The browser you are using is not supported by this website. All versions of Internet Explorer are no longer supported, either by us or Microsoft (read more here: https://www.microsoft.com/en-us/microsoft-365/windows/end-of-ie-support).

Please use a modern browser to fully experience our website, such as the newest versions of Edge, Chrome, Firefox or Safari etc.

A diet rich on fat and sugar damaged the memory in mice – but not permanently

Photo of soft drink and french fries.
A diet rich in sugar and fat led to memory impairment in mice, but the damage does not have to be permanent.

Food impacts not only the body but also the brain. Researchers at Lund University strive to understand how a diet rich on fat and sugar impacts memory functions in relation to obesity and type 2 diabetes. Their new study on mice shows that although an unhealthy diet leads to memory impairment, the damage does not have to be permanent.

Obesity is a risk factor for developing type 2 diabetes and cardiovascular diseases. These diseases may, in turn, increase the risk for dementia and Alzheimer’s disease. Previous research has shown that a diet rich in fat and sugar induces obesity and diabetes in mice, and may impact their memory. Until now, it has been unknown whether the damage to the brain is temporary or permanent. 

Researchers at Lund University have investigated how a diet rich in fat and sugar altered the hippocampus and cortex in mice of both genders. Their study shows that animals who were given a diet rich in fat and sugar displayed major metabolic alterations in the hippocampus and cortex, and also had impaired memory. 

“An important result of this study is that we could see that the impairments do not have to be permanent. We saw the same results in mice of both genders,” says Joao Duarte, a researcher in diabetes and brain function at Lund University Diabetes Centre (LUDC) and one of the main authors behind the study in the scientific journal Aging and Disease. 

Behavioral experiments

A total of 72 mice were included in the study and randomly assigned to three experimental groups. One group had a diet that consisted of 60 percent saturated fat and sugary drink for four months followed by a diet low in fat for two months. Another group was given the diet of 60 percent fat and sugary drink during six months. The third group was given a control diet of ten percent fat. 

The researchers assessed brain metabolites over time with magnetic resonance spectroscopy (MRS). A metabolite is a byproduct of breakdown of any substance in tissues and organs. The metabolic profile of the brain may reflect alterations in energy levels, neuron communication and cell death.  Several behavioral experiments were carried out to study the impact of the diet in the memory functions of the mice.

“Our measurements with magnetic resonance spectroscopy show that mice who had been given unhealthy foods had an altered metabolic profile compared to animals who had eaten more healthy foods. We could also see that an unhealthy diet led to memory impairment. However, the brain structure and important memory functions were restored in mice who were assigned to the group who first had a diet high in fat followed by a reversed diet low in fat. This is a very positive result,” Joao Duarte.

”Healthier ageing”

Memory functions were studied in object recognition tasks, where the ability to recognise new objects was assessed. Animals who were given a diet high in fat did not explore new objects to the same extent as mice who had a diet low in fat. Mice who were assigned to the group who had a high fat diet followed by a period of a diet low in fat recovered their ability to recognise new objects. 

The knowledge may contribute to a healthier ageing for people with type 2 diabetes. The disease requires lifelong treatment and may lead to different complications. There is no cure against dementia and Alzheimer’s disease.

“It is hard to conduct a similar study in human beings, and we have to keep in mind that research on mice has its limitations. However, metabolism supporting brain function is very similar in the two species. We believe that our results are robust and add to the evidence base that an unhealthy diet may harm important cognitive functions. It is important that people with type 2 diabetes are encouraged to develop a healthy lifestyle, as this may contribute to better ageing without dementia,” says Joao Duarte, affiliated with Wallenberg Centre for Molecular Medicine (WCMM).

Hippocampus and the cerebral cortex

Hippocampus is a region of the human brain associated with memory. The hippocampus is thought to be principally involved in storing and retrieving long-term memories. It also plays an important role in spatial processing and navigation. 

The cerebral cortex is the outer layer of the brain and is divided into fields with different functions. This part of the brain controls higher functions such as speech, thinking and memory in humans. 

The function of hippocampus and cerebral cortex is similar in mice. The cerebral cortex is much more developed in humans. 

Photo of the researcher behind the study.

Contact

Joao Duarte
Senior lecturer and researcher at Lund University Diabetes Centre and Wallenberg Centre for Molecular Medicine

+46 724 52 56 31 
joao [dot] duarte [at] med [dot] lu [dot] se

Link to Joao Duarte’s profile in Lund University’s research portal

Quick facts

Research subject: Brain metabolism, obesity and diabetes
Research area: Basic research
Study design: Quantitative study, researcher-initiated study, animal study with 72 male and female mice
Experimental investigation: In vivo, randomized intervention
Observational study: Longitudinal

Link to the study on the website of Aging and Disease

Funders

Swedish Research Council, Crafoord Foundation, Diabetesfonden, Direktör Albert Påhlssons stiftelse, Demensfonden, Royal Physiographic Society of Lund, Stiftelsen Lars Hiertas Minne, Swedish foundation for International Cooperation in Research and Higher Education, and Young IBRO Regions Connecting Award. The Knut and Alice Wallenberg foundation, the Medical Faculty at Lund University and Region Skåne are acknowledged for generous financial support. The study has been supported by Lund University Diabetes Centre, which is funded by the Swedish Research Council (the strategic research area EXODIAB) and the Swedish Foundation for Strategic Research.