Medical Bulletin 30/June/2026 - Video

A newly identified type of stem cell may help explain why belly fat tends to increase with age, according to a study published in Science. Researchers found that aging activates a previously unknown population of fat-producing stem cells that appear to drive the formation of new abdominal fat cells, offering fresh insight into age-related weight gain and metabolic disease.

Scientists at City of Hope studied white adipose tissue, the body's primary fat-storage tissue, in mice and confirmed key findings using human tissue samples. While fat cells are known to enlarge with age, the researchers investigated whether aging also increases the production of entirely new fat cells.

The team focused on adipocyte progenitor cells (APCs), stem cells that develop into mature fat cells. When APCs from older mice were transplanted into young mice, they generated large numbers of new fat cells. In contrast, APCs from young mice produced very few new fat cells, even when placed in older animals, suggesting the age-related changes were built into the stem cells themselves.

Further analysis revealed that aging transforms some APCs into a newly identified stem cell population called committed preadipocytes, age-specific (CP-As). These cells appeared only in middle-aged mice and showed a strong ability to generate new fat cells. Researchers also identified the leukemia inhibitory factor receptor (LIFR) signaling pathway as a key driver of this process, helping CP-As multiply and produce fat cells.

Importantly, similar CP-A cells were also detected in human fat tissue, where they were more abundant in middle-aged individuals and showed the same fat-producing potential.

Although the findings require further validation in humans, the researchers believe targeting CP-A cells or the LIFR pathway could eventually lead to new treatments aimed at reducing age-related belly fat, improving metabolic health, and supporting healthier aging.

REFERENCE: Guan Wang, Gaoyan Li, Anying Song, Yutian Zhao, Jiayu Yu, Yifan Wang, Wenting Dai, Martha Salas, Hanjun Qin, Leonard Medrano, Joan Dow, Aimin Li, Brian Armstrong, Patrick T. Fueger, Hua Yu, Yi Zhu, Mengle Shao, Xiwei Wu, Lei Jiang, Judith Campisi, Xia Yang, Qiong A. Wang. Distinct adipose progenitor cells emerging with age drive active adipogenesis. Science, 2025; 388 (6745) DOI: 10.1126/science.adj0430

Breastfeeding for Six Months Linked to Lower ADHD Risk in Children: Study

Exclusive breastfeeding for up to six months may be associated with a lower risk of attention-deficit/hyperactivity disorder (ADHD) symptoms during early childhood, according to a new study from the University of Bergen.

Researchers analyzed data from more than 37,600 families participating in the Norwegian Mother, Father and Child Cohort Study (MoBa). They examined whether the duration of exclusive breastfeeding during the first six months of life was linked to ADHD symptoms at ages three, five, and eight years.

The findings showed that children who were exclusively breastfed for longer periods had lower levels of ADHD symptoms throughout childhood. The association was observed in both boys and girls and was strongest at ages three and five, although it remained evident, though weaker, at age eight. Researchers also found that while any breastfeeding was associated with lower ADHD symptoms, the strongest relationship was seen with exclusive breastfeeding for up to six months.

Because ADHD has a strong genetic component, the researchers accounted for several potential confounding factors, including genetic risk for ADHD, maternal ADHD symptoms, and sociodemographic characteristics. They also performed sibling analyses, comparing children within the same family who had different breastfeeding durations.

Even after these adjustments, exclusive breastfeeding remained associated with a modest reduction in ADHD symptoms, suggesting that factors beyond genetics may contribute to neurodevelopment.

The researchers caution that the study was observational and cannot prove that breastfeeding directly prevents ADHD

The team says further research is needed to determine whether the relationship is causal and to better understand how breastfeeding may influence early brain development and the risk of ADHD symptoms later in childhood.

REFERENCE: Solberg, B. S., et al. (2026). Breastfeeding and Development of Attention-Deficit/Hyperactivity Disorder Symptoms Across Childhood. Biological Psychiatry. DOI: 10.1016/j.biopsych.2026.06.009. https://www.sciencedirect.com/science/article/pii/S000632232601348X?via=ihub

Researchers Discover Why Fructose Fails to Suppress Hunger Like Glucose

Fructose and glucose may contain the same number of calories, but they communicate with the brain through different biological pathways, according to a study published in Neuron. The findings suggest that the type of sugar consumed-not just its calorie content-may influence hunger, food preferences, and eating behavior.

Researchers at the Monell Chemical Senses Center investigated how the two sugars affect brain activity in mice. They found that fructose and glucose send distinct signals from the gut to the brain, producing different effects on neurons that regulate appetite.

Fructose increased levels of the gut hormone peptide YY (PYY), which transmitted signals through the vagus nerve and modestly reduced the activity of agouti-related protein (AgRP) neurons, brain cells known to stimulate hunger. When researchers blocked this signaling pathway, fructose no longer influenced these hunger-related neurons.

Glucose, however, followed a different route. Rather than relying on the PYY-vagus nerve pathway, it produced a much stronger suppression of AgRP neuron activity, suggesting it has a greater impact on reducing hunger signals.

Although both sugars had similar short-term effects on food intake, the mice gradually developed food preferences that reflected the different levels of AgRP neuron suppression. The researchers also tested a sweetener containing both fructose and glucose. This mixture reduced hunger-neuron activity more than fructose alone, and the mice showed a stronger preference for it.

The findings challenge the long-standing belief that hunger-regulating neurons respond primarily to the number of calories consumed. Instead, the results suggest that the brain can distinguish between different types of sugars and process them through separate gut-brain communication pathways.

While the research was conducted in mice, the authors say the findings improve understanding of how different dietary sugars influence appetite and food preferences and may help explain why some sweetened foods and beverages are particularly appealing.

REFERENCE: Aaron D. McKnight, Alan de Araujo, Fang-Yu Hsu, Alexandra G. Vargas-Elvira, Alisha A. Acosta, Miliani M. Smith, Wisdom Iwueze, Guillaume de Lartigue, Amber L. Alhadeff. Attenuated hypothalamic response to fructose via a dedicated gut-brain pathway. Neuron, 2026; DOI: 10.1016/j.neuron.2026.05.013