine mammal without a layer of blubber. Instead, they have a thick coat of dense hairs, 1000x denser than human hair–the thickest on earth. This enables sea otters to trap large amounts of air within their fur coat, acting as insulation. (This is the same reason why sea otters float: the air trapped in their fur coat makes them buoyant).

But with that said, can you stay warm in a fleece jacket? Possibly. What if you were wearing it while in the ocean? That might be somewhat difficult. Similarly, fur can’t solely protect these animals from losing too much heat. These mammals are still living in water, which transfers heat 23 times as efficiently as air. Since sea otters are the smallest aquatic mammals, they have a lot of surface area relative to their volume, making it even harder for these animals to maintain homeostasis.

So how do they do it? Researchers have already understood that sea otters have an extreme metabolism, how food gets converted to energy in cells, eating about twenty-five percent of their body mass in food every day. But the pieces were still not adding up, which prompted researcher T. Wright to investigate this question on a cellular level. He and his colleagues searched for the source of heat in otters’ muscles. Playing a pivotal role in the body’s metabolism, the skeletal muscle makes up 40 to 50 percent of the sea otters’ entire body mass. His study required the collection of tissue from 21 sea otters of different ages and then measured the muscle cells’ respiratory capacity compared to that of other animals. The sea otters’ oxygen flow rate would roughly indicate the measurement of the cells’ heat production.

Mitochondria pump protons across their cell membranes to store energy in the form of ATP, like we learned in AP Biology’s diffusion unit. From this study, T. Wright concluded that the protons are diffusing back through the membrane before being used for work, resulting in excess heat. Since some of the energy is lost as heat, sea otters need to eat more food to compensate for the lost energy. This “leak in energy” is what contributes to the sea otters’ speedy metabolism.

It’s unknown if sea otters develop leaky mitochondria by living in cold water or simply inherit it. Future research into the fascinating design of sea otters may potentially reveal intriguing insight into their evolution, behavior, and maybe someday, their cuteness.



Nobel Prize awarded to Researchers for Key Discoveries in Cellular Respiration

Recent findings about the change in oxygen levels in cells show new important factors about oxygen that translate to one’s well-being. William G. Kaelin Jr., Sir Peter J. Ratcliffe and Gregg L. Semenza discovered how cells can “sense and adapt to changing oxygen availability,” and are now being awarded the Nobel Prize in Physiology or Medicine. Oxygen is a crucial aspect to how a cell’s functionality. Mitochondria in cells use oxygen to aid in converting food into ATP (energy), a process known as cellular respiration.

A representation of the reaction of cell respiration.


Gregg Semenza wanted to further look into the rise of levels of the hormone erythroprotein (EPO), a response to low levels of oxygen, or hypoxia. He found that “oxygen sensing mechanisms were present in virtually all tissues, not only in the kidney cells where EPO is normally produced.” While Semenza analyzing cultured liver cells, Semenza found a protein complex that was unknown to science. He named unidentified DNA segment the “hypoxia-inducible factor (HIF).”

Over the course of 24 years, Semanza continued to explore aspects of HIF and found two different DNA-binding proteins, now named “HIF-1a and ARNT.” Researchers worked with Semanza in finding out which parts of the HIF assist in cellular respiration. While Semenza and Ratcliffe were researching regulation of EPO, Kaelin Jr. was researching von-Hippel-Lindau’s disease (VHL). Kaelin Jr.’s research showed that VHL gene “encodes a protein that prevents the onset of cancer,” and that cancer cells lacking a functional VHL gene have “abnormally high levels of hypoxia-related genes.” But when the VHL gene was reintroduced into cancer cells, “normal levels were restored.” Eventually, Kaelin Jr. and his team found that VHL needs HIF-1a for degradation at normal oxygen levels.

Kaelin Jr. and Ratcliffe both published articles that center around protein modification called prolyl hydroxylation which “allows VHL to recognize and bind to HIF-1α degradation with the help of oxygen-sensitive enzymes.” The papers also wrote that the gene activating function of HIF-1α “was regulated by oxygen-dependent hydroxylation.” The researchers now had a much clearer idea of the effects of how oxygen is sensed within cells.

These groundbreaking finds give the science world more information about how oxygen levels are regulated in cells in physiological processes. Sensing oxygen levels is important for muscles during physical exercise, as well as the generation of blood cells and strength of one’s immune system.

Cuts, Scrapes, and Hair Loss a Thing of the Past!


Can adults repair their tissues as easily as children can? A study currently conducted at Boston Children’s hospital is attempting to find the answer to this question. Researchers have found that by activating a gene called Lin28a, they were able to “regrow hair and repair cartilage, bone, skin and other soft tissues in a mouse model.”  The scientists found that Lin28a works by enhancing metabolism in mitochondria—which, as we learned in class, are the “powerhouses” of the cells. This in turn helps generate the energy needed to stimulate and grow new tissues.
This discovery is a very exciting one for the field of medicine. The study’s senior investigator George Daley said, “[Previous] efforts to improve wound healing and tissue repair have mostly failed, but altering metabolism provides a new strategy which we hope will prove successful.” Scientists were even able to bypass Lin28a and directly activate the mitochondrial metabolism with a small compound and still enhance healing. Researcher Shyh-Chang says of this, “Since Lin28 itself is difficult to introduce into cells, the fact that we were able to activate mitochondrial metabolism pharmacologically gives us hope.” Since it is difficult for scientist to actually introduce Lin28a into a cell, it might be easier to simply synthetically create a substitute and introduce that. Either way, I think this is a very promising discovery! What other uses can you think of for this discovery?



What CAN’T Exercise Do?!

As I’m sure you’re all well aware, exercise makes you stronger. This is because exercise increases the amount of muscle mitochondria and basically the more mitochondria you have in your muscle cells, the more durable and fatigue-resistant (strong) your muscles are.

Credit: PictureYouth Flickr

Well guess what? You’re brain is a muscle too.

Studies show that brain cells are also fueled by mitochondria, and therefore also get stronger through working out. This is because “the brain has to work hard to keep the muscles moving” (J. Mark Davis, University of South Carolina Professor).

J. Mark Davis and his fellow scientists at the Arnold School of Public Health at the University of South Carolina conducted a test with mice for 8 weeks to figure out how this actually works. There was one group of mice that exercised every day, and one group that just lounged around. At the end of 8 weeks, the group that exercised performed extremely well on an endurance test and had a huge surge of “newborn mitochondria” in their brain cells. Of course no improvement was seen for the lounging mice, because they were lazy and didn’t exercise!

This is extremely good news, especially for neurologists studying Alzheimer’s and Parkinson’s disease, which are believed to be caused by mitochondria deficiencies in human brain cells.

Credit: Jules.K. Flickr

But the benefits don’t stop there! By working out, you are decreasing bodily or mental fatigue. That’s why the more you work out, the longer you can spend working out. Also, by decreasing mental fatigue, you’re making your brain sharper.

So the next time you stay up all night studying for your AP Bio test, don’t forget to take a casual 30-minute jog or just do some yoga. It will really help (plus it’s always good to take a break from studying)!

For more information about the benefits of exercise, please visit the following site.

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