Mice Exposed to High-Sugar Diet More Susceptible to IBD, Especially Colitis, Study Shows

Mice Exposed to High-Sugar Diet More Susceptible to IBD, Especially Colitis, Study Shows
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A high-sugar diet may increase susceptibility to inflammatory bowel diseases (IBD), and specifically colitis, a study in mice suggests.

Titled “A high-sugar diet rapidly enhances susceptibility to colitis via depletion of luminal short-chain fatty acids in mice,” the study was published in the journal Scientific Reports.

Although the importance of diet in the development of inflammatory bowel disease (IBD) remains unclear, dietary factors do appear to play a role in triggering disease flares.

Researchers at the University of Alberta were particularly interested in the impact of a “western diet” — a diet high in fat and refined sugars — on IBD.

To date, most studies that have investigated the impact of a western diet on IBD have focused on either a high-fat diet alone or a high-fat diet in combination with high sugar. Therefore, the isolated effect of a high-sugar diet on IBD is not well-understood.

To learn more, the researchers set out to investigate the impact of short-term dietary exposure to high sugar on a person’s susceptibility to colitis, one of the two major forms of IBD.

The investigators used healthy adult mice from the same litter that were fed either regular chow (control group) or a high-sugar diet.

After two days on the diet, the mice were treated with dextran sodium sulfate (DSS) to induce colitis. This is one of the most common methods of establishing a mouse model of IBD.

Disease severity was assessed daily. Mice were sacrificed at day 10 and tissue from the colon was analyzed for markers of inflammation.

Additionally, researchers measured gut permeability — the degree to which compounds and cells can pass from inside the gut into the rest of the body — and the population of microbes (gut microbiome) that colonize the intestine.

Maintenance of gut permeability, diversity of different microbial groups, and production of short-chain fatty acids (SCFAs) from gut microbes are all required for optimal intestinal health.

Mice that were on a high-sugar diet were found to have increased gut permeability, decreased microbial diversity, and reduced SCFAs compared with mice that were on a normal diet.

The researchers speculate that a loss of SCFA-producing microbes, as well as loss of overall microbial diversity, is likely responsible for the reduction in SCFAs in mice on the high-sugar diet.

“It’s been previously shown that the type of diet that you are on can change your susceptibility to disease,” Karen L. Madsen, lead author of the study, said in a press release.

“We wanted to know how long it takes before a change in diet translates into an impact on health. In the case of sugar and colitis, it only took two days, which was really surprising to us. We didn’t think it would happen so quickly,” Madsen said.

Next, researchers obtained bone marrow-derived macrophages (BMDM), a type of immune cell, from the mice. BMDM were then incubated with LPS, a component of bacteria.

BMDM obtained from high-sugar-fed mice were significantly more responsive to LPS and secreted high levels of pro-inflammatory cytokines compared with chow-fed mice, the study showed.

Hence, high-sugar-fed mice had increased susceptibility to inflammation and colitis compared with chow-fed mice.

The researchers concluded that a high-sugar diet plays a role in “the triggering and perpetuation of inflammation in patients with inflammatory bowel disease.” High sugar levels led to the colon’s “lack of ability to repair damage.”

“Surprisingly, our study shows that short-term sugar consumption can really have a detrimental impact, and so this idea that it’s OK to eat well all week and indulge in junk food on the weekend is flawed,” Madsen said.

One of the study’s major findings is that a high-sugar diet leads to a reduction in the levels of short-chain fatty acids. Madsen said the results suggest that SCFAs could possibly be used as supplements to protect the body against the detrimental effects of sugar — namely the higher risk of IBD — and may aid tissue repair.

Follow-up studies could pave the wayfor such use, she said.

“Changing someone’s diet is one of the hardest things to do, even if you tell them that it will fix their health problems,” Madsen said.

Iqra holds a MSc in Cellular and Molecular Medicine from the University of Ottawa in Ottawa, Canada. She also holds a BSc in Life Sciences from Queen’s University in Kingston, Canada. Currently, she is completing a PhD in Laboratory Medicine and Pathobiology from the University of Toronto in Toronto, Canada. Her research has ranged from across various disease areas including Alzheimer’s disease, myelodysplastic syndrome, bleeding disorders and rare pediatric brain tumors.
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Margarida graduated with a BS in Health Sciences from the University of Lisbon and a MSc in Biotechnology from Instituto Superior Técnico (IST-UL). She worked as a molecular biologist research associate at a Cambridge UK-based biotech company that discovers and develops therapeutic, fully human monoclonal antibodies.
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Iqra holds a MSc in Cellular and Molecular Medicine from the University of Ottawa in Ottawa, Canada. She also holds a BSc in Life Sciences from Queen’s University in Kingston, Canada. Currently, she is completing a PhD in Laboratory Medicine and Pathobiology from the University of Toronto in Toronto, Canada. Her research has ranged from across various disease areas including Alzheimer’s disease, myelodysplastic syndrome, bleeding disorders and rare pediatric brain tumors.
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