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Diet and Weight Loss

Uncovering the Cellular Culprit Behind Age-Related Abdominal Fat: A New Target for Future Therapies

It’s no secret that our waistlines often expand in middle-age, but the problem isn’t strictly cosmetic. Belly fat accelerates aging and slows down metabolism, increasing our risk for developing diabetes, heart problems and other chronic diseases. Exactly how age transforms a six pack into a softer stomach, however, is murky. New research shows how aging shifts stem cells into overdrive to create more belly fat.

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The article reveals that age-related abdominal fat is not just a cosmetic issue but also accelerates aging and increases the risk of developing chronic diseases such as diabetes and heart problems. The research, conducted by City of Hope and UCLA, has uncovered the cellular culprit behind this phenomenon: adult stem cells called adipocyte progenitor cells (APCs). These cells are responsible for producing new fat cells, especially around the belly.

The study’s findings suggest that aging triggers the arrival of a new type of adult stem cell, which enhances the body’s massive production of new fat cells. The researchers discovered that APCs from older mice rapidly generate a colossal amount of fat cells when transplanted into young mice. In contrast, APCs from young mice do not produce many new fat cells when transplanted into older mice.

Using single-cell RNA sequencing, the scientists compared APC gene activity in young and older mice. They found that while barely active in young mice, APCs woke up with a vengeance in middle-aged mice and began pumping out new fat cells. This is the first evidence that our bellies expand with age due to the APCs’ high output of new fat cells.

A signaling pathway called leukemia inhibitory factor receptor (LIFR) proved critical for promoting these cells to multiply and evolve into fat cells. The researchers also identified similar CP-A cells in human tissue samples from people of various ages, illustrating that CP-As have a high capacity for creating new fat cells.

The study’s findings highlight the importance of controlling new fat-cell formation to address age-related obesity. Understanding the role of CP-As in metabolic disorders and how these cells emerge during aging could lead to new medical solutions for reducing belly fat and improving health and longevity. Future research will focus on tracking CP-A cells in animal models, observing CP-A cells in humans, and developing new strategies that eliminate or block the cells to prevent age-related fat gain.

Colitis

Unlocking the Missing Link Between Obesity and Insulin Production: The Role of Colonic Inflammation

How does obesity affect insulin production? Researchers are shining light on new stages of the ERK pathway.

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The relationship between obesity and diabetes has long been a subject of scientific interest. Researchers at Tohoku University Graduate School of Medicine have made a groundbreaking discovery that sheds light on the missing link between these two conditions. Their study reveals that colonic inflammation, triggered by obesity, plays a crucial role in regulating glucose homeostasis through the hepatic ERK pathway.

Insulin is a hormone produced by β-cells in the pancreas that unlocks cells to let glucose enter from the blood. However, individuals with obesity often become insulin-resistant, causing their pancreas to secrete more insulin to try and keep up. This study shows that inflammation in the colon, triggered by obesity, activates the ERK pathway in the liver, which stimulates the neuronal relay pathway and increases β-cell production.

The researchers conducted a series of experiments on mice to determine if colonic inflammation due to obesity could impact the hepatic ERK pathway. They found that causing inflammation in the colon activated the ERK pathway in the liver, stimulated the neuronal relay pathway, and increased β-cells even in mice without obesity. By analyzing colons of mice with induced obesity, they also found that colonic inflammation had occurred along with both hepatic ERK pathway activation and increased β-cells.

Moreover, when the researchers treated obese mice with colon inflammation by lowering their inflammation, it actually stopped the ERK pathway in the liver from activating. This exciting finding suggests that targeting colon inflammation could be a potential way to prevent or treat diabetes.

This research has significant implications for understanding the mechanism behind β-cell proliferation and maintaining normal blood glucose levels. It is anticipated that these findings will lead to advancements in developing treatments and prevention methods for diabetes, ultimately improving the lives of millions of people worldwide.

The study was published in JCI Insight on May 8, 2025, and was supported by various grants from the Japan Society of the Promotion of Science (JSPS), Japan Science and Technology Agency (JST), and Japan Agency for Medical Research and Development (AMED).

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The Hidden Dangers of Ultra-Processed Foods: A Risk Factor for Your Health?

Consumption of ultra-processed foods, such as sugar-sweetened beverages, potato chips and packaged cookies, may be associated with adverse health outcomes. Study finds each additional 100 grams/day consumption of ultra-processed foods increased risk of hypertension, cardiovascular events, cancer and more.

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The consumption of ultra-processed foods has been linked to various adverse health outcomes, including hypertension, cardiovascular events, cancer, digestive diseases, and mortality. Research presented at the ACC Asia 2025 Together with SCS 36th Annual Scientific Meeting suggests that for every 100 grams of ultra-processed food consumed daily, the risk for these health issues increases.

Ultra-processed foods are characterized by high sugar, salt, and non-nutritive components, exhibiting low nutritional density yet high caloric content. These products may contribute to adverse health outcomes through mechanisms such as dysregulation of blood lipid profiles, alterations in gut microbiota composition, promotion of obesity, induction of systemic inflammation, exacerbation of oxidative stress, and impairment of insulin sensitivity.

A systematic review of 41 prospective cohort studies, spanning the Americas, Europe, Asia, and Oceania, found that ultra-processed food consumption was associated with increased risks for:

* Hypertension: 14.5% higher risk per 100g/day consumed
* Cardiovascular events: 5.9% higher risk per 100g/day consumed
* Cancer: 1.2% higher risk per 100g/day consumed
* Digestive diseases: 19.5% higher risk per 100g/day consumed
* All-cause mortality: 2.6% higher risk per 100g/day consumed

Researchers observed increased risks for obesity/overweight, metabolic syndromes/diabetes, and depression/anxiety.

The study’s findings suggest that clinicians should inform patients about the nutritional imbalance in ultra-processed foods and encourage them to reduce their consumption. Governments may consider implementing measures to mitigate the associated health impacts, such as establishing stringent food labeling regulations and requiring manufacturers to provide explicit ingredient disclosures.

Emerging evidence has linked health benefits to whole foods, simple ingredients, and culturally appropriate healthy eating patterns like the Mediterranean or DASH diet. Further high-quality studies on this topic are needed to inform public health recommendations and promote healthier eating habits.

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Diet and Weight Loss

A Healthy Diet in Childhood Linked to Later Menstrual Periods

Eating a healthy diet as a child is linked to girls having their first menstrual period at an older age than those who consumed a less healthy diet, according to a new study. The findings remained unaltered by the girls’ body mass index or height, both of which have been associated with the earlier onset of periods. The study has implications for health in later life as it is well known that women who started their periods at an early age may be at higher risk for diabetes, obesity, breast cancer and diseases of the heart and blood vessels.

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A Healthy Diet in Childhood Linked to Later Menstrual Periods

Eating a healthy diet during childhood has been linked to later menstrual periods, according to a new study published in Human Reproduction. Researchers found that girls who consumed a healthier diet were more likely to have their first period at an older age than those with less healthy diets.

The study’s findings remained unchanged even when taking into account body mass index (BMI) or height, both of which have been associated with earlier onset of periods. This suggests that a healthy diet is crucial for girls’ reproductive health, regardless of their weight or stature.

Researchers used data from over 7,500 children aged between 9 and 14, who were enrolled in the Growing Up Today Study (GUTS) in the USA. The participants completed questionnaires about their diets at two different times: when they joined the study and then every one to three years thereafter. They also reported their age when their first period started.

The researchers assessed the girls’ diets against two established dietary patterns: the Alternative Healthy Eating Index (AHEI) and the Empirical Dietary Inflammatory Pattern (EDIP). The AHEI scores diets based on healthier foods, such as vegetables, legumes, and whole grains. The EDIP scores diets in a way that reflects their overall potential for causing inflammation in the body.

The results showed that girls with the highest AHEI score, indicating they had the healthiest diet, were 8% less likely to have their first period within the next month compared to those with the lowest AHEI score. Similarly, girls with the most inflammatory diet, as indicated by EDIP scores, were 15% more likely to have their first period in the next month.

The study’s lead author, Holly Harris, stated that these findings highlight the importance of providing all children and adolescents with access to healthy meal options. She also emphasized the significance of school-based breakfasts and lunches being based on evidence-based guidelines.

These results suggest that a healthier diet may be associated with menstrual periods starting at an older age, which is an important period for reducing the risk of chronic diseases such as diabetes, obesity, cardiovascular disease, and breast cancer. The researchers now plan to investigate how childhood and adolescent dietary patterns relate to characteristics of menstrual cycles in adulthood.

The study’s strengths include collecting data on diet prospectively and examining whether BMI and height influence the association with age at menarche. However, limitations exist, such as information on diet, weight, height, and age at menarche being collected via questionnaires, which may be subject to error. Additionally, the participants were predominantly white, and the researchers were unable to see if results varied by race.

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