How liver responds to food

Minutes after eating, as nutrients rush into the bloodstream the body makes massive shifts in how it breaks down and stores fats and sugars. Within half an hour, the liver has made a complete switch  from burning fat for energy to storing as much glucose, or sugar, as possible. It's too short a time span for the liver's cells to activate genes and produce the RNA blueprints needed to assemble new proteins to guide metabolism.

Liver cells store up pre-RNA molecules involved in glucose and fat metabolism. ''The switch from fasting to feeding is a very quick switch and human physiology has to adapt to it in the right time frame," says Satchidananda Panda, a professor in the Salk Institute's Regulatory Biology Laboratory. It was known that a RNA-binding protein called NONO was implicated in regulating daily ("circadian") rhythms in the body.

Researchers analyzed levels of NONO in response to feeding and fasting in mice. After the animals ate, speckled clumps of NONO suddenly appeared in their liver cells, newly attached to RNA molecules. Within half an hour, the levels of corresponding proteins-those encoded by the NONO-bound RNA increased.

After mice eat, it looks as if NONO brings all these RNAs together and processes them so they can be used to make proteins. When mice lacked NONO, it took more than three hours for levels of the same proteins involved in processing glucose to increase. During that time lag, blood glucose levels shot up to unhealthy levels.

Since blood glucose levels are also heightened in diabetes, the researchers think that the mice without NONO may act as a model to study some forms of the disease. NONO has been found at high levels in the brain and muscle cells.
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How to live longer

Many cells in human body, such as those which make up brain need to last a lifetime. To do this human cells have developed ways of protecting themselves. One way is through a process called autophagy, which literally means self-eating, where damaged components are collected together and removed from the cell.This is very important as accumulation of damage in cells has been linked to several diseases including dementia.

Lead author, Dr Viktor Korolchuk explains: "As we age, we accumulate damage in our cells and so it is thought that activating autophagy could help us treat older people suffering from dementia. In order to be able to do this we need to understand how we can induce this cell cleaning." In this study the authors were able to identify how a protein called p62 is activated to induce autophagy. They found that p62 can be activated by reactive oxygen species (ROS). ROS are by-products of our metabolism that can cause damage in the cell.

This ability of p62 to sense ROS allows the cell to remove the damage and to survive this stress. In lower organisms, such as fruit flies, p62 is not able to do this. The team identified the part of the human p62 protein which allows it to sense ROS and created genetically modified fruit flies with 'humanised' p62. These 'humanised' flies survived longer in conditions of stress. Abilities like sensing stress and activating protective processes like autophagy may have evolved to allow better stress resistance and a longer lifespan.

Specific mutations in human p62, which cause a neurodegenerative disease called amyotrophic lateral sclerosis (ALS), can prevent activation of p62 by ROS. These cells are then unable to induce protective autophagy, and the authors explain that this could underlie the premature death of neurons in patients with this devastating age-related disease. In contrast, 'humanised' p62 fruit flies did not live longer suggesting that other mechanisms may be required. The research demonstrates that a collection of small adaptations like that of human p62 could have accumulated over time and these adaptations could underlie our increased natural defences and longer lifespans. The discovery of these adaptations allows a better understanding of how to treat age-related diseases.
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Secret of longevity protein

Klotho proteins play an important role in the regulation of longevity and metabolism. In a recent Yale-led study, researchers revealed the three-dimensional structure of one of these proteins, beta-Klotho, illuminating its intricate mechanism and therapeutic potential. The study findings could have implications for therapies developed to treat a wide range of medical conditions, including diabetes, obesity, and certain cancers, the researchers said.

The Klotho family of two receptor proteins are located on the surface of cells of specific tissues. The proteins bind to a family of hormones, designated endocrine FGFs, that regulate critical metabolic processes in the liver, kidneys, and brain, among other organs. To understand how beta-Klotho works, the research team used X-ray crystallography, a technique that provides high-resolution, three-dimensional views of these proteins.

The researchers' analysis yielded several insights. First, beta-Klotho is the primary receptor that binds to FGF21, a key hormone produced upon starvation. When bound to beta-Klotho, FGF21 stimulates insulin sensitivity and glucose metabolism, causing weight loss. This new understanding of beta-Klotho and FGF21 can guide the development of therapies for conditions such as type 2 diabetes in obese patients.

Like insulin, FGF21 stimulates metabolism including glucose uptake. In animals and in some clinical trials of FGF21, it shows that you can increase burning of calories without changing food intake, and we now understand how to improve the biological activity of FGF21.
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Winter work out is better than summer sweat

According to personal trainers and exercise physiologists, the body's primary goal is to maintain stasis, or stability, and that includes keeping a steady temperature. In the cold, the body needs to burn extra fat, to produce energy to heat it back up to the ideal temperature.

Working out in the cold weather can shake off some extra calories. During the winter, the body ramps up its production of a chemical called ATLPL, which helps it to store up fat for the evolutionary scarce season, so staying active in the winter is important to counteracting that.

Working out in the cold makes it difficult for the body to stay warm and burn a ton of calories, the cold acts as a 'thermal stressor,' forcing the body's temperature regulation out of work. To keep the core, vital organs at the right temperature, blood flow to the extremities is reduced, and kept concentrated closer to the heart and internal organs.

The heart rate and metabolism slow, trying to save up energy and keep the warm blood in place. That's when the shivering starts. Those shakes are a series of fast muscle contractions and releases, a way for the body to produce some extra warmth by burning energy stored in fat.

When you get into a relatively consistent, high intensity workout - though you'll feel like you're working harder at first, against your slower heart rate and metabolism - the body begins warming up from more robust fat burning. As your heart rate rises, blood and warmth return to your hands, feet and other extremities, and shivering is no longer necessary.

Once you hit that point, you're burning calories as you would during exercise at any temperature. During the winter, the body crave extra simple carbohydrates found in sugary foods like baked goods and get vitamin D deficient spending too much time indoors. Getting some winter sun will boost your vitamin D to break those sweet indulgences.

Walking in moderately warm clothing on a cold day will keep the heart rate from getting high enough to cancel out the shivers, but enough activity is require for burning some fat for energy. Body temperature will be  lower when you are closer to the cold while playing in the snow, making the body ready to fight to stay warm.
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Cancer alters the circadian clock to survive

Tumor cells use the unfolded protein response to alter circadian rhythm, which contributes to more tumor growth, Hollings Cancer Center researchers at the Medical University of South Carolina (MUSC) find. A key part of the circadian clock opposes this process. For tumors to grow and spread, cancer cells must make larger than normal amounts of nucleic acids and protein, so they can replicate themselves. Yet in both normal and cancer cells that increase their synthesis of protein, a small percent of those proteins do not fold properly.

When that happens, the cell activates its unfolded protein response (UPR), which slows down the making of new proteins while the misfolded proteins are refolded. Eventually, the buildup of misfolded proteins becomes toxic and leads to cell death. However, cancer cells have learned to use the UPR to slow protein synthesis when needed, in order to handle the backlog of misfolded proteins. This helps them survive in conditions that would kill normal cells.

This pattern of adaptation is often seen in tumor cells. UPR and circadian rhythm are linked together to lead the clockwork of the cell and also that cancer cells use the UPR to manipulate the circadian clock in ways that allow them to survive conditions that are toxic to normal cells. Researchers formulated a new idea based on what was known about protein synthesis in the cell. The UPR is altered in tumors, and second, cells establish a circadian rhythm to regulate metabolism by producing levels of certain proteins that rise and fall in coordination with natural cycles of light and dark.

 Scientists had observed that circadian rhythm is altered in tumor cells. Since protein production is tied to circadian rhythm. Research team used chemicals to activate the UPR in osteosarcoma cells. They found that, when activated, the UPR changes levels of an important protein called Bmal1, which is a transcription factor that rises and falls with cycles of light and dark. As it does, it regulates the expression of major circadian rhythm genes.

When cells were exposed to cycles of light and dark, Bmal1 levels peaked during dark hours. But when the UPR was chemically activated, Bmal1 stayed low during both light and dark phases, which caused a phase shift in the expression of circadian genes. When one of the main parts of the UPR machinery was absent in cells, the phase shift did not happen.

Levels of the circadian protein Bmal1 continued to decrease, as the UPR was increasingly activated. In rodents that had their light-dark cycles suddenly reversed, Bmal1 stopped rising and falling - a clear sign that their circadian rhythms were disrupted. Shifts in light exposure activated the UPR in those rodents' cells.

 The team found that patients with breast, gastric or lung cancers survived longer when they had higher levels of Bmal1 protein. In myc-driven cancers, the UPR was causing the loss of Bmal1 protein, which caused the tumors to grow. Myc-driven tumors lost circadian rhythm, whereas normal cells maintained it. Conversely, high levels of Bmal1 overtook the UPR, thereby allowing protein synthesis to continue, which was toxic to tumor cells . In this way, Bmal1 directly encourages protein synthesis.

Human cancer suppresses circadian rhythm by controlling protein synthesis through Bmal1. Cancer cells survived longer by using the UPR to suppress Bmal1 and short-circuit their circadian rhythms. These results are important for human biology. Every single normal cell in human body has circadian oscillation, resetting the circadian rhythms in cancer cells slows down their proliferation.
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Using mouthwash increases the risk of obesity and diabetes

Using mouthwash twice a day significantly raises the risk of obesity and developing type 2 diabetes, according to a new study. Swilling with the anti-bacterial fluid could be killing beneficial microbes which live in the mouth and protect against the conditions. People who used the product twice a day were around 55 percent more likely to develop diabetes or dangerous blood sugar spikes.

Popular mouthwash solutions include ingredients that kill good and bad bacterial. Most of these antibacterial ingredients in mouthwash are not selective- they do not target specific oral bacteria-instead, these ingredients can act on a broad range of bacteria.
Researchers looked at overweight people who were at risk of developing diabetes. Over the study period, around 17 per cent developed diabetes or pre-diabetes, but that rose to 20 per cent for those using mouthwash once a day, and 30 per cent for those using it in the morning and evening.

Helpful bacteria in the mouth can protect against obesity and diabetes, as it helps the body produce nitric oxide. This important molecule helps trillions of our cells to communicate with each other by transmitting signals throughout the entire body and regulates insulin levels and our metabolism. Commonly-used mouthwashes typically contain powerful bacteria-killing formulas including cetylpyridinium chloride, chlorhexidine, triclosan, alcohol, fluoride, peroxide and essential oils. However, the researchers warn killing off good helpful bacteria also makes room for harmful bacteria to thrive.
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Eggs can select semen

According to the latest research, female's eggs are able to select sperm with the best genes to ensure the healthiest offspring. Semen does not appear to have the same ability to detect bad genes, this shows that fertilisation is not random and specific pairings between certain eggs and sperm are more common than others. Researchers bred female mice carrying one normal and one mutant copy of a gene that increased the chance of getting testicular cancer.

 The resulting offspring followed Mendel's rules and there was a random dispersal of the mutated form among offspring. Researchers reversed the breeding- gave males the mutant copy of the cancer gene while the females had the normal version. Only 27 per cent of the offspring had the mutant variant, compared to the 75 per cent. Researchers found no evidence the mutated mice embryos were dying shortly after fertilisation, rather they were never fertilised.

The rate of metabolism folic acid - which is an important signalling molecule - is different in sperm and eggs. Research has revealed that these molecules play an important role in fertilisation. Changes in these signals may impact how much sperm and egg are attracted to one another. When sperm from multiple males arrive at an egg concurrently, eggs are able to choose the sperm whose recognition proteins are best suited for healthy fertilization. This selection process can spur the evolution of new recognition proteins, eventually resulting in reproductive isolation and, in some cases, the creation of new species altogether.
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How protein breakdown causes leukemias and brain cancer

An enzyme that is responsible for the breakdown of specific amino acids in food plays a key role in the development of leukemias and brain cancer. The researchers have discovered a surprising link between energy metabolism and the epigenetic code. These labels in the DNA of cancer stem cells determine the activity of genes and many cellular functions.

Acute myeloid leukemia AML is an aggressive type of blood cancer that often relapses in the wake of successful initial treatment. Stem cells that are resistant to therapy are believed to be responsible. Reseachers examined patient samples by comparing the composition of proteins of AML stem cells and leukemia cells without stem cells properties.

The investigators found suspiciously high levels of an enzyme called BCAT1 in the stem cells. These levels rose even higher during a cancer recurrence. The researchers considered this to be a clue that BCAT1 might be linked to therapy resistance. Cancer researchers have suspected for some time that the BCAT1 enzyme, which is responsible for the breakdown of specific proteins in food, plays a role in the development of malignant tumors.

 They discovered that an overproduction of BCAT1 increases the aggressiveness of malignant brain tumors and breast cancer. BCAT1 reduces the levels of this key molecule and this leads to increased levels of chemical labels in the DNA. The tiny methyl groups that are attached to DNA determine whether particular genes are active or silent and, thus, have an immense impact on all cellular functions.

They increase cancer-promoting methylation of DNA. AML is known for an extremely heterogeneous pattern of genetic alterations. However, misregulated methylation with its drastic consequences for the whole cell appears to be a common characteristic of this malignant disease.

The finding that BCAT1 drives cancer-promoting methylation in AML stem cells and other cancer stem cells opens up new options for therapy. A blockade of the enzyme using a targeted agent might normalize DNA methylation and thereby reduce cancer spread and therapy resistance.
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How bones affect appetite and metabolism

Human skeleton is more than the structure supporting the muscles and other tissues, it produces osteocalcin hormone. The hormone affects how we metabolize sugar and fat. It increases insulin production which reduces blood glucose levels, it can also protects us from obesity by increasing the use of energy.

Changes in blood concentrations of osteocalcin may stave off the development of diabetes. Osteocalcin is produced by osteoblasts, the cells responsible for making human bones. The hormone builds up in bone, and then, through a series of chemical reactions, is released into the blood.

Inactive osteocalcin has one more piece than active osteocalcin. The researchers examined in mice the different enzymes present in cells where osteocalcin was produced. Furin causes osteocalcin to become active and the hormone is then released into the blood.

When there was no furin in bone cells, inactive osteocalcin built up and was still released, but this led to an increase in blood glucose levels and a reduction in energy expenditure and insulin production. The absence of furin reduced the mice's appetite, osteocalcin has no effect on appetite, the existence of a new bone hormone that controls food intake.
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How obesity causes breast cancer

Obesity leads to the release of cytokines into the bloodstream which impact the metabolism of breast cancer cells, making them aggressive to treatment.
Severe overweight can lead to various health impairments. Besides inducing cardiovascular diseases, obesity for example also promotes the development of cancer and metastases.

ACC1 acetyl-CoA-carboxylase 1, a central component of fatty acid synthesis. ACC1 mediates the chemical addition of carbon dioxide to acetyl-CoA, which results in malonyl-CoA. This reaction is the first and speed determining step in the fatty acid synthesis of all living organisms.

ACC1 enzymes is a key component of fatty acid synthesis, its function is impaired by the cytokines leptin and TGF-β. The levels of these cytokines are increased particularly in the blood of severely overweight people.

Fatty acid precursors promote metastasis. The inhibition of ACC1 leads to the accumulation of the fatty acid precursor acetyl-CoA. This precursor is transferred to certain gene switches that in turn increase the metastatic capacity of cancer cells by activating a specific gene program.

Scientists used human tissue from breast cancer metastases to show that ACC1 was less active. When the scientists blocked the unknown signaling pathway with an antibody directed against the leptin receptor, this led to a significantly reduced metastatic spread of breast cancer tumors in an experimental model.
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Dangers of disrupting body clock

Body clock regulates day and night cycle that guides sleep and eating patterns and hormones. Nature can have serious consequences ranging from impulsive behaviour to life-threatening conditions such as obesity and cancer if the body clock is disrupted.

Human body can not adapt to operating outside the normal cycle of working by day, and sleeping at night. Shift workers' biological clocks are set by the rising and setting of the sun. There is no drug for speed up or slow down of body clock.

When workers force themselves to stay awake, it triggers the release of stress hormones such as cortisol- the hormone release into the blood in a life-or-death situation. Cortisol works to suppress the immune system and in the long run increases the risk of illnesses.

Working when you are supposed to sleep also opens you up to eating outside of normal times, when the body's metabolism might be lower and the calories are more likely to be converted into fat instead of being burnt up.

Short time disruptions of the circadian clock can wreak havoc within the body-raising heart rate, raising blood pressure and insulin levels. Circadian dysfunction has been linked to depression, bipolar disorder, cognitive function, memory formation and some neurological diseases.

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Immune cells hinder metabolism in adult

Older people do not burn the energy stored in fat cells as efficiently as younger people, this leads to the accumulation of harmful belly fat. The underlying cause for this unresponsiveness in fat cells was unknown.

Researchers discovered a new type of macrophage that resides on the nerves in belly fat. These nerve-associated macrophages become inflamed with age and do not allow the neurotransmitters, which are chemical messengers, to function properly.
The researchers also isolated the immune cells from fat tissue of young and old mice, and then sequenced the genome to understand the problem.

They discovered that the aged macrophages can break down the neurotransmitters called catecholamines, and thus do not allow fat cells to supply the fuel when needed. Lowering a specific receptor that controls inflammation, the NLRP3 inflammasome, in aged macrophages, the catecholamines could act to induce fat breakdown, similar to that of young mice.

Researchers blocked an enzyme that is increased in aged macrophages, restoring normal fat metabolism in older mice, monoamine oxidase and MAOA, is prevented by existing drugs in the treatment of depression. When immune cell interact with nerves and fat cells to reduce belly fat, this enhance metabolism, improve performance and belly fat loss in older people.
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The use of metabolism to subtype hepatoblastoma tumors

Hepatoblastoma is a rare pediatric liver cancer, usually diagnosed in the first three years of life. There are many subtypes of hepatoblastoma, the two major ones are fetal and embryonal.
Scientists have identified new biomarkers that could accurately classify the two main subtypes of hepatoblastoma, a children liver cancer.

Different types of hepatoblastoma use different nutrients to grow. Some use glucose or fatty acids. The genetics of hepatoblastoma involves frequent mutations in the gene CTNNB1. This gene produces the protein beta-catenin, which is involved in cell-cell adhesion and gene transcription. Because of its dual function, mutations of the CTNNB1 gene can cause hepatoblastoma cancer.

Beta-catenin is a component of a signaling pathway known as Wnt/beta-catenin, which is responsible for regulating the expression of multiple genes. Many components of the Wnt/beta-catenin pathway are affected and overactive in various tumors.

Researchers examined the relationship between the CTNNB1 gene and the cell's metabolism, they discovered that beta-catenin, as part of the Wnt signaling pathway directly regulates the expression of a gene that produces a glucose transporter protein. GLUT3

They used RNA sequencing to identify molecular and metabolic features that are specific to hepatoblastoma. This approach revealed that several enzymes involved in the metabolism of glucose are overexpressed in embryonal hepatoblastoma cells as compared to fetal hepatoblastoma cells.

Embryonal hepatoblastoma cells show high levels of glucose uptake, they also discovered that these cells are very sensitive to the perturbation of an enzyme involved in the cell's use of glucose. They immunohistochemistry of the three metabolic biomarkers to distinguish embryonal from fetal components out of a large panel of human hepatoblastoma biopsies.

The study shows that the Wnt/beta-catenin pathway is important for reprograming the energy management of tumor cells. It also provides a new
metabolic classification of human hepatoblastoma that can help oncologists develop novel diagnostic methods and treatments.
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Third-hand smoke exposure affects liver and kidney

Third-hand smoke exposure can damage brain, liver, increase the risk of neurodegenerative diseases, and destroy metabolism. The research team analyzed how people were affected by inhaling smoke from smoker's clothes, hair, home, or car.

Being a third-hand smoker for one month can cause type 2 diabetes, hyperactivity, liver and lung damage, and wound-healing complications.
Exposure for two months resulted in further molecular damage, and at four to six months caused more damage, long-term exposure can leads to insulin resistance.

Researchers discovered that stress hormones, such as epinephrine, increased in one month of exposure.
Additional stress hormones are seen at two months, four months, and six months, eventually leading to immune fatigue.

Contaminants can be absorbed through the skin and through breathing. Exposure to tobacco smoke deposited on surfaces in homes and dust is a new form of toxicity. Noxious chemicals in tobacco smoke once deposited change in chemistry to become even more toxic and carcinogenic.
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Premature babies get metabolic boost from breast milk

Researchers compared the breast milk of mothers with babies born between 28, 37, 38 and after 38 weeks, they examined whether there were differences in the composition of the breast milks' microRNAs, snippets of RNA that affect gene expression and can be passed to the infant.

They discovered that there are differences in these microRNA profiles, and that the majority of the altered microRNAs influence metabolism, giving the microRNAs to babies could potentially impact how the newborn processes energy and nutrients.

Prematurely babies are at risk of different problems like failure to thrive and neurodevelopmental delays. They also tend to be born at a lower weight than term infants, premature babies have different nutritional needs than babies born at term.

The breast milk of mothers with premature babies has different amounts of microRNA than that of mothers with babies born at term, this improves growth and development in premature babies. Presently, there is no infant formula that have the special variations in microRNA profile for premature babies, breast milk is recommended for them because of their special needs.
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Low fat intake can cause untimely death

Low-fat diets could increase the risk of an early death, fats have protective effect on human health, people with the lowest fat intake may die young.

Human body needs fat; it carries vitamins and provides essential acids.
Low levels of fat in the body will affect important vitamins and minerals in the body.

Eating excess fat is not healthy, low fat intake is malnutrition, moderation is the key when you are eating fatty foods. Replacing fat with other food is not good for proper body metabolism.

Limiting total fat consumption may have adverse effects on health, high carbohydrate intake increases the risk of mortality while higher intake of fats, including saturated fats, are associated with lower risk of mortality.

Low fat diets increased the risk of cardiovascular disease, moderate consumption of healthy fatty foods would be a healthy choice for longevity.
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Microbes compete for nutrients and hinder metabolism

Choline is a water soluble nutrient, it supports energy, brain function and keeps the metabolism active. It contributes to resources that cells used to make modifications to DNA, and with less choline the cell's ability to modify and regulate genes can be impaired.

Tissues from the liver to the brain had altered epigenetic patterns in mice with high levels of choline-eating microbes.
Epigenetic modifications change how genes are expressed. The nutritional demand for the nutrient increases during pregnancy to support epigenetic regulation and cellular health in the developing fetus, and studies have linked choline deficiency during pregnancy in humans with altered behavior in children.

 Choline is found in high amounts in soybeans, eggs, meat, fish, cauliflower, milk and other foods. To test whether microbiomes could compete with their hosts for the nutrient. Researchers used germ-free mice that were colonized with defined populations of microbes to test whether microbiomes could compete with their hosts for the nutrient.

Some mice had choline eaters; others had communities where choline consumption was disrupted by mutating a single gene. When the mice were fed with a high-fat diet, which induces a range of metabolic diseases in mice, the animals with choline-eating microbes added more abdominal fat, and had fattier livers, than their counterparts with microbes that couldn't eat choline.

The offspring of mice with choline-eating bacteria had altered epigenetic patterns in their brains, suggesting problems with normal development. In mice that were genetically susceptible to behavioral problems, those that had choline-eating microbes showed anxious behaviors.

Epigenetic regulation explains the negative effects of choline-eating microbiomes, the byproduct of bacterial choline metabolism, known as Trimethylamine N-oxide TMAO, is also linked to negative outcomes. In another experiments, researchers observed much higher levels of TMAO in the mice that hosted choline-eating bacteria.

The toxic TMAO might work together with disrupted epigenetic patterns to create the long list of metabolic and developmental disruptions seen in these animals. The toxic effects of TMAO accumulation also complicate potential dietary remedies, more choline in the diet might lead to more TMAO rather than fixing nutritional shortages.
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Faulty gene caused obesity

 Researchers have discovered that reduced function of a gene that impacts the breakdown of fats resulted in adult-onset obesity and fatty liver. In normal metabolism, fat and carbohydrate in our diets was broken down to produce the energy that our bodies required by the cellular energy plants, known as mitochondria.

Faulty mitochondrial gene had major impacts on normal metabolic function, if mitochondria are compromised or damaged, the breakdown of fat and carbohydrates will be poorly regulated, which can lead to adult-onset obesity.

Healthy adults will have two copies of the Pentatricopeptide repeat-containing protein 1, PTCD1 gene, PTCD1 is vital for the breakdown of fats, carbohydrates and energy production. When one copy of this gene is lost, it results in obesity, fatty liver and heart disease

PTCD1 affects the way mitochondria are formed by changing their shape and making them less connected with each other. Excess weight and obesity are major risk factors for diabetes, cardiovascular disease, musculoskeletal disease and cancers.
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Genetic variants determined strength of immune system

Genetic differences in human affects cellular response to infections. Defense against microbial pathogens is carried out by white blood cells. White blood cells activate cellular defense programs and repressing the expression of hundreds of genes when they come across microbes.

Human immune system plays a central role in autoimmune inflammatory diseases, cancer, metabolism and aging. The researchers discovered hundreds of genes where the response to immune stimulus depended on the genetic variants possessed by the individual.

These genes demonstrate that genetic variation has an important role in how the human immune system works.
The study discovered genetic variants whose effects on gene regulation was different depending on the different infectious state of the cells.

Genetic disease risk is sometimes driven not by genetic variants causing constant cellular dysregulation, but by causing a failure to respond properly to environmental conditions such as infection.

Researchers analyzed how cells from different individuals respond to infection by measuring gene expression both during the early and late immune response.

 Integrating the gene expression profiles with genome-wide genetic data of each individual, they were able to discovered how genetic variants affect gene expression and how this genetic effect changes with immune stimulus.

Diseases have both genetic and environmental risk factors.
The analyses of gene expression patterns provide comprehensive information about the immune responses and show wide variation among individuals exposed to different pathogens at different time.

The research identified population differences in immune response and demonstrated that immune response modifies genetic associations to disease.
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Stress hormone may affect your health

Cortisol is a steroid hormone that regulates a wide range of processes throughout the body. It controls the body’s blood sugar levels, regulates
metabolism, it prevents inflammation, controls salt and water balance.

Blood levels of cortisol are high in the morning and fall throughout the day.  Steady daytime levels of the stress hormone cortisol are associated with health problems like inflammation, obesity and cancer.

Chronic stress may hinder variability of cortisol levels, this is known as stress-related circadian dysregulation.
Inflammation and the immune system dysfunction are the major cause of the loss of variation in cortisol levels.
Fatigue, cancer, depression, and obesity are associated with less variation in cortisol.

Viral infections, vigorous exercises, caffeine and sleep deprivation can cause abnormal increase in cortisol levels. Healthy lifestyle of regular exercise, sound sleep and eating healthy diet can restore cortisol rhythms.
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