Energy Metabolism in Adipose Tissue


Author: Sude Sak

Adipose tissue is a type of connective tissue that plays an important role in energy metabolism. It includes adipocytes. Adipocytes, which are closely associated with small blood vessels, are found singly or in groups, often within lobules surrounded by fibrous septa. Adipose tissue contains different cell types. Only one-third of the tissue consists of adipocytes. The rest form fibroblasts, macrophages, stromal cells, monocytes, and preadipocytes.

Adipose tissue is a critical regulator of systemic energy homeostasis by acting as a calorie reservoir. Under nutrient-excess conditions, adipose tissue stores excess nutrients in the form of neutral lipids, while under nutrient-deficient conditions, it provides nutrients to other tissues through lipolysis.

It is a dynamic tissue that is involved in the synthesis and storage of lipids in order to meet the energy needs of the body, and that constantly changes in volume in terms of cell number and size. Excess energy is stored in lipid droplets in the form of triglycerides.

Triglycerides, which are the most concentrated form of metabolic energy storage in humans, store twice as much energy as carbohydrates and proteins.

Simultaneously, various stromal vascular cells in adipose tissue undergo numerical and/or functional changes, contributing to the maintenance of adipose tissue’s function as an energy store and endocrine organ.

There are three types of adipose tissue

White adipose tissue (WAT) is the predominant type of fat in the human body. WAT has several biological functions, including energy storage, prevention of heat loss, protection of vital organs, and hormone secretion. Some hormones include leptin, adiponectin, and resistin.

Beige adipocyte tissue, the third and most recent type of adipocyte, can emerge in VAT in response to thermogenic stimulation, a process known as the browning of WAT. Recent research suggests that the browning of WAT deserves more attention and that therapies that target the browning of WAT can help reduce obesity. Beige adipocytes reside within WAT and expend energy to generate heat during cold exposure (called cold-induced thermogenesis). It is well known that activated beige adipose tissue can stimulate weight loss and promote resistance to obesity, making it an attractive therapeutic target tissue. Ageing is the primary risk factor for obesity and is associated with loss of beige adipose tissue, suggesting that loss of energy expenditure capacities may contribute to an obesity-prone phenotype with increasing age.

Almost every mammal has brown adipose tissue (BAT). In newborns and hibernating mammals, brown adipose tissue is especially abundant. It is also present in adults and is metabolically active, but its prevalence decreases with age. The primary function of this gland is thermoregulation. The mitochondria of BATS cells are observed to be brown in colour due to the presence of large amounts of cytochromes. It is also called the hibernating gland because these fat stores function for the animal during its awakening from hibernation.

Energy Metabolism

The metabolism and mobilization of lipids are under the control of adipose tissue. Lipogenesis is the process through which carbohydrates are converted into fatty acids, promoting the biosynthesis of triglycerides (TG) and the expansion of lipid droplets within adipocytes. Conversely, lipolysis breaks down TG into free fatty acids (FFA) and glycerol, which can be oxidized or released.

The uptake of circulating FFAs by the liver, muscles, and other tissues constitutes a primary pathway for lipid mobilization. Both the pathways of lipogenesis and lipolysis are highly sensitive to nutritional factors and hormones such as insulin, norepinephrine, and glucagon. As a result, the intricate regulation of these processes is essential for maintaining systemic energy homeostasis and insulin sensitivity.

Lipolysis and Lipogenesis

Lipogenesis is the term used to describe the synthesis of triglycerides and fatty acids from acetyl coenzyme A. In contrast, lipolysis involves the breakdown of triglycerides, leading to the formation of fatty acids. The key distinction between these two processes lies in their fundamental nature. Specifically, lipolysis is centered around the hydrolysis of fats and various lipid molecules, resulting in the production of fatty acids. Conversely, lipogenesis entails the creation of fatty acids and triglycerides from substrates like acetyl coenzyme A and other precursors.

adipose tissue difference of lipolysis and lipogenesis

Adipose tissue serves as a crucial energy storage reservoir, housing triglycerides (TGs) that are released as fatty acids through processes called lipogenesis and lipolysis, respectively.

The systemic intake of food triggers the activation of the lipogenic pathway, encouraging TG storage in adipose tissue. Conversely, fasting initiates the lipolytic pathway, prompting the breakdown of TGs and the subsequent release of fatty acids from adipose stores. This intricate balance involves lipogenesis, a process of creating fresh fatty acids from acetyl-coenzyme A (acetyl-CoA), and TG synthesis.

The metabolism of glucose generates acetyl-CoA, a pivotal component for fatty acid synthesis. This process also boosts the expression of acetyl-CoA carboxylase, the rate-controlling enzyme in lipogenesis, and triggers the release of pancreatic insulin, further propelling lipogenesis. In essence, adipose tissue functions as an energy reservoir, effectively mitigating fatty acid fluxes and averting lipotoxicity and insulin resistance. This tissue also manages the clearance of plasma TGs, averting their accumulation in other bodily tissues.

Consequently, the adipose tissue’s lipid storage capacity plays a pivotal role in systemic insulin resistance and the infiltration of lipids into organs such as the liver and muscles. On the contrary, lipolysis entails the catabolic breakdown of stored TGs within adipocytes, liberating free fatty acids and glycerol.

Starvation triggers lipolysis, yielding glycerol for hepatic gluconeogenesis and free fatty acids for oxidation, catering to the energy requirements of other organs. When fatty acids abound and carbohydrates are scarce, the liver can further metabolize fatty acids to create ketone bodies, a process termed ketogenesis, which serves as an energy source for the brain. This dynamic interplay between lipogenesis and lipolysis is pivotal for maintaining systemic energy equilibrium and insulin sensitivity. Overall, adipose tissue’s multifaceted functions underscore its significance as an energy reservoir and regulator within the body’s energy homeostasis.”

Adipose tissue acts like an endocrine organ

White adipose tissue emerges as a pivotal endocrine organ, playing a dual role in lipid storage or release and energy equilibrium by engaging in the secretion of essential adipokines. Among these, adipocytes secrete polypeptides like leptin, resistin, and adiponectin, which orchestrate a delicate balance crucial for glucose and lipid metabolism homeostasis. The intricate interplay of these adipocytokines emanating from adipocytes fundamentally contributes to sustaining optimal energy levels.

Leptin, a key player, responds to factors such as excessive energy intake, insulin levels, and glucose levels, resulting in varying production rates. Conversely, fasting, exposure to cold, β-adrenergic agonists, and testosterone lead to decreased leptin secretion. Adiponectin, a collagen-like plasma protein synthesized within adipose tissue, plays a significant role. While its concentration is higher in subcutaneous white adipose tissue, visceral white adipose tissue and hypertrophic adipocytes are inversely correlated with circulating adiponectin levels. Weight loss and periods of hunger trigger an increase in plasma adiponectin levels, which in turn activate glucose utilization within muscles. This cascade drives enhanced fatty acid oxidation in the liver and muscles, subsequently curbing glucose production due to inhibited gluconeogenesis.

The regulation of adaptive thermogenesis

Thermogenin (uncoupling protein 1, or UCP1), a distinctive molecule inherent to cold-induced thermogenesis, assumes a crucial role as it is selectively expressed within brown adipose tissue. It orchestrates a remarkable metabolic shift by diverting oxidative phosphorylation away from ATP synthesis, and channeling the energy towards heat generation instead of ATP production.

Instances of cold exposure and heightened nutritional intake trigger a surge in brown adipose tissue activity, accompanied by elevated expression levels of norepinephrine and UCP1, which emanate from the central nervous system. Notably, a repertoire of agents, including β-adrenergic antagonists, thyroid hormones, insulin, and cAMP analogues, also contribute to the augmentation of UCP1 expression.

In response to cold and nutrient availability, sympathetic nerve activity intensifies within adipose tissue. Noradrenaline binds adeptly to β-adrenergic receptors, thereby instigating a cascade of molecular signals that culminate in the hydrolysis of triglycerides. The ensuing liberation of fatty acids plays a dual role, not only energizing UCP1 but also fueling thermogenesis in cold-induced thermogenic pathways, with glucose serving as the exclusive carbon source for degradation.

Notably, the activation extends to beige cells, further enhancing the thermogenic response. Consequently, this orchestrated mechanism precipitates a surge in whole-body energy expenditure while concurrently reducing body fat mass. In essence, the interplay of these intricate processes orchestrates a metabolic symphony that elevates energy expenditure and diminishes body fat mass.

This article has been prepared from the presentation of our student Sude Sak.


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Hormones in Control of Metabolism

hormones in control of metabolism

Author: Barış Ataseven

Metabolism is a complex process that involves various chemical reactions and pathways that occur within an organism. These reactions are essential for maintaining life and include the breakdown of food into energy, the production and storage of nutrients, and the elimination of waste products.

The regulation of metabolism is crucial for maintaining the balance between energy intake and expenditure, and hormones play a key role in this process. Hormones are signalling molecules produced by endocrine glands that regulate various physiological processes, including metabolism.


Insulin is produced by the pancreas and is responsible for regulating glucose levels in the blood. When glucose levels rise, insulin is released to facilitate the uptake of glucose by cells for energy production or storage. Insulin also promotes the storage of excess glucose as glycogen in the liver and muscle cells.


Glucagon, on the other hand, is also produced by the pancreas, but it has the opposite effect of insulin. Glucagon stimulates the breakdown of glycogen in the liver to release glucose into the bloodstream when glucose levels are low. It also promotes the breakdown of fats in adipose tissue to release fatty acids for energy production.


Cortisol is a steroid hormone produced by the adrenal glands in response to stress. It plays a crucial role in the metabolism of carbohydrates, proteins, and fats. Cortisol promotes the breakdown of proteins in muscle cells to release amino acids for gluconeogenesis, the production of glucose from non-carbohydrate sources. It also promotes the breakdown of fats in adipose tissue and the release of fatty acids for energy production.

cortisol, hormones in control of metabolism
Functions of Cortisol

Thyroid Hormones

Thyroid hormones, produced by the thyroid gland, play a critical role in the regulation of metabolism. They increase the metabolic rate by promoting the production of ATP, the energy currency of cells. Thyroid hormones also increase the activity of enzymes involved in carbohydrate, protein, and fat metabolism

Thyroid hormones affect both physiological and pathological events.


Leptin is another hormone that plays a crucial role in the regulation of metabolism. It is produced by adipose tissue and is involved in the regulation of energy balance. Leptin suppresses appetite and increases energy expenditure, promoting weight loss.


Ghrelin is a hormone produced by the stomach that stimulates appetite and promotes food intake. It also plays a role in the regulation of energy balance by promoting the release of growth hormone, which increases the breakdown of fats for energy production.


Adiponectin is a hormone produced by adipose tissue that regulates glucose and lipid metabolism. Adiponectin increases insulin sensitivity, promoting glucose uptake by cells for energy production. It also promotes the breakdown of fats in adipose tissue and the utilization of fatty acids for energy production.

In conclusion, hormones play a crucial role in the control of metabolism. Insulin and glucagon regulate glucose levels in the blood, while cortisol promotes the breakdown of proteins and fats for energy production.

Thyroid hormones increase the metabolic rate by promoting the production of ATP.

Leptin and ghrelin regulate appetite and energy balance, while adiponectin regulates glucose and lipid metabolism.

The proper regulation of hormones is essential for maintaining metabolic balance and overall health.

This article has been prepared from the presentation of our student Barış Ataseven.



Oxidative stress and the effect on different organs

Author: Aline Donker

Oxidative stress is a process that occurs due to an imbalance between reactive oxygen species (ROS) or free radicals and antioxidants in the body. ROS are molecules formed as a by-product of cellular metabolism.

Several molecules take part in the process of oxidative stress, such as superoxide anion (O2), hydrogen peroxide (H2O2), and hydroxyl radical (•OH). As well as antioxidants like glutathione, vitamin C and E. They can cause damage to cellular components like proteins, lipids, and DNA. This can result in a variety of diseases.

Figure 1: The balance during homeostasis and the imbalance during oxidative stress.

Oxidative stress can occur in many organs, such as the liver, lungs, pancreas, intestines, and even in the eyes.

The liver plays a critical role in detoxification and metabolism, which can generate reactive oxygen species (ROS) as by-products. Excessive ROS production in the liver can result in oxidative stress and damage to liver cells. The liver produces antioxidant enzymes and molecules that can neutralize ROS. But if the liver’s antioxidant defences get overstimulated, it can lead to the accumulation of ROS which results in oxidative stress in other organs.

To counteract oxidative stress, the liver relies on antioxidant molecules such as glutathione and vitamins C and E, to neutralize ROS and prevent damage to cellular components.
Some diseases related to oxidative stress in the liver are viral hepatitis, non-alcoholic fatty liver disease and liver fibrosis.

oxidative stress in liver

Figure 2: Factors causing oxidative stress in the liver and conditions occurring as a result of oxidative stress

The lungs are highly susceptible to oxidative stress due to their constant exposure to environmental toxins and pollutants. Oxidative stress in the lungs can lead to inflammation and damage to the lung tissue.

Pancreatic beta cells are very susceptible to oxidative stress because of their high production of reactive oxygen species and their low capacity for antioxidants.
ROS can damage pancreatic beta cells. This impairs the secretion of insulin and glucose metabolism. Oxidative stress can also promote inflammation and pancreatic fibrosis, which can contribute to the development of cancer.
The pancreas plays a role in the regulation of the blood sugar level by producing insulin. Dysfunction of the pancreas can lead to insulin resistance and diabetes. This can impact other organs like the kidneys, eyes and cardiovascular system.

The eyes are also vulnerable to oxidative stress. This can lead to multiple diseases like cataracts, dry eyes and glaucoma. Reactive oxygen species are able to damage the lens and retina, which results in impaired vision and the increased risk of blindness. They can also damage the proteins in the lens of the eye. As an individual ages, this damage accumulates, which contributes to the development of cataract.

oxidative stress in eye diseases

Figure 3: Diseases related to oxidative stress in the eyes.

Oxidative stress can also occur in the intestines. Here it can cause alteration in the microbiotics and dysfunction of the intestinal barrier. Oxidative stress can cause dysbiosis in the intestines. As a result of this, the proliferation of harmful bacteria can occur. There is a decrease in beneficial bacteria, which can further contribute to oxidative stress and inflammation in the intestines. Oxidative stress can also damage the intestinal barrier, which prevents harmful substances from entering the bloodstream. As a result of this, intestinal permeability can increase. This leads to the leakage of toxins, bacteria and other harmful substances into the bloodstream.

This article has been prepared from the presentation of our student Aline Donker.


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Metabolism of Amino Acids in Muscle Tissue

Author: Tala Abdallah

Amino acid metabolism is the collective term for the metabolic processes that produce, break down, and use amino acids. The amino groups and ammonia that are provided by the six amino acids are necessary for the synthesis of glutamine and alanine, which muscles release in enormous amounts.

The 6 amino acids metabolized in resting muscle are Leucine, Isoleucine, Valine, Asparagine, Aspartate, and Glutamate. In addition to playing other vital roles in human metabolism, glutamine generated by muscles is an important source of energy and regulates the synthesis of DNA and RNA in the immune system and mucosal cells. Furthermore, protein synthesis and degradation are both required for the organism to maintain balance. Moreover, Acetyl-CoA can only be made by converting leucine and a portion of the isoleucine molecule, and the TCA-cycle intermediates and glutamine are synthesized using the carbon skeleton of the other amino acids.

The breakdown of amino acid carbon skeletons results in the creation of six metabolites: acetyl-CoA, acetoacetyl-CoA, pyruvate, α-ketoglutarate, fumarate, and oxaloacetate and each has a different fate in the energy metabolism. Amino acids are categorized as either ketogenic or glucogenic based on what happens to their breakdown products. Therefore Acetyl-CoA and acetoacetyl-CoA are produced by the ketogenic amino acids leucine and lysine. Many amino acids operate as direct energy-producing substrates and regulate the activity of several enzymes involved in the metabolism of glucose. Both isolated animal and human myocardium exhibit improved contractile performance as a result.

amino acids
The many different ways and outcomes of Amino Acid Metabolism in Muscles.

Branched-chain amino acids (BCAAs) are the primary amino acid source for skeletal muscle anabolism and are crucial for maintaining energy balance. Skeletal muscle oxidizes the bulk of the body’s BCAAs, followed by brown adipose tissue, the liver, kidneys, the heart, and other tissues. Skeletal muscle participates disproportionately in BCAA catabolism due to the fact that BCAA transamination, the initial stage of the process, occurs predominantly there.

The amino acid alanine is necessary for the synthesis of proteins and it provides the central nervous system and muscles with energy. The liver uses alanine, which is secreted from skeletal muscle, as a substrate for gluconeogenesis, then the amino group of alanine is changed into urea by the urea cycle, which is then eliminated. The alanine-derived glucose produced in the liver may subsequently be able to re-enter the skeletal muscle and serve as an energy source.

Glucose – Alanine cycle and the pathways between muscle and liver.

Transamination, a chemical process in which an amino group is added to a keto acid to create new amino acids, is a crucial step in the metabolism of amino acids. The bulk of amino acids undergoes transamination during degradation. Transaminases are specific examples of enzymes that are frequently discovered as markers of potential injury to the liver cells, such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST).

Aspartate transferase (AST), an essential enzyme in amino acid metabolism, is found in the liver, heart, pancreas, muscles, and other biological tissues. AST catalyzes a reaction between the amino acids aspartate and glutamate.

An enzyme called aspartate transaminase is released when your muscles or liver are injured and the main sources of AST are liver tissues, myocardium, and striated muscle. Like with all transaminases, aspartate transaminase recognizes two amino acids (Asp and Glu) with different side chains and is able to discriminate between them and bind them.

The quick oxidation of the branched-chain amino acids appears to be connected to the synthesis of alanine in muscle. Alanine is transformed into pyruvate by ALT primarily for cellular energy production moreover the enzyme ALT, which is regarded to be most closely related to the liver, is produced by the kidneys, skeletal muscle, and cardiac muscle. The intermediate metabolism of glucose and protein depends on the enzyme glutamate pyruvate transaminase, often known as alanine aminotransferase (ALT). In order to create pyruvate and glutamate, it catalyzes the reversible transamination of alanine and 2-oxoglutarate.

Leucine, alanine, and proline, three amino acids in particular, suggest they can enhance muscle repair, boost endurance, and grow muscle mass more effectively when paired with other amino acids, carbohydrates, or whey protein. Because glutamine fuels multiple cells throughout the body, it is the best recovery ingredient for all types of exercise. These acids, which are the building blocks of protein, have been demonstrated to help muscle recovery. Beyond protein, glutamine and BCAAs are two of the most important nutrients for athletes to recover and develop muscle, although BCAAs support muscle growth and prevent tiredness glutamine aids in muscle healing and rebuilding after exercise.

Process of Rhabdomyolysis in muscle then kidney.

For those with muscular dystrophy, defective genes hinder the body from producing the proteins required for proper muscle growth. A serious medical condition called rhabdomyolysis can be fatal or result in permanent disability. Rhabdo arises when muscle tissue is damaged because the electrolytes and proteins are discharged into the bloodstream, for instance, Myoglobin is a protein that is secreted into the bloodstream and then removed from the body by the kidneys which then produces dark-coloured urine.

This article has been prepared from the presentation of our student Tala Abdallah.


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emDocs Cases: Evidence-Based Recommendations for Rhabdomyolysis

Ancient Cheesemaking and Diversified Dairy Herd in Late Neolithic Poland: New Evidence Uncovered by Archaeologists

In a recent study, evidence has been found for cheesemaking using milk from multiple animals during the Late Neolithic period in Poland. This research suggests that early farmers reduced the lactose content in milk by making it into cheese or other dairy products, such as yogurt, and utilized dairy products from several different animals, including cows, sheep, and goats.

During the Neolithic period until the Late Bronze Age, almost everyone in Europe had lactose intolerance. However, genetic mutations became widespread, enabling adults to produce lactase, the enzyme that breaks down lactose in the body. The researchers investigated dairy processing during the Late Neolithic period by identifying high curd-content residues in pottery, indicating cheesemaking, and revealing that multiple dairy species were utilized. By using a multi-stranded proteomic and lipid-analysis approach, the scientists and archaeologists from the Universities of York, Cambridge, Toruń, and Kraków investigated ceramics and deposits on their surface from the site of Sławęcinek in central Poland.

This new development provides evidence that cheesemaking (and other curd-enriching dairy processing) can be directly detected by scrutinizing the proportion of curd proteins, by comparing proteomic data. These results are the first of their kind in Europe and contribute significantly to our understanding of the use of dairy products by some of the earliest farmers in Central Europe.

While previous research has shown that dairy products were widely available in some European regions during this period, the present study provides clear evidence for a diversified dairy herd, including cattle, sheep, and goats, from the analysis of ceramics.

Despite widespread lactose intolerance during the Neolithic period, there is evidence of dairy being consumed, such as animal bones with kill patterns expected for dairy herds, dairy lipids in ceramic vessels, and dairy proteins in ancient dental calculus or plaque.

Lead author Miranda Evans, a Ph.D. student at Cambridge’s Department of Archaeology, said that the proteomic results showed that the ancient residues closely resembled both the modern cheesemaking residues and cheese itself and not whole milk. This reveals that the people of Sławęcinek practiced cheesemaking or another form of curd-enriching dairy processing.

Evidence of multiple species used for cheesemaking was backed up by the presence of both cow and sheep or goat bones on the site.

Dr. Harry Robson from the Department of Archaeology at the University of York said that these results contribute significantly to our understanding of the use of dairy products by some of the earliest farmers of Central Europe. Furthermore, Dr. Jasmine Lundy from the Department of Archaeology highlighted how complementary lipid and proteomic analyses are, particularly in understanding the use of the ceramic vessel over time. From this, for example, we could see that some techniques waterproof or seal the ceramics, and we could also determine what foods were being produced in them.

Overall, this study provides significant insights into the use of dairy products during the Late Neolithic period in Central Europe and how cheesemaking was practiced using milk from multiple animals. The use of proteomic and lipid-analysis approaches is an innovative and informative method for analyzing ancient residues, and the findings offer valuable contributions to our understanding of the development of food production and consumption in the Neolithic period.

Reference: Evans M, Lundy J, Lucquin A, Hagan R, Kowalski Ł, Wilczyńki J, Bickle P, Adamczak K, Craig OE, Robson HK, Hendy J. Detection of dairy products from multiple taxa in Late Neolithic pottery from Poland: an integrated biomolecular approach. Royal Society Open Science, 2023; 10 (3) DOI: 10.1098/rsos.230124

The world’s oldest cat, Flossie, is 27 years old.

27-year-old ‘Flossie’ crowned world’s oldest living cat

Described as an affectionate and playful cat, Flossie was born on the streets of England in 1995. Flossie took its place in the Guinness Book of Records as the longest-living cat and became immortal. Flossie’s record was confirmed at 26 years 316 days on November 10.

Born and later adopted in a cat colony in Merseyside, England, Flossie lives in Orpington, London, with her current owner, Vicki Green.

“I knew all along that Flossie was a special cat, but I didn’t think I would share my home with a Guinness World Record holder,” says Green, Flossie’s owner. “She’s so loving and playful, especially sweet when you remember how old she is. She is deaf and has poor eyesight, but none of that seems to bother her.” she continues.


Flossie is currently the oldest confirmed cat inside and is at least 120 years old to human age.

Happy new year Flossie…

Source: Guinness World Records

Does Toxoplasma turn immune cells into zombies?

toxoplasma gondii

Toxoplasma, an intracellular parasitic protozoan, is carried globally by a considerable proportion of the human population. So how does Toxoplasma spread within the body or how does it reach the brain?

Studies on how Toxoplasma protozoa spread within the body are continuing. One of them was recently published in the journal Cell Host & Microbe (IF=31.316, JCR Ranking Q1). Researchers shared the question and answer in the title of the article with the scientific world.

Ten Hoeve AL, Braun L, Rodriguez ME, Olivera GC, Bougdour A, Belmudes L, Couté Y, Saeij JPJ, Hakimi MA, Barragan A. The Toxoplasma effector GRA28 promotes parasite dissemination by inducing dendritic cell-like migratory properties in infected macrophages. Cell Host Microbe. 2022 Nov 9;30(11):1570-1588.e7. doi: 10.1016/j.chom.2022.10.001.

It is known that the roles of immune cells in the fight against infections are tightly regulated. It is important to illuminate how Toxoplasma has managed to infect so many human and animal species and spread so efficiently. At this point, Ten Hoeve and his team stated that they had found an answer. The key element of this response was the discovery of a protein. Researchers have identified a protein (GRA28) that Toxoplasma uses to reprogram the immune system.

The study findings indicated that Toxoplasma injects this particular protein into the nucleus of the immune cell, thereby changing the cell’s identity. Thus, it was shown that Toxoplasma tricked the immune cell into being another type of cell, in other words, it changed the gene expression and behavior of the immune cell. This situation was described by researchers as “Toxoplasma transforming immune cells into Trojan horses or wandering zombies that spread the parasite”. The study also highlighted that the parasite is much more targeted in its spread than previously thought.

Briefly about Toxoplasmosis (Toxoplasmosis)

The disease caused by toxoplasma is defined as toxoplasmosis and is one of the most common parasitic infections in humans worldwide, perhaps the most common. WHO estimates that at least 30% of the world’s human population are carriers of the parasite.

Domestic cats (not just domestic cats, but all felines) occupy a special place in the life cycle of Toxoplasma: sexual reproduction takes place only in the cat’s gut. Reproduction in other hosts, for example, humans, dogs, or birds, takes place by parasite division. At this point, the one health concept to fight the disease is important. Therefore, veterinarians play an important role in the detection, prevention, and treatment processes of both infected cats and cats in the final host role. This directly affects human health.

Toxoplasma (Toxoplasma gondii) infection is common in cats, but the clinical picture is rare. Up to 50% of cats, especially free-range ones, have antibodies that indicate infection and the presence of cystic stages. Clinical signs usually occur when cats are immunocompromised – in these cases, the cystic stages can be reactivated. Commonly affected organs are the central nervous system, muscles, lungs, and eyes. When cats shed oocysts, they can pose a risk to humans. However, this only happens once in their lifetime, usually for three to ten days after tissue cysts have been ingested.

Toxoplasma is transmitted to humans through food and contact with cats. In nature, the parasite spreads preferentially from rodents to cats, rodents, and the like. The parasites are “dormant” in the rodent’s brain, and when the cat eats the mouse, they multiply in the cat’s gut and are expelled through the feces. The parasite terminates in the vegetation and becomes infected when the rodent eats the vegetation. It is transmitted to humans through the consumption of meat or contact with cats, especially cat feces.

The disease caused by toxoplasmosis is defined as toxoplasmosis. When a person is first infected, they show symptoms similar to a cold or flu. After the initial infection stage, the parasite enters the “sleeping” stage in the brain and begins a chronic, silent infection that can last for decades or a lifetime. Chronic infection usually does not cause symptoms in healthy individuals. However, toxoplasma can cause a life-threatening brain infection (encephalitis) in people with compromised immune systems (HIV, transplant recipients, post-chemotherapy) and can be dangerous to the fetus during pregnancy. Eye infections can occur in healthy individuals.