Sugar can have a surprising impact on obesity and the human gut, study finds
Dietary sugar can alter the gut microbiome, setting off a chain of events that leads to metabolic disease, pre-diabetes, and weight gain. (CREDIT: Creative Commons)
Recent research led by Dr. Ivaylo Ivanov, an associate professor of microbiology & immunology at Columbia University Vagelos College of Physicians and Surgeons, has shed light on the intricate relationship between dietary sugar, the gut microbiome, and the development of metabolic disease, pre-diabetes, and weight gain.
This groundbreaking study, published in the prestigious journal Cell, brings forth compelling evidence that underscores the significance of maintaining a balanced diet alongside a healthy gut microbiome to stave off metabolic syndrome, diabetes, and obesity.
Dietary Sugar Alters the Microbiome
The prevalence of Western-style diets, characterized by high levels of both fat and sugar, has been strongly linked to the emergence of obesity, metabolic syndrome, and diabetes. Yet, until now, the precise mechanisms through which these diets initiate detrimental changes in the body have remained a mystery.
Image of segmented filamentous bacteria in the mouse intestine from Ivalyo Ivanov, Columbia University Irving Medical Center.
Dr. Ivanov and his team embarked on a journey to unravel this enigma by investigating the initial effects of a Western-style diet on the gut microbiome of mice.
Upon subjecting mice to this diet for a mere four weeks, a remarkable transformation occurred within their bodies. They exhibited hallmark signs of metabolic syndrome, including weight gain, insulin resistance, and glucose intolerance.
Concurrently, their gut microbiomes underwent dramatic alterations. A notable decline in segmented filamentous bacteria, commonly found in the gut microbiota of rodents, fish, and chickens, was observed. In their stead, other bacterial populations increased in abundance.
Microbiome Changes Uncover the Role of Th17 Cells
The reduction in filamentous bacteria, the researchers discovered, held the key to understanding the mice's deteriorating health. This microbial shift had a profound impact on Th17 immune cells within the gut.
Notably, the decrease in filamentous bacteria led to a corresponding reduction in Th17 cells, which proved to be pivotal in preventing metabolic disease, diabetes, and weight gain.
Dr. Ivanov elaborated on this connection, stating, "These immune cells produce molecules that slow down the absorption of 'bad' lipids from the intestines and they decrease intestinal inflammation. In other words, they keep the gut healthy and protect the body from absorbing pathogenic lipids."
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A significant revelation emerged from the study regarding the role of dietary components in this intricate process. The research team discovered that sugar was the primary culprit responsible for the depletion of filamentous bacteria and the subsequent disappearance of protective Th17 cells.
Dr. Ivanov emphasized this finding, explaining, "Sugar eliminates the filamentous bacteria, and the protective Th17 cells disappear as a consequence. When we fed mice a sugar-free, high-fat diet, they retained the intestinal Th17 cells and were completely protected from developing obesity and pre-diabetes, even though they ate the same number of calories."
However, it's important to note that the absence of sugar did not yield the same positive results for all mice. In cases where mice lacked any filamentous bacteria to begin with, eliminating sugar failed to exert any beneficial effects, leading to obesity and diabetes.
Microbiota-induced Th17 cells protect from diet-induced obesity and metabolic disease. Sugar eliminates commensal Th17 cells to increase the risk for metabolic disease. (CREDIT: Cell)
"This suggests that some popular dietary interventions, such as minimizing sugars, may only work in people who have certain bacterial populations within their microbiota," Dr. Ivanov pointed out. In such instances, certain probiotics could offer a potential solution.
In the study, supplementing mice with filamentous bacteria facilitated the recovery of Th17 cells, affording protection against metabolic syndrome despite the continued consumption of a high-fat diet.
Dietary sugar displaces Th17 microbiota by increasing Faecalibaculum rodentium. (CREDIT: Cell)
While humans do not possess the same filamentous bacteria as mice, Dr. Ivanov remains optimistic about the potential therapeutic implications. He believes that other bacterial species present in the human microbiome may exert similar protective effects.
An intriguing aspect of the study is the profound impact of Th17 cells on overall protection against metabolic diseases. Dr. Ivanov stressed, "Microbiota are important, but the real protection comes from the Th17 cells induced by the bacteria."
This insight opens up avenues for potential therapeutic interventions that target Th17 cell induction to bolster the body's defenses against metabolic disorders.
As the scientific community continues to delve deeper into the intricate mechanisms that underlie metabolic diseases, this research serves as a beacon of hope, offering potential strategies to mitigate the growing health challenges associated with obesity and related conditions.
The findings reinforce the idea that a holistic approach, encompassing diet, microbiome health, and immune system support, may hold the key to a healthier future for individuals at risk of metabolic disorders.
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