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الوسم: metabolism

  • Scientists Discover New Method to Boost Body Fat Burning

    Scientists Discover New Method to Boost Body Fat Burning

    Credit: Unsplash+.

    Most of today’s new weight-loss medications work by suppressing appetite, helping people eat less. However, researchers at the University of California, Berkeley, are exploring an alternative approach that targets energy expenditure instead.

    Rather than focusing primarily on reducing food intake, an experimental drug appears to increase how much energy the body burns.

    The compound is called TOFA, short for 5-tetradecyloxy-2-furoic acid.

    In recent mouse studies, scientists observed that TOFA helped lower body fat, improved blood sugar regulation, and decreased unhealthy blood fats. These results were published in Science Advances.

    This research comes amid a significant shift in obesity treatment options. Medications like Ozempic and Wegovy contain semaglutide, while Mounjaro and Zepbound include tirzepatide.

    These drugs target hormones that influence appetite, blood sugar, and digestion, often leading to significant weight loss for many users.

    While these medications offer benefits for those with obesity, diabetes, and related health issues, they can also cause side effects such as nausea, vomiting, diarrhea, or constipation—especially when starting treatment or increasing doses.

    Because patients often eat less while using these drugs, doctors also focus on ensuring proper nutrition and preventing muscle loss during weight reduction.

    Muscle loss is concerning since total body weight doesn’t fully reflect overall health. Losing excess fat can boost metabolic well-being, but losing too much muscle can weaken strength and reduce physical function.

    This is particularly problematic for older adults and individuals already at risk for frailty.

    The Berkeley team aimed to find another strategy to encourage weight loss. Body weight depends partly on the balance between calories consumed and calories burned. While GLP-1 medications mainly influence appetite, this study focused on boosting energy expenditure.

    TOFA isn’t a newly discovered chemical. It’s been known for decades and is understood to interfere with enzymes called ACCs, which help the body convert food into fatty acids that can be stored or used for energy.

    Blocking ACC enzymes sounds promising for reducing fat, but previous efforts faced challenges. Some ACC inhibitors unexpectedly increased triglycerides in the blood, raising concerns since high triglycerides are linked to cardiovascular risk, which limited enthusiasm for this approach.

    However, the new findings suggest TOFA might behave differently, as it appears to affect multiple aspects of metabolism simultaneously. Besides slowing fat production (like cholesterol and triglycerides), it also activates genes involved in fat utilization, causing cells to burn more fuel.

    This effect is partly linked to two cell receptors called PPAR-alpha and PPAR-delta, which regulate genes related to fat processing and energy production. When activated, these receptors promote the uptake and use of fatty acids as fuel.

    In treated mice, this resulted in up to an 18% increase in energy expenditure. Notably, this wasn’t due to increased activity or heat production, as body temperature remained stable. This indicates that the metabolism itself was driving the increased energy use.

    Additionally, TOFA improved several indicators associated with type 2 diabetes. The mice became more responsive to insulin, leading to better blood sugar control, and their triglyceride levels decreased instead of rising.

    The compound also positively impacted fatty liver disease, a condition characterized by excess fat accumulation in the liver, strongly linked to obesity and insulin resistance. Over time, fatty liver can progress to inflammation, scarring, and serious liver damage.

    One of the most striking results was the change in body composition. Obese mice treated with TOFA lost fat without losing significant muscle mass, suggesting a potential way to achieve weight loss while preserving strength.

    The researchers also tested whether combining two separate drugs—one that inhibits fat production and another that stimulates energy burning—could replicate TOFA’s effects. Surprisingly, this two-drug combo was less effective overall than the single molecule, indicating TOFA may trigger a coordinated response in the body.

    Lead author Justin Y. Lee explained that TOFA seems to activate a linked process where fat production decreases and the body becomes more efficient at handling excess fat and glucose. Fully understanding this mechanism could be key to designing future therapies.

    Further, when TOFA was combined with existing GLP-1-based treatments like semaglutide or tirzepatide in mice, results improved even more. These animals showed greater reductions in body weight and better metabolic profiles compared to using each treatment alone. Blood sugar, insulin, and triglyceride levels all improved more with combination therapy.

    This combined approach is promising because these meds target different pathways — GLP-1 drugs mainly curb appetite, while TOFA boosts energy use. Targeting both sides of energy balance could yield stronger results.

    Nevertheless, caution is essential. TOFA’s safety and effectiveness in humans remain unproven. While animal studies reveal important biological insights, many promising drugs fail when tested in people.

    Questions about long-term safety also remain. Modifying how the body produces and burns fats could impact vital organs like the liver and heart. Further research will need to evaluate toxicity, dosing strategies, potential drug interactions, and whether increased energy expenditure can be maintained safely over time.

    The team has founded ReRx Therapeutics to continue developing this approach. More comprehensive safety studies are necessary before human trials can determine if TOFA or similar compounds could be viable treatments. Until then, TOFA stays in the experimental stage.

    This research broadens understanding of obesity therapies. While current GLP-1 drugs have shown that controlling appetite can produce significant weight loss, future treatments might also include medications that safely increase energy expenditure or help preserve muscle mass.

    What’s most encouraging is that TOFA improved multiple health issues in mice—excess fat, insulin resistance, elevated triglycerides, and fatty liver disease. Its enhanced effect when combined with GLP-1 medications is noteworthy, though human data is needed before any conclusions can be made regarding its benefit for people.

    The study was conducted at UC Berkeley and published in the peer-reviewed journal Science Advances.

  • Scientists Discover Surprising Cause of Common Gut Disorder

    Scientists Discover Surprising Cause of Common Gut Disorder

    Scientists have uncovered a groundbreaking discovery that could transform how healthcare professionals understand irritable bowel syndrome (IBS), a common digestive disorder affecting over 10% of the global population. IBS often leads to recurring stomach pain, bloating, constipation, diarrhea, or a combination of these symptoms. Despite its prevalence, medical experts have yet to fully grasp why some individuals develop this condition, complicating efforts to develop universally effective treatments.

    For years, the prevailing theory linked IBS primarily to disrupted communication between the brain and the gut. The digestive system is densely populated with millions of nerve cells that constantly exchange signals with the brain. Emotional factors like stress, anxiety, and mood disorders are known to worsen IBS symptoms, and many patients report that emotional stress exacerbates their digestive issues. Still, this explanation has never fully explained all cases of IBS.

    A recent international study suggests a new piece of the puzzle: metabolism, especially how the body processes fats in the blood, may play a role in susceptibility to IBS. Led by Professor Mauro D’Amato of LUM University and CIC bioGUNE, the research was published in the journal Gut. This extensive genetic analysis is among the largest ever conducted on IBS, involving the genetic and health data of more than 2.7 million individuals from 22 major biobanks globally. The team compared the DNA of those with IBS against those without to pinpoint genetic factors associated with the condition.

    The study identified 35 specific regions within the human genome linked to IBS. Some of these regions involved genes connected to the nervous system, reinforcing earlier findings. Unexpectedly, the research also uncovered a significant link with cardiometabolic health, particularly involving blood triglycerides—the fats that circulate in the bloodstream and store excess energy. Elevated triglyceride levels are already known to increase the risk of cardiovascular disease and fatty liver disease.

    The strongest connection was found with a gene called GCKR, which plays a crucial role in how the liver manages sugar and fat. A particular variation in this gene was associated with higher triglyceride levels and an increased likelihood of developing IBS. These results suggest that alterations in liver metabolism might influence digestive health in ways previously unrecognized.

    The study further explored existing medications that could potentially reverse the biological changes associated with IBS. Several drugs affecting fat metabolism and cardiovascular health emerged as promising candidates, indicating that some medications already available might be repurposed for IBS treatment after further testing.

    This research broadens the understanding of IBS, highlighting that the condition may involve a complex interplay between the gut, brain, liver, and metabolic processes. The immense size of the study enhances confidence in the genetic findings, although it doesn’t establish a direct cause-and-effect relationship between high triglycerides and IBS. Clinical trials will be necessary before any new treatments are endorsed. Nonetheless, these findings pave the way for innovative research directions and could eventually lead to more personalized therapies for patients who don’t respond well to current options.

    For additional insights into gut health, recent studies emphasize the vital connection between diet, immune function, and gut integrity. Notably, low-gluten, high-fiber diets have been shown to improve gut health and support weight management. Other research highlights how dietary choices, such as incorporating mycoprotein, may reduce the risk of bowel cancer and promote gut well-being.

    Source: LUM University.

  • Can Sugar Alternatives Raise Diabetes Risk?

    Can Sugar Alternatives Raise Diabetes Risk?

    Millions of Australians consume artificial sweeteners daily, believing they offer a healthier alternative to sugar. But is that really true? A recent study from the University of Adelaide is exploring how low-calorie sweeteners impact the body’s glucose regulation systems and whether they might influence the development of diabetes.

    These sweeteners are found in a wide range of products—from sodas and yogurts to protein bars and sugar-free snacks—making them a common fixture in modern diets. Despite their popularity, our understanding of how they affect metabolism remains incomplete. The Adelaide research project, funded by the National Health and Medical Research Council, the Medical Research Future Fund, and Diabetes Australia, aims to fill this knowledge gap.

    The team is examining five of the most widely used sweeteners—aspartame, stevia, sucralose, saccharin, and acesulfame potassium—to see how they interact with key organs involved in blood sugar management, such as the intestines, pancreas, and kidneys, along with the gut microbiome. Associate Professor Tongzhi Wu from the university explains that understanding how different sweeteners impact glucose levels could lead to safer dietary guidelines and help identify new pathways for preventing and managing diabetes.

    “Many people looking to lose weight or control their blood sugar choose low-calorie sweeteners because they believe they’re healthier than sugar,” Wu notes. “But, although these sweeteners were created to replace sugar without adding calories, accumulating evidence suggests they may not be as metabolically neutral as previously thought.”

    The study aims to determine how sweeteners affect glucose absorption and excretion, alter gut bacteria, and whether these changes could influence diabetes risk. Researchers are especially interested in whether sweeteners can impact blood glucose regulation through mechanisms independent of calorie consumption, and if some alternatives are safer than others.

    Diabetes is the fastest-growing chronic illness worldwide, affecting over 462 million people globally and nearly 1.2 million within Australia. Artificial sweeteners like NutraSweet (aspyrteme), Natvia (stevia), Splenda (sucralose), Sugarine (saccharin), and Equal (acesulfame potassium) form a market worth over $4.3 billion and are projected to grow to nearly $6.2 billion by 2034.

    Professor Chris Rayner, another lead researcher at the university, emphasizes that excess body weight is one of the biggest risk factors for type 2 diabetes. “People often view sweeteners as a simple switch for sugar, but the science is more complex than that,” he explains. “While these products can help reduce sugar intake, we still lack a full understanding of their long-term effects on metabolism.”

    By comparing these popular sweeteners, the researchers hope to identify whether certain products influence the body differently and to provide solid evidence to inform future dietary advice. The study is expected to conclude by year’s end, with hopes that its findings will support more informed choices and better health outcomes.

    Individuals interested in participating in the ‘Sweet n Sour’ study can visit the university’s website for more details.

  • Joint Pain Supplements Linked to Accelerated Alzheimer’s Progression

    Joint Pain Supplements Linked to Accelerated Alzheimer’s Progression

    Credit: Unsplash+

    Glucosamine has gained popularity worldwide as a common dietary supplement. Many individuals take it daily to relieve joint pain, support cartilage health, and stay active as they age.

    Since it has been accessible for years and sold without a prescription, many perceive glucosamine as a harmless supplement that can easily be incorporated into a healthy lifestyle.

    However, a recent study conducted by the University of Florida questions that assumption. The research indicates that glucosamine use might be associated with an increased risk of cognitive decline in those already experiencing memory issues. The findings were published in Nature Metabolism.

    This research centers on Alzheimer’s disease, a condition characterized by memory loss, impaired reasoning, and difficulties with daily tasks. It is the leading cause of dementia, affecting millions around the world.

    Despite breakthroughs in neuroscience, the reasons why some individuals develop Alzheimer’s or why it progresses faster in certain people remain unclear.

    One area gaining attention is metabolism—the sum of chemical reactions within cells that produce energy and facilitate essential functions. Scientists increasingly believe that metabolic shifts might play a critical role in brain aging and neurodegenerative conditions.

    The team from the University of Florida examined whether glucosamine could influence these metabolic processes. While it’s primarily known for supporting joints, researchers noted that glucosamine can cross the blood-brain barrier and enter the central nervous system.

    This suggests that glucosamine might directly impact brain cells instead of only acting on joints and connective tissues.

    To explore this, researchers analyzed patient records from the university’s healthcare system between 2012 and 2024, utilizing advanced AI techniques to identify links between glucosamine consumption and cognitive decline.

    The results revealed a notable trend: individuals taking glucosamine were about 25% more likely to transition from mild cognitive impairment to dementia or Alzheimer’s when compared to those not using the supplement.

    Mild cognitive impairment often serves as an intermediate stage—signifying noticeable forgetfulness or thinking issues, yet allowing individuals to live independently. Nonetheless, many eventually develop Alzheimer’s or other dementias.

    The study also indicated that among those already diagnosed with Alzheimer’s or dementia, glucosamine users faced roughly a 25% higher risk of death during the study period.

    Further analysis targeted potential biological mechanisms behind these results. The focus was on a process where sugar molecules attach to proteins inside cells, a modification essential for protein function.

    Proteins are vital for cell survival and operation. Many require small chemical modifications, like sugar additions, to fold correctly and carry out their tasks effectively.

    Researchers discovered evidence suggesting this sugar-tagging process becomes overly active in Alzheimer’s disease. Instead of aiding cellular health, excessive sugar attachment might contribute to damaging changes in brain tissue.

    Additionally, experiments with genetically modified mice showed that those given glucosamine exhibited increased sugar-modified proteins and memory deficits. When this sugar-tagging was reduced, memory function improved.

    Human brain tissue samples stored at the university’s brain and tissue bank supported these findings. Elevated levels of sugar-modified proteins were observed in Alzheimer’s-affected brains, indicating this pathway may also be active in humans.

    Based on this evidence, researchers propose that glucosamine might amplify an already overactive metabolic process in Alzheimer’s, possibly speeding up disease progression in vulnerable individuals.

    While these findings are concerning, experts emphasize that the study does not establish causation. Observational data can show associations but cannot definitively prove that glucosamine causes Alzheimer’s. Many factors, including genetics, heart health, lifestyle, education, and other medical conditions, influence dementia risk.

    The study’s strength lies in its comprehensive approach, combining large-scale human data, laboratory experiments, animal models, and direct examination of brain tissue. This layered analysis makes the findings particularly compelling.

    Despite this, numerous questions remain. It is unclear whether all glucosamine products pose similar risks, whether certain people are more vulnerable, or if effects vary with dosage and duration of use.

    Further research is essential to confirm these results and determine whether changing supplement habits might impact cognitive decline.

    This study underscores that dietary supplements, even those deemed natural, are biologically active substances capable of affecting complex bodily systems. Understanding these effects is crucial as scientists continue their efforts to prevent and treat Alzheimer’s disease.

    These revelations suggest that metabolic pathways may play a significant role in Alzheimer’s progression. If future studies verify these findings, targeting metabolism could become a key strategy alongside existing treatments focused on amyloid plaques and tau tangles.

    For now, individuals taking glucosamine are advised not to make abrupt changes based solely on this single study. Instead, those worried about memory issues, dementia risk, or supplement use should consult their healthcare providers.

    Ongoing research will clarify whether glucosamine directly influences Alzheimer’s or if the observed association stems from other factors.

    If you’re interested in Alzheimer’s prevention, consider reading about vitamin D deficiency links to dementia or how strawberries might serve as a protective food. Keep up with recent studies on foods that may lower Alzheimer’s risk or explorations into cannabis-based therapies for symptom relief.

    Source: University of Florida.

  • A Popular Antioxidant Might Accelerate Cancer Growth

    A Popular Antioxidant Might Accelerate Cancer Growth

    A recent scientific breakthrough is transforming researchers’ understanding of cancer and nutrition. Scientists have discovered that cancer cells may rely on a common antioxidant called glutathione as a fuel source.

    This unexpected finding opens up new possibilities for cancer therapy and sheds light on how tumors survive and flourish in challenging environments. The study, conducted by researchers at the Wilmot Cancer Institute at the University of Rochester and published in the journal Nature, was led by Dr. Isaac Harris. The team examined how cancer cells acquire and utilize nutrients differently than normal cells.

    Like healthy cells, cancer cells need energy to grow and spread. However, tumors often exist in harsh conditions with limited nutrients. To survive, they develop unique strategies to find and utilize alternative fuels. The research reveals that glutathione is one such surprising resource.

    Naturally produced by the body, glutathione is primarily recognized as an antioxidant that guards cells against damage. It’s also available as a supplement, often linked to immune support and inflammation reduction. Due to these benefits, many people assume glutathione is universally good for health.

    However, this new research indicates a more complicated role. Scientists found that cancer cells can break down glutathione and repurpose it as energy. Essentially, glutathione isn’t just protecting cells but may also be aiding tumor growth.

    In their investigation, researchers analyzed fluid from breast tumors and detected elevated levels of glutathione, suggesting that cancer cells store and consume it. Further experiments showed that interfering with the ability of cancer cells to use glutathione slowed tumor growth.

    This discovery highlights a potential vulnerability in cancer cells. If new drugs can be developed to prevent tumors from using glutathione, it might be possible to slow or halt cancer progression without harming normal cells. Early evidence suggests that this mechanism may be relevant across various tumor types, not just breast cancer, hinting at broader implications for treatment.

    The findings also prompt questions about antioxidant supplements. While often regarded as beneficial, this research suggests that in certain cases, these supplements might inadvertently support tumor growth. It’s important to emphasize that consuming fruits and vegetables—rich in essential nutrients—remains beneficial, but caution should be exercised with high-dose supplements that aren’t strictly regulated.

    The study also identified a promising drug that can block cancer cells from utilizing glutathione. Originally developed years ago, this drug is now under renewed investigation for its potential to treat cancer. Researchers are working on refining this approach and understanding its effects in the body.

    Building on previous research linking diet and cancer growth, this study deepens awareness of how metabolism and nutrition influence disease progression. Although the findings are significant, much of the work has been done in laboratory and preclinical models. Further research involving patients is essential to determine safety and effectiveness.

    In summary, this research uncovers that cancer cells might exploit glutathione as an unseen energy supply. Discovering this role opens new pathways for therapies targeting cancer cell metabolism. While ongoing studies are needed, this development offers hope for more precise and effective cancer treatments in the future.

    For those interested in cancer-related research, consider reading about how a low-carb diet could increase overall cancer risk, or about a berry with potential to prevent cancer, diabetes, and obesity. Additionally, insights into how drinking milk may influence heart disease and cancer risks, as well as the potential of vitamin D supplements to significantly reduce cancer mortality, are also worth exploring.