Medical Bulletin 14/Jun/2025 - Video

The study found that oleic acid, a monounsaturated fat associated with obesity, causes the body to make more fat cells. By boosting a signaling protein called AKT2 and reducing the activity of a regulating protein called LXR, high levels of oleic acid resulted in faster growth of the precursor cells that form new fat cells.

Researchers fed mice a variety of specialized diets enriched in specific individual fatty acids, including those found in coconut oil, peanut oil, milk, lard and soybean oil. Oleic acid was the only one that caused the precursor cells that give rise to fat cells to proliferate more than other fatty acids.

"You can think of the fat cells as an army," said Michael Rudolph, Ph.D., assistant professor of biochemistry and physiology at the University of Oklahoma College of Medicine and member of OU Health Harold Hamm Diabetes Center. "When you give oleic acid, it initially increases the number of 'fat cell soldiers' in the army, which creates a larger capacity to store excess dietary nutrients. Over time, if the excess nutrients overtake the number of fat cells, obesity can occur, which can then lead to cardiovascular disease or diabetes if not controlled."

Unfortunately, it's not quite so easy to isolate different fatty acids in a human diet. People generally consume a complex mixture if they have cream in their coffee, a salad for lunch, and meat and pasta for dinner. However, Rudolph said, there are increasing levels of oleic acid in the food supply, particularly when access to food variety is limited and fast food is an affordable option.

Reference: Allison Wing, Elise Jeffery, Christopher D. Church, Jennifer Goodell, Rocío del M. Saavedra-Peña, Moumita Saha, Brandon Holtrup, Maud Voisin, N. Sima Alavi, Mariana Floody, Zenan Wang, Thomas E. Zapadka, Michael J. Garabedian, Rohan Varshney, Michael C. Rudolph, Matthew S. Rodeheffer. Dietary oleic acid drives obesogenic adipogenesis via modulation of LXRα signaling. Cell Reports, 2025; 44 (4): 115527 DOI: 10.1016/j.celrep.2025.115527

New Nanoparticles Therapy for Patients with Lung Cancer, Cystic Fibrosis: Study Finds

New Delhi: For treating respiratory diseases, scientists have developed a new drug delivery system that transports genetic therapies directly to the lungs, opening possibilities for patients with conditions like lung cancer and cystic fibrosis. Findings were published in a pair of papers, in Nature Communications and the Journal of the American Chemical Society.

Scientists created and tested more than 150 different materials and discovered a new type of nanoparticle that can safely and effectively carry messenger RNA and gene-editing tools to lung cells. In studies with mice, the treatment slowed the growth of lung cancer and helped improve lung function that had been limited by cystic fibrosis, a condition caused by one faulty gene.

Researchers also developed a chemical strategy to build a broad library of lung-targeting lipids used in the nanocarriers. These materials form the foundation for the new drug delivery system and could be customized to reach different organs in the body, Gaurav Sahay of Oregon State University's College of Pharmacy, said.

"The streamlined synthesis method makes it easier to design future therapies for a wide range of diseases," he said. "These results demonstrate the power of targeted delivery for genetic medicines. We were able to both activate the immune system to fight cancer and restore function in a genetic lung disease, without harmful side effects."

Reference: K. Yu. Vlasova, A. Kerr, N. D. Pennock, A. Jozic, D. K. Sahel, M. Gautam, N. T. V. Murthy, A. Roberts, M. W. Ali, K. D. MacDonald, J. M. Walker, R. Luxenhofer, G. Sahay. Synthesis of ionizable lipopolymers using split-Ugi reaction for pulmonary delivery of various size RNAs and gene editing. Nature Communications, 2025; 16 (1) DOI: 10.1038/s41467-025-59136-z

Study Links Low Oral Microbiome Diversity to Depression Symptoms

New Delhi: Published in BMC Oral Health, a new study led by researchers at NYU Rory Meyers College of Nursing reveals that individuals with less diverse oral microbiomes are more likely to experience symptoms of depression. This research sheds light on the underexplored connection between oral bacteria and mental health.

The mouth, home to between 500 billion and 1 trillion bacteria, houses the second-largest community of microorganisms in the human body after the gut. This new research emphasizes that the oral microbiome may play a role in mood disorders.

To explore this connection, researchers examined data from over 15,000 U.S. adults aged 18 and older, drawn from the National Health and Nutrition Examination Survey (NHANES) conducted by the Centers for Disease Control and Prevention between 2009 and 2012. Participants completed surveys measuring depression symptoms, and provided saliva samples that underwent gene sequencing to identify bacterial content and assess microbiome diversity.

The study found that individuals with lower microbial diversity in their saliva were more likely to report symptoms of depression. Additional analysis revealed that factors such as smoking, alcohol use, and dental care habits—known to affect oral bacterial composition—also influenced the relationship between microbiome diversity and depression.

“It’s possible that the oral microbiome influences depressive symptoms through inflammation or changes to the immune system. Conversely, depression can drive changes including dietary intake, poor oral hygiene, increased smoking and drinking, or the use of medications—all of which have the potential to alter the oral microbiome,” said Bei Wu, vice dean for research at NYU Rory Meyers and senior author of the study.

While the direction of the relationship remains unclear, these findings open new avenues for research into mental health diagnostics and treatment.

Reference: Qiu, X., Xu, T., Huang, Y. et al. Relationship between depression and oral microbiome diversity: analysis of NHANES data (2009–2012). BMC Oral Health 25, 914 (2025). https://doi.org/10.1186/s12903-025-06274-x