Unveiling Metabolism’s Secrets: How to Trick Your Body into Burning More Calories

Many of us who have embarked on a weight loss journey know the frustration all too well: at some point, the pounds stop shedding. Despite our best efforts to cut calories, our bodies seem to betray us by slowing down metabolism, burning fewer calories than before. But why does this happen, and can we outsmart our metabolism? A new study from the University of Southern Denmark offers some promising insights.

The Metabolic Paradox

When we reduce our calorie intake, our body perceives a potential threat of starvation. In response, it adapts by conserving energy, ensuring essential functions can still be carried out. Unfortunately, this adaptation works against our weight loss goals, causing our metabolism to slow down and hold on to calories.

A Glimpse of Hope: New Research Findings

Researchers at the University of Southern Denmark have identified a potential way to maintain calorie burning even when consuming fewer calories. This discovery could be significant for patients using weight-loss or diabetes medicines like Wegovy and Ozempic, who often find their weight loss plateaus after shedding about 20-25% of their body weight.

According to Kim Ravnskjaer, a Principal Investigator and associate professor at the Department of Biochemistry and Molecular Biology, University of Southern Denmark, this stall is likely due to the body’s natural response. “It usually goes well at first, but as people lose some of the weight they aim to shed, their progress stalls because the body’s metabolism adapts,” he explains.

The Study and Its Implications

The study, published in the prestigious journal Cell Metabolism, explores the function of a gene called Plvap in certain mouse liver cells. The researchers discovered that the Plvap gene enables the body’s metabolic shift from burning sugar to fat when fasting. When Plvap is turned off, the liver does not recognize that the body is fasting and continues burning sugar.

“If we could develop a medication that helps maintain fat or sugar burning at its original high level alongside weight-loss treatments, people could continue losing weight beyond the usual plateau,” says Ravnskjaer.

Unexpected Discoveries

The researchers’ discovery was unexpected while investigating the role of the Plvap gene. They found that turning off this gene in mouse liver cells prevented the liver from shifting to fat burning during fasting, keeping the metabolism in sugar-burning mode. This shift resulted in the mice experiencing improved insulin sensitivity and lower blood sugar levels without negative effects.

Beyond the intriguing ability to “trick” the liver into thinking it is not fasting, the study made several other important observations:

  • The signal that triggers metabolic changes during fasting comes from the liver’s stellate cells rather than hepatocytes, suggesting a new mode of cell-to-cell communication.
  • Fat was redirected to the muscles instead of the liver, improving insulin sensitivity and lowering blood sugar levels.

Potential for Future Treatments

This discovery could have far-reaching implications—not just for obesity treatments, but also for improving our understanding of how fat and sugar are processed in metabolic diseases. In the long run, it may open new avenues for treating conditions like type 2 diabetes and steatotic liver disease.

“It’s well known that elevated blood sugar may lead to chronic complications for people with type 2 diabetes. Understanding Plvap could help diabetics better regulate their blood sugar in the future,” says Ravnskjaer.

Conclusion

The findings of this study underscore the complexity of our metabolism and the potential for groundbreaking treatments. While human trials and potential treatments are still a long way off, this research offers a promising glimpse into the future of weight loss and metabolic health. Understanding and controlling our metabolism may one day help us achieve our weight loss goals more effectively and improve overall health.

Obesity Starts in the Brain

Non-alcoholic fatty liver disease warning signs

Tübingen study highlights the brain’s central role in the development of obesity.

Published by: Deutsches Zentrum fuer Diabetesforschung DZD

In recent decades, obesity has become a pressing issue, impacting millions worldwide and posing significant challenges for healthcare systems. But did you know that the hormone insulin plays a crucial role in the brain’s involvement in obesity? A recent study by the University Hospital of Tübingen, the German Center for Diabetes Research (DZD), and Helmholtz Munich delves into this fascinating connection, offering new insights into the origins of type 2 diabetes and obesity.

Obesity: A Growing Epidemic

Officially recognized as a disease in Germany since 2020, obesity is known to contribute to various illnesses, including diabetes, heart attacks, and even cancer. With over one billion individuals affected globally and nearly 16 million in Germany alone, obesity has reached epidemic proportions. While poor diet and lack of exercise are often blamed, the mechanisms behind obesity are more complex than they appear.

The Brain’s Role in Obesity and Insulin Sensitivity

Unhealthy body fat distribution and chronic weight gain are linked to the brain’s sensitivity to insulin. What role does insulin play in the brain, and how does it affect those of normal weight? Prof. Dr. Stephanie Kullmann and her team at Tübingen University Hospital found that even a brief consumption of highly processed, unhealthy foods can significantly alter the brain of healthy individuals. This alteration may be the initial trigger for obesity and type 2 diabetes.

“In a healthy state, insulin has an appetite-suppressing effect in the brain. However, in people with obesity, insulin no longer properly regulates eating behavior, leading to insulin resistance,” explains Prof. Kullmann. She adds, “Interestingly, in our healthy participants, the brain shows a similar decrease in insulin sensitivity after short-term high-calorie intake as observed in people with obesity. This effect can persist even a week after returning to a balanced diet.”

Focusing on the Brain

Prof. Dr. Andreas Birkenfeld, Medical Director of Internal Medicine IV and DZD Board Member, suggests that the brain’s insulin response adapts to short-term dietary changes before any weight gain occurs, promoting the development of obesity and other secondary diseases. He calls for further research to explore the brain’s role in obesity and metabolic disorders.

A Short-Term Study with Long-Term Implications

The study involved 29 male volunteers of average weight, divided into two groups. For five days, one group supplemented their regular diet with 1500 kcal from high-calorie snacks, while the control group did not. Using magnetic resonance imaging (MRI), researchers examined liver fat content and brain insulin sensitivity.

The results were striking: the liver fat content increased significantly in the high-calorie group, and their brain’s insulin sensitivity remained lower even a week after returning to a regular diet. This effect, previously observed only in obese individuals, highlights the brain’s critical role in the early stages of obesity development.

As obesity challenges global health, understanding the brain’s role in this complex condition may pave the way for new strategies to combat it.

Can Cutting Ultra-Processed Foods Change Your Life?

Researchers found ultra-processed foods, even diet ones, bring distinct risks for people with diabetes.

Most diet programs aim to help people lose weight or follow U.S. nutrition guidelines, which don’t mention ultra-processed foods (UPFs). These mass-produced, packaged products—like chips and candy—contain little to no natural ingredients and are linked to higher risks of diseases and early death.

Recognizing the gap, researchers from Drexel University’s College of Arts and Sciences created an intervention program specifically targeting the problematic aspects of UPFs, including their addictive nature. Their program includes education about UPFs, mindfulness and acceptance strategies to cope with cravings, one-on-one meal planning, involving a household member in the process, and financial support to purchase healthy foods like fresh fruits and vegetables.

Recently published in Obesity and Science Practice, the researchers tested their two-month intervention with 14 adults who regularly consumed UPFs. The results were promising: participants cut their UPF intake nearly in half.

“Reducing UPF intake can be extremely difficult because the food industry wants us hooked on these ultra-delicious, convenient, cheap, and omnipresent foods,” said lead author Charlotte Hagerman, PhD.

The program participants halved their UPF consumption and reduced their calorie intake by an average of over 600 calories per day. They cut their sugar intake by 50%, saturated fat by 37%, and sodium by 28%. On average, participants lost 7.7 pounds and reported improved mood and energy.

Interestingly, the study found no significant increase in fruit and vegetable consumption, suggesting that further encouragement might be needed to improve overall dietary habits.

The intervention involved weekly group sessions with health behaviour change coaches, discussions, and activities. Participants learned to identify UPFs and their harmful effects and developed strategies to cope with cravings and reduce UPF intake. They also received a $100 grocery store gift card for meal planning.

Participants reported everything they ate over the past 24 hours to assess dietary intake using the Automated Self-Administered 24-Hour Dietary Assessment Tool (ASA-24). The data helped the team track changes in UPF, sodium, sugar, and saturated fat intake, as well as weight and fruit/vegetable intake.

“The findings suggest that with the right tools, people can reduce their UPF intake and be enthusiastic about interventions designed for this purpose,” said Hagerman. “Reducing UPF intake can lead to meaningful health improvements such as weight loss and better mood in as short as eight weeks.”

The research team plans to continue testing the intervention with a larger sample and different populations to confirm its effectiveness and explore its components further.

New Hope for Reducing Alcohol Cravings: Semaglutide Shows Promise!

Summer, Teenagers, and Alcohol A Deadly Combination

The blockbuster drug semaglutide, famously known as Ozempic for diabetes and Wegovy for obesity, could soon help people reduce their alcohol intake, according to new research from the University of North Carolina Health Care.

The Research

Led by Christian Hendershot, PhD, and Klara Klein, MD, PhD, the study found that weekly injections of semaglutide reduced alcohol cravings, drinking quantity, and the frequency of heavy drinking days in adults with symptoms of alcohol use disorder. These groundbreaking findings were published in JAMA Psychiatry.

A Potential Lifesaver

Alcohol use disorder is a significant public health issue, with an estimated 178,000 U.S. deaths per year attributed to alcohol-related causes, including liver disease and cardiovascular disease. Despite this, few people seek or receive treatment. The popularity of Ozempic and other GLP-1 receptor agonists could increase the adoption of these treatments for alcohol use disorder.

The Clinical Trial

In the trial, 48 adults with alcohol use disorder were recruited. One week before the first injection, participants were invited to drink their preferred alcoholic beverages in a lab setting, and their drinking patterns were documented. Participants were then randomly assigned to receive weekly injections of semaglutide or a placebo for nine weeks, with their drinking patterns continually measured.

Promising Results

After treatment, those in the semaglutide group consumed lower amounts of alcohol in the lab, as measured by grams of alcohol consumed and breath alcohol concentration. Clinical assessments showed that semaglutide reduced weekly alcohol cravings, average drinks on drinking days, and heavy drinking days compared to placebo.

Unexpected Benefits

Among a small subgroup of participants who smoked cigarettes, those treated with semaglutide also saw significant reductions in average cigarettes per day compared to the placebo group. This finding is particularly noteworthy as there are currently no medications approved for both alcohol reduction and smoking cessation.

Future Research

Though these preliminary results are promising, further research is needed to understand the mechanisms by which GLP-1 receptor agonists reduce alcohol cravings. Dr. Klein suggests that these effects are likely mediated in the brain and involve changes in reward processing. Additional studies are required to evaluate the long-term effects on alcohol consumption and determine the ideal doses and treatment durations.

Conclusion

“These data suggest the potential of semaglutide and similar drugs to fill an unmet need for the treatment of alcohol use disorder,” said Klein. “Larger and longer studies in broader populations are needed to fully understand the safety and efficacy in people with alcohol use disorder, but these initial findings are promising.”

Stay tuned for more updates on this exciting development in the fight against alcohol use disorder!

The Surprising Side Effects of Popular Weight Loss Drugs Explained

Risk factors for depression included loneliness, chronic pain and being female.

New research reveals that some weight loss medications might have unexpected behavioural side effects, but the reasons behind these effects are not fully understood.

Published in Diabetes, Obesity and Metabolism, the study looked at glucagon-like peptide 1 receptor agonists (GLP1RA)—drugs commonly used for type 2 diabetes and obesity. These medications mimic the GLP-1 hormone, which helps control insulin and blood glucose levels while promoting feelings of fullness.

The researchers examined genetic data from diverse populations to see how variants in the GLP1R gene might explain these side effects. The study involved over 400,000 individuals from various ethnic backgrounds and found that GLP1R gene variants were linked with both cardiometabolic traits (like blood pressure and type 2 diabetes) and behavioral traits (such as risk-taking behavior and mood instability).

Interestingly, the genetic variants influencing cardiometabolic traits were different from those affecting behavioral changes, suggesting that the side effects are likely indirect.

Although it’s not possible to directly compare these genetic findings to the effects of a drug, the study provides new insights into the complex mechanisms behind the unexpected side effects of GLP1RAs. Understanding these factors could help guide safer use of these popular weight loss drugs in the future.

Are you curious about how these findings could impact weight loss treatments? Dive into the full study to uncover more! 🚀