fat cells – BioQuakes

Are you sick and tired of spending all of your time running on the treadmill and eating restrictive diets? Are you looking for a way to hack fat loss without ruining your way-of-life? Look no further than CRISPR gene-editing!

In humans, stubborn body fat can be attributed to either white or brown fat. Brown fat, specifically, is used in humans primarily for insulation, and can be tapped into when we are cold or need to ramp up our metabolism to generate heat. This fat is caused by a caloric surplus in humans, and is burned off by engaging in caloric deficit. However, in mice studies conducted by Steven Romanelli, Ormand MacDougald, and colleagues, CRISPR gene-editing offers promising results regarding the topic of brown fat loss in humans.

But what exactly is CRISPR gene-editing? CRISPR, or Clustered Regularly Interspaced Short Palindromic Repeat, gene-editing entails organizing short, palindromic DNA sequences of bacteria. These DNA sequences are surprisingly important in the immune function of these bacteria and other microorganisms, making CRISPR an incredibly promising and innovative tool in science research.

Bacteria have short sequences of variable DNA called “spacers” in between CRISPR DNA sequences. This DNA helps protect the bacterium from reinfection from viruses. If any virus were to attack the bacterium, the CRISPR DNA sequences would cut up that viral DNA matching any spacer within the genetic code of the bacterium, preventing it from reinfection.

CRISPR gene-editing works by processing invading viral DNA into short fragments that are inserted into the CRISPR DNA as spacers. Then, CRISPR replicates and spacers in the DNA of the bacterium experience transcription, in which DNA becomes RNA and CRISPR RNAs. These CRISPR RNAs help bacteria kill viruses, as they match the exact DNA as the viral DNA attacking the bacterium.

In mice experiments conducted by Romanelli, MacDougald, and colleagues, has used CRISPR gene-editing to have an enzyme named Cas9 break strands of DNA and a single piece of RNA to be packed into a harmless virus cell that will be delivered into cells in the study, which are brown fat cells in this case. This process has shown to delete several genes, namely the UCP1 gene in mice, that allows brown fat to exist and create heat. However, the mice in the study did not die when exposed to cold environments. They were able to survive despite a huge loss in brown fat.

Accordingly, using CRISPR gene-editing as a tool for brown fat loss in humans provides incredibly promising results. It is certain that, once CRISPR gene-editing becomes available for use in the reduction of brown fat in humans, I will no longer be using the treadmill as my mode of fat-burning and shift toward this method instead.

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

By elendometrium

On November 7, 2021

In Student Post

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.

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!!

Sometimes less is better. Especially in the case of germs.

By sheasexual

On March 3, 2016

In Student Post

Scanning electron micrograph of Escherichia coli

Photo by NIAID

Apparently we’re healthier than we thought!!

Throughout the 20th century, scientists who studied the microbiome had thought that humans contain around 9000 times more germs than human cells. Scientists now believe, however, that that number is more like 30 percent.

Micro biologists: Ron Sender, Ron Milo, and Shai Fuchs took on the challenge to actually find out the ratio of bacteria to cells in the human body. First, its important to know the types of cells that make up the human body. One might think that muscle and fat cells make up the largest portion of human cells in the body but that is wildly incorrect. In fact, despite their weight and size dominance, they make up a measly .2 percent of the body’s cells while blood cells make up 90 percent (mostly red blood cells).

The colon houses the most bacteria in the human body by a long shot. This makes sense as it is the pathway for human feces out of the body and reaches up to 5 feet in length. The “trio” of scientists estimate that the human body contains somewhere between 30 trillion and 50 trillion cells and that the bacterial count is around 30 to 60 percent higher than the amount of cells.

Now, despite the insightful findings of Sender, Milo, and Fuchs, the microbiome community still has a lot of research to do into the subject of germ:cell ratio in humans and scientists believe that the trio missed some important factors in their experiments and as geneticist Julie Segre points out, “Other researchers also point out that the new paper’s calculations focused on bacteria. Yet the body can host other types of microbes as well. Those include viruses, fungi and archaea (Ar-KEE-uh). Viruses tend to vastly outnumber bacteria, so they could skew the microbe-to-human cell ratio upwards.”

The most important and prevailing part of the trio’s research was that the amount of bacteria that we have in our body and attached to human cells is much less than we had previously believed.

https://student.societyforscience.org/article/cell-recount-people-host-far-fewer-germs?mode=topic&context=79

Original Article

BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: fat cells

Away With Treadmills and Low Carb Diets: Is CRISPR the New Hack For Fat Loss?

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

Sometimes less is better. Especially in the case of germs.

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