FatCells – BioQuakes

Fat, which is made up of cells that have been distended with greasy or oily materials, or triglycerides, is required for the body to function, but it may also be hazardous if consumed in excess. Fat cells are distinct from other cells such that they lack surface receptors and constitute only a small percentage of the cells in fat tissue. While restricting diets can assist those who are obese lose weight, the results are typically solely temporary. If only there were a way to target fat cells specifically… Well, there just might be!

A group of doctors discuss a potential prospective breakthrough utilizing CRISPR-Cas9, a technology that has proven particularly elusive in the study of adipose tissue, in a recent publication published in the Journal of Biological Chemistry. Their study was tested on mice, in order to see how it worked and what it targeted. The gene-editing technology CRISPR-Cas9 changes genes by precisely cutting DNA and then allowing natural DNA repair mechanisms to take charge. This technology has changed the ability of deleting or inserting certain genes of interest into an organism. Cas9, an enzyme that can break DNA strands as well as a piece of RNA that directs the Cas9 enzyme to a specific location in the genome for modification, is encased in a non-harmful virus and supplied to the cells being studied. The equipment has also been used to study the heart, liver, neurons, and skin cells, to name a few. However, brown fat adipose cells have never been studied.

Using CRISPR-Cas9 components, the physicians were eventually able to target brown fat adipose cells. In mature mice, they were able to knock off the UCP1 gene, which specifies brown adipose tissue and allows it to generate heat. They discovered that knockout mice were able to adjust to the absence of the gene and maintain their body temperature under freezing settings, indicating the existence of additional mechanisms involved in temperature regulation. Overall, the CRISPR interference system assisted mice in losing about twenty percent of their body weight, proving that CRISPR can accurately target fat cells.

Genetics can have a significant impact on the quantity of fat cells you are born with. However, the proportion of tendency to becoming overweight differs by individual. For example, in some people, genes account for just 25 percent of the tendency, but in others, the genetic effect might be as high as 70 percent to 80 percent. Obesity is most commonly associated with the FTO gene. This FTO gene is not found in everyone. For example, around 20 percent of white people have a variation of the gene that increases their risk of obesity. The FTO gene is located on chromosome 16, which is one of the 23 pairs of chromosomes in humans. While this chromosome pair represents under 3 percent of the total DNA in cells, if FTO is present, it can affect whether if one is obese or not, depending on the alleles of the gene. CRISPR has the potential to target this gene as well as other genes that affect body weight, such as brown fat adipose cells.

Your health is essential for the rest of your life! A healthy lifestyle can aid in the prevention of chronic diseases and long-term ailments. The alleles on the FTO gene can have an impact on your health and are linked to type 2 diabetes, obesity, and other health concerns.

COVID-19 has a plethora of underlying effects. However, researchers may have just identified the most dangerous long-term impact.

While researchers have been studying COVID-19 for the past two years, pharmacy technician Nola Sullivan of Kellogg, Idaho, has uncovered the virus’s extending underlying conditions. Sullivan faced an additional struggle as a result of being infected with COVID-19 last year, despite the virus’s long-term effects, which included a loss of taste and smell, nausea, and diarrhea. Many COVID-19 patients too are grappling with an additional struggle: the onset of diabetes. In a research involving nearly 3,800 patients infected with the virus, cardiologist James Lo and colleagues discovered that just under half of the patients acquired elevated blood sugar levels that were not previously present. How is it conceivable for COVID-19 patients to develop diabetes? Many researchers have been tackling this exact issue for a long time.

When a patient develops diabetes, he or she must learn to control the illness and live an active life due to an insulin shortage. Because diabetes is incurable, the prospect that it is a long-term side effect of COVID-19 is very troubling. Insulin is essential in the human body because it lowers triglycerides by boosting lipoprotein lipase activity, which degrades triglycerides into glycerol and fatty acids. A lack of pancreatic B-cells, which release proper quantities of insulin, has a direct impact on mitochondria and the glycolysis process which is utilized for energy synthesis by all cells in the human body, eventually prompting the pyruvate product to join the Krebs cycle for ongoing energy production. Both processes are required for continual energy generation. Glucose is broken down into pyruvate and energy during glycolysis. The process can take place in the absence of oxygen, making it anaerobic. Insulin promotes glycolysis by raising the rate of glucose transport across the cell membrane and the rate of glycolysis by boosting the activities of hexokinase and 6-phosphofructokinase.

Nonetheless, people with COVID-19 have experienced sugar surges. The elevated blood sugar levels were new after infection for the majority of the patients, suggesting that many of them had not been diagnosed with diabetes prior to contracting the virus. According to Lo and other experts, the mechanism by which COVID-19 causes diabetes is currently being investigated. Patients with ARDS caused by COVID-19 and a high blood sugar level were in the hospital three times longer than those with normal blood sugar levels. While the exact cause of diabetes is unknown, researchers have discovered evidence that the coronavirus attacks pancreatic B-cells, which produce insulin. This does not yet address the question because patients who received COVID-19 continued to generate significant amounts of C-peptide, indicating that pancreatic cells were still generating insulin. Despite this, their blood sugar levels remained elevated, suggesting that something else was at fault. The virus-infected fat cells must be stimulating other cells in a detrimental way, resulting in diabetes. As a result, Lo and colleagues observed that individuals with COVID-19 had low amounts of adiponectin, a hormone generated by fat cells that helps other cells respond to insulin’s urge to take up sugar. COVID-19 can clearly infect fat cells. The virus may also cause replication in human fat, which provides another indication as to how fat is implicated in the virus and, as a result, diabetes. While obesity has a significant impact on the onset of diabetes as a result of the virus, this is not always the case. The miscommunication of fat cells is to blame.

How may fat cell miscommunication be controlled, and who is directly affected? This is the next question that has to be addressed in order to develop a deep understanding of the long term effects of the virus.

BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: FatCells

How CRISPR Can Help Individuals Overcome Obesity

How Diabetes Is Emerging In Patients With COVID-19

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