Medical Bulletin 11/ February/ 2025 - Video

In a study published in Science, researchers at the University of Michigan used mice to show that dysfunctional mitochondria trigger a response that affects the maturation and function of insulin-producing pancreatic β-cells.

Mitochondrial defects are associated with the development of diseases such as type 2 diabetes. Patients who suffer from this disorder are unable to produce enough insulin or use the insulin produced by their pancreas to keep their blood sugar at normal levels.

Researchers damaged three components that are essential for mitochondrial function: their DNA, a pathway used to get rid of damaged mitochondria, and one that maintains a healthy pool of mitochondria in the cell.

“In all three cases, the exact same stress response was turned on, which caused β-cells to become immature, stop making enough insulin, and essentially stop being β-cells,” said Emily M. Walker, Ph.D, a research assistant professor of internal medicine and first author of the study.

“Our results demonstrate that the mitochondria can send signals to the nucleus and change the fate of the cell.”

The researchers also confirmed their findings in human pancreatic islet cells. The team repeated their mouse experiments in liver cells and fat-storing cells and saw that the same stress response was turned on. Both cell types were unable to mature and function properly.

Regardless of the cell type, the researchers found that damage to the mitochondria did not cause cell death. This observation brought up the possibility that if they could reverse the damage, the cells would function normally. To do so, they used a drug called ISRIB that blocked the stress response. They found that after four weeks, the β-cells regained their ability to control glucose levels in mice.

Reference: Emily M. Walker et al., Retrograde mitochondrial signaling governs the identity and maturity of metabolic tissues.Science0,eadf2034DOI:10.1126/science.adf2034

A new study found that heavy drinkers with either diabetes, high blood pressure or a high waist circumference are as much as 2.4 times more likely to develop advanced liver disease. The findings are published in Clinical Gastroenterology and Hepatology.

Diabetes, high blood pressure and a high waist circumference (35 inches for women; 40 inches for men), which is associated with obesity, belong to a cluster of five health conditions that influence an individual’s risk for heart attack and stroke known as cardiometabolic risk factors.

Cardiometabolic risk factors have been linked to the buildup of fat in the liver (also known as metabolic dysfunction-associated steatotic liver disease), which can lead to fibrosis, or scarring of the liver.

Researchers analyzed data from the National Health and Nutrition Examination Survey looking at the intersection of heavy drinking, individual cardiometabolic risk factors and the incidences of significant liver fibrosis. Significant liver fibrosis refers to liver scarring that can lead to liver failure.

For the study, heavy drinking was characterized as 1.5 drinks a day for women (20 grams) and two drinks a day for men (30 grams).

Researchers discovered that heavy drinkers with either diabetes or a high waist circumference were 2.4 times more likely to develop advanced liver disease and those with high blood pressure 1.8 times more likely. They found that the other two cardiometabolic risk factors — high triglycerides and low HDL had less significant correlations to liver disease.

Author emphasize that the study does not imply it is safe for those without these three cardiometabolic risks to consume large amounts of alcohol. “We know that alcohol is toxic to the liver and all heavy drinkers are at risk for advanced liver disease,” said Brian P. Lee, MD, MAS, a hepatologist and liver transplant specialist with Keck Medicine and principal investigator of the study.

Reference: Association of Alcohol and Incremental Cardiometabolic Risk Factors with Liver Disease: A National Cross-Sectional Study, Lee, Brian P. et al.Clinical Gastroenterology and Hepatology, Volume 0, Issue 0

Researchers in a new study showed that curcumin, the compound that gives turmeric its characteristic bright yellow color, can potentially be used to reduce antibiotic resistance.

The study showed that when curcumin is intentionally given to bacteria as food and then activated by light, it can trigger deleterious reactions within these microbes, eventually killing them. This process, they demonstrated, reduces the number of antibiotic-resistant strains and renders conventional antibiotics effective again. The results of the study are published in the journal Scientific Reports.

Photodynamic inactivation, a technique that has shown promise in combating bacterial resistance, uses light and light-sensitive molecules, called photosensitizers, to produce reactive oxygen species that can kill microorganisms by disrupting their metabolic processes. In their experiments, the team used curcumin, which is also a natural food for bacteria. They tested this technique on strains of Staphylococcus aureus that are resistant to amoxicillin, erythromycin, and gentamicin.

The researchers exposed the bacteria to many cycles of light exposure and then compared the minimum concentration of antibiotics needed to kill the bacteria after light exposure versus those that did not get light exposure.

The team noted that photodynamic inactivation using curcumin has tremendous potential as an adjuvant or additional therapy with antibiotics for diseases, like pneumonia, caused by antibiotic-resistant bacteria.

“When we have a mixed population of bacteria where some are resistant, we can use photodynamic inactivation to narrow the bacterial distribution, leaving behind strains that are more or less similar in their response to antibiotics,” said Dr. Vanderlei Bagnato, professor in the Department of Biomedical Engineering and senior author on the study. “It’s much easier now to predict the precise antibiotic dose needed to remove the infection.”

People’s ability to interpret emotions or focus on performing a task is reduced by short-term exposure to particulate matter (PM) air pollution, potentially making everyday activities, such as the weekly supermarket shop, more challenging, a new study reveals.

Scientists discovered that even brief exposure to high concentrations of PM may impair a person’s ability to focus on tasks, avoid distractions, and behave in a socially acceptable manner. Findings are published in Nature Communications.

Researchers exposed study participants to either high levels of air pollution - using candle smoke - or clean air, testing cognitive abilities before and four hours after exposure. The tests measured working memory, selective attention, emotion recognition, psychomotor speed, and sustained attention.

Researchers reveal that selective attention and emotion recognition were negatively affected by air pollution – regardless of whether subjects breathed normally or only through their mouths.

The experts suggest that inflammation caused by pollution may be responsible for these deficits noting that while selective attention and emotion recognition were affected, working memory was not. This indicates that some brain functions are more resilient to short-term pollution exposure.

Co-author Dr Thomas Faherty, from the University of Birmingham, commented: “Our study provides compelling evidence that even short-term exposure to particulate matter can have immediate negative effects on brain functions essential for daily activities, such as doing the weekly supermarket shop.”

Reference: Faherty, T., Raymond, J. E., McFiggans, G., & Pope, F. D. (2025). Acute particulate matter exposure diminishes executive cognitive functioning after four hours regardless of inhalation pathway. Nature Communications, 16(1), 1-14.