Eating olive oil before carbs has a surprising effect on blood sugar

 

New findings suggest that meal order could become a practical tool for managing blood sugar, although human studies are still needed. Credit: Shutterstock

The order in which you eat different foods may have a surprising effect on blood sugar levels. Research in mice suggests that consuming fat before carbohydrates can reduce the sharp rise in blood sugar that typically follows a meal. The findings also reveal how hormones and nerve signals work together to influence this response.

Keeping blood sugar from rising too high after eating is an important part of diabetes management. Previous clinical studies have shown that eating vegetables, protein, or fat before carbohydrates can help limit these increases. This suggests that changing the sequence of foods during a meal could offer a practical, sustainable way to improve blood sugar control without eliminating entire food groups.

Scientists have generally explained this effect through two main mechanisms. The first is slower gastric emptying, which means food moves from the stomach into the small intestine more gradually. The second involves increased release of hormones called incretins, including GLP-1, which help the body regulate blood sugar.

However, researchers have not fully understood how hormones produced by the gut and pancreas interact with the nervous system to produce these effects. To investigate, an international research team examined how consuming fat before or after glucose influences blood sugar, hormone activity, and the speed at which the stomach empties.

"Our group has long been interested in practical dietary approaches that people can continue in everyday life," says corresponding author Daisuke Yabe of Kyoto University. "Meal-sequencing is appealing because it merely changes how a meal is eaten rather than requiring people to avoid entire food groups."

Testing How Olive Oil Changes Blood Sugar Levels

The researchers conducted a series of experiments in mice to determine whether the timing of fat consumption affected how the body processed glucose.

After an overnight fast, the mice were assigned to three groups. One group received water followed by glucose. A second group was given olive oil, followed 15 minutes later by glucose. The third group received glucose first, with olive oil administered 15 minutes afterward.

The scientists then measured blood glucose levels and several hormones involved in blood sugar regulation, including insulin, glucagon, GIP, and GLP-1. Glucagon is normally associated with increasing blood sugar, while GIP and GLP-1 help regulate glucose levels after eating.

To determine how quickly material was leaving the stomach, the researchers also administered acetaminophen, a common pain reliever. By measuring how much of the drug appeared in the bloodstream after oral administration, they could estimate the rate of gastric emptying.

The team extended the experiments to additional groups of mice, including animals with type 2 diabetes and others that lacked the receptor needed to respond to GLP-1.

They also performed experiments that blocked glucagon or GLP-1 signaling, surgically interrupted the vagus nerves below the diaphragm on both sides, and examined whether different dietary fats produced similar results. The vagus nerve is an important communication pathway between the brain and digestive system, helping coordinate functions such as digestion and hormone release.

Eating Fat First Slows Blood Sugar Spikes

The results showed a clear difference depending on when the mice received olive oil.

When olive oil was given before glucose, the initial rise in blood sugar was smaller than when the oil was administered afterward. The earlier fat intake also slowed gastric emptying, delaying the movement of glucose from the stomach into the intestine.

At the same time, consuming fat before glucose stimulated an early increase in several hormones, including glucagon, GIP, and GLP-1.

Importantly, these effects were also observed in mice with type 2 diabetes and severe insulin deficiency. This suggested that the response could still function even when normal insulin regulation was significantly impaired.

A Surprising Role for a Blood Sugar Hormone

One of the most unexpected findings involved glucagon, a hormone generally known for raising blood sugar by stimulating the liver to release stored glucose.

The researchers discovered that blocking glucagon signaling alone did not eliminate the blood sugar lowering effect of consuming olive oil before glucose. Blocking GLP-1 signaling by itself also failed to remove the benefit.

However, when both signaling pathways were blocked simultaneously, the beneficial effect was reduced.

This finding suggests that glucagon and GLP-1 work together as part of a more complex system that helps moderate blood sugar after fat is consumed before carbohydrates. It also reveals that glucagon, despite its familiar role in increasing blood sugar, can contribute to a response that ultimately limits the rise in glucose after eating.

The vagus nerve experiments provided another important clue. When the researchers interrupted these nerve pathways, the results suggested that communication through the vagus nerve also contributes to the body's response to nutrient order.

Together, these findings point to a coordinated interaction between digestive hormones, pancreatic signals, and the nervous system.

Could Changing Meal Order Help Manage Diabetes?

The findings offer a clearer biological explanation for why eating fat before carbohydrates may help reduce blood sugar spikes. Rather than relying on a single hormone or digestive process, the effect appears to involve multiple systems working together to control how quickly glucose enters the intestine.

This could have practical implications for diabetes management. Adjusting the order in which foods are eaten is relatively simple and may be easier to maintain than diets that require avoiding particular food groups.

However, the experiments were conducted in mice, and the same effects have not yet been established in humans through this research. Additional clinical studies will be needed to determine whether the mechanisms identified in the experiments can be used to improve blood sugar regulation in people with or without diabetes.

"Our findings suggest that the order in which nutrients reach the gut can engage a coordinated hormone-nerve response that changes how quickly the stomach delivers glucose to the intestine," says Yabe.

Journal Reference:

1. Yanyan Liu, Hiromi Tsuchida, Sodai Kubota, Saki Kubota-Okamoto, Takehiro Kato, Yukio Horikawa, Shin Tsunekawa, Hitoshi Kuwata, Yuuka Fujiwara, Yuji Yamazaki, Yuichiro Yamada, Hiroki Fujita, Katsumi Iizuka, Naoya Murao, Shinji Ueno, Yusuke Seino, Atsushi Suzuki, Yoshitaka Hayashi, Tsuyoshi Nakanishi, Daniel J. Drucker, Takahiko Shiina, Yasutake Shimizu, Yusaku Iwasaki, Toshihiko Yada, Yohei Seno, Yuya Takahashi, Toshinori Imaizumi, Takaaki Murakami, Michael Horowitz, Yutaka Seino, Daisuke Yabe. Olive Oil Before Oral Glucose Delays Gastric Emptying and Lowers Glycemia Through Partially Redundant Glucagon and GLP-1 Signaling in Mice. Diabetes, 2026; DOI: 10.2337/db26-0531

Courtesy:

Kyoto University. "Eating olive oil before carbs has a surprising effect on blood sugar." ScienceDaily. ScienceDaily, 11 October 2026. <www.sciencedaily.com / releases / 2026 / 10 / 261008102700.htm>.

 

 

 

A plastic once thought harmless may be fueling fatty liver disease

 

Scientists have discovered that polyethylene, a plastic commonly found in food packaging and containers, may contribute to fatty liver disease and make its effects worse when combined with an unhealthy diet. Credit: Shutterstock

Microplastics have spread into nearly every corner of the environment. These tiny plastic particles have been found in ocean water, drinking water, and even inside the human body. Although their presence is well documented, scientists are still working to understand what prolonged exposure could mean for human health.

Researchers at the Texas A&M College of Veterinary Medicine and Biomedical Sciences (VMBS) have now identified a potential health concern involving polyethylene, one of the most widely used plastics in the world. Their findings suggest that polyethylene microplastics may contribute to fatty liver disease, particularly when exposure occurs alongside an unhealthy diet.

Polyethylene accounts for approximately one-third of plastic production worldwide. It is used in numerous everyday products, including food wrappers, storage containers, plastic packaging, and the linings of beverage cups. Despite its widespread use, scientists have devoted relatively little attention to its potential effects on the liver compared with other types of microplastics.

"No studies have really looked into polyethylene's effect on liver health, and it's the most widely produced plastic," said Dr. Adi Joshi, associate professor in VMBS' Department of Veterinary Physiology and Pharmacology. "What we now know is that these microplastics, especially polyethylene, affect our liver's natural defense and repair mechanisms."

Common Microplastics May Contribute to Fatty Liver Disease

To investigate the possible health effects of polyethylene, Joshi and his colleagues examined whether exposure to this common plastic could promote fatty liver disease.

The condition develops when excessive fat accumulates inside liver cells. According to the American Liver Foundation, it affects approximately 25% of people worldwide, making it a major global health concern.

The researchers discovered that polyethylene exposure increased indicators of fatty liver disease even without the added influence of an unhealthy diet. When the plastic was combined with a diet rich in fat, fructose, and cholesterol, the signs of liver disease became more severe.

These results suggest that exposure to environmental pollutants and poor dietary habits may reinforce each other's harmful effects, potentially worsening liver damage.

"Those who have a more Western-style diet, including foods like burgers and sodas, may have a greater chance of progressing to fatty liver disease if they are also exposed to polyethylene," Joshi said.

The results were especially unexpected because polyethylene has traditionally been regarded as a relatively biologically inert material. In other words, scientists generally considered it less likely to interact with biological systems than more reactive substances.

However, the findings indicate that polyethylene may influence liver function in ways that were previously overlooked. Its effects appeared both independently and alongside dietary risk factors, raising important questions about how this common plastic interacts with the body's metabolism and protective mechanisms.

Scientists Pinpoint How Microplastics Affect the Liver

Understanding where and how polyethylene causes biological changes could help explain its potential role in liver disease.

To investigate these effects in greater detail, the Texas A&M team partnered with scientists at the University of Oklahoma and applied a powerful technique called spatial transcriptomics.

This technology allows researchers to study gene activity while preserving information about where individual cells are located within a tissue. Rather than simply measuring which genes are active, scientists can identify precisely where biological changes are occurring.

Using this approach, the team mapped areas of liver damage associated with polyethylene exposure and identified molecular pathways that may help explain the effects.

One important finding involved PPAR-alpha, a protein that helps regulate fat metabolism in the liver. The researchers found that polyethylene activated this protein, suggesting that it plays a significant role in the liver's response to microplastics.

They also identified ANXA2, a gene associated with tissue repair, as another possible contributor to the disease process.

Together, these discoveries provide a more detailed picture of how polyethylene may interfere with the liver's normal functions, including the mechanisms involved in protecting and repairing damaged tissue.

Joshi believes that understanding these biological pathways could eventually help researchers identify potential treatments that reduce the harmful effects of microplastic exposure.

Could Microplastics Contribute to More Serious Liver Damage?

Although the findings reveal a previously underexplored connection between polyethylene and fatty liver disease, several important questions remain unanswered.

The researchers plan to investigate whether polyethylene exposure could contribute to more advanced forms of liver disease, including fibrosis. This condition occurs when repeated or ongoing liver damage leads to the accumulation of scar tissue, which can interfere with the organ's ability to function properly.

The team also intends to examine other molecular processes involved in the liver's response to polyethylene. One particular focus will be determining whether targeting the PPAR-alpha pathway could help protect the liver against microplastic-related damage.

"This is the pioneering study showing that polyethylene can contribute to fatty liver disease and the use of spatial transcriptomics has determined exactly where the damage has happened within the liver," Joshi said. "The other microplastics might also be harmful to the liver, and we definitely need to look into other classes of microplastics."

The findings add to growing concerns about the possible health consequences of microplastics, although further research is needed to establish how these experimental observations translate to everyday human exposure.

For Joshi, the discovery highlights why scientists need to look beyond familiar risk factors such as diet when investigating chronic diseases. As research continues, understanding how common environmental pollutants interact with the body could reveal previously unrecognized contributors to long-term health problems.

Journal Reference:

1. Woncheol Jung, Hassan Abushukair, Nikhil Y. Patil, Felix Ampadu, Maryam Firouzi, Iulia Rus, Jinhyuk Choi, Sree Deepthi Muthukrishnan, Surendra Shukla, Stefano Tarantini, Anna Csiszar, Kamiya Mehla, Dongin Kim, Je-Hyun Yoon, Dowoon Kim, Juyang Kim, Jaehak Jung, Oxana Klementieva, Yatrik M. Shah, Eiji Yoshihara, Pankaj K. Singh, Aditya D. Joshi, Tae Gyu Oh. Spatial transcriptome mapping identifies Ppara-Anxa2 cross-talk in microplastic-induced hepatotoxicity. Science Advances, 2026; 12 (25) DOI: 10.1126/sciadv.aec8681

Courtesy:

Texas A&M University. "A plastic once thought harmless may be fueling fatty liver disease." ScienceDaily. ScienceDaily, 10 October 2026. <www.sciencedaily.com / releases / 2026 / 10 / 261008102718.htm>.