Pregnant women who suffer from metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as non-alcoholic fatty liver disease, are more likely to give birth prematurely. A new study published in the journal eClinicalMedicine has found that these women have a significantly higher risk of preterm birth, and this increased risk cannot be attributed solely to their weight or obesity.

According to the research conducted by Karolinska Institutet, one in five people in Sweden may have MASLD, while globally, it could affect as many as three out of ten individuals. Common risk factors for developing the disease include metabolic disorders like type 2 diabetes and being overweight or obese. The study’s findings are based on Swedish registry data and included a total of 240 births among women with MASLD, along with 1140 matched births from the general population.

Alarmingly, the research revealed that women with MASLD were more than three times as likely to give birth prematurely compared to those without the disease. This increased risk persisted even after adjusting for factors such as weight and metabolic disorders. The study’s lead author suggests that this association may not solely be due to a high BMI, implying that the liver disease itself could have negative effects on pregnancy outcomes.

Moreover, women with MASLD had a 63 percent higher risk of caesarean section compared to the control group. However, this increased risk seemed to be explained by their high BMI, as no significant difference was observed when comparing them to overweight or obese women without fatty liver disease.

While the study’s findings are concerning, it is essential to note that MASLD itself did not increase the risk of congenital malformations in the children born to these women. The authors acknowledge that their research may have been influenced by other factors and emphasize the importance of closely monitoring pregnant women with MASLD to reduce the risk of complications.

The study’s conclusions highlight the need for specific recommendations regarding pregnancy care for women with MASLD, which could potentially be added to clinical guidelines for managing the disease.

The intricate dance of protein quality control within cells has been revealed by researchers led by biochemist Alexander Buchberger at Julius-Maximilians-Universität Würzburg (JMU). A recent study published in Nature Communications sheds light on the crucial role played by the ubiquitin-selective unfoldase p97/VCP enzyme in eliminating malformed proteins and aggresomes.

In cells, proteins are constantly being produced, assembled, transported, and broken down. This delicate balance is vital to prevent serious illnesses, as even small changes can have devastating consequences. To maintain this balance, cells have developed complex systems to control protein quality. One such system involves the formation of aggresomes – a type of cage that collects and isolates proteins prone to clumping.

While the formation of aggresomes has been extensively studied, their protein content and degradation pathways remained poorly characterized. The recent study changes this by revealing that the breakdown of aggresomes requires multiple players, with p97/VCP enzyme emerging as the most critical.

The researchers conducted experiments blocking p97/VCP enzyme and observed that aggresomes no longer disintegrated and were destroyed. This indicates that p97/VCP plays a pivotal role in breaking down aggresomes into smaller components. The findings have significant biomedical implications, particularly for understanding neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s disease.

Mutations in the p97/VCP enzyme cause neuro-muscular degenerative diseases, including certain forms of dementia and ALS – amyotrophic lateral sclerosis. Moreover, disrupted degradation processes within cells could also contribute to Parkinson’s disease, which is characterized by Lewy bodies – roundish inclusions containing harmful protein deposits that disrupt nerve cell metabolism.

The research team concludes that their findings suggest mutations in the p97/VCP enzyme disrupt aggresome degradation, potentially contributing to Lewy body formation and neuro-muscular degenerative diseases. This study highlights the importance of understanding protein quality control mechanisms within cells and how disruptions in these processes can lead to devastating diseases.

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).