A study published in the journal cell It demonstrates that dietary sugar increases the risk of metabolic syndrome by disrupting the gut microbiota and suppressing protective T helper 17 (Th17) cells.
Consuming a high-fat diet increases the risk of diabetes, obesity, cardiovascular disease, and metabolic syndrome. Although the causal relationship between a high-fat diet and metabolic risk is not fully known, it has been hypothesized that diet-induced intestinal inflammation could be a potential contributor.
The intestinal immune system is a vital regulator of metabolic homeostasis. CD4 T cells are key regulators of the intestinal immune responses to food antigens. Studies have identified specific cell types that show both pro- and protective effects in metabolic syndrome. These cell types are Th17 cells and innate lymphoid type 3 (ILC3) cells.
Gut bacteria play an important role in regulating intestinal immune responses, including Th17 cell responses and ILC3 responses. It is known that diet-induced changes high in fat in the composition of the gut microbiota promote the metabolic syndrome by altering energy metabolism and immune responses.
In the current study, scientists determined the relationship between bacteria-controlled intestinal immune responses and diet-induced obesity and metabolic syndrome.
The effect of a high-fat diet on metabolic syndrome
Comparison of immune responses elicited by the standard diet and the high-fat diet in mice revealed that the high-fat diet induces symptoms of metabolic syndrome, including increased body weight, insulin resistance and glucose intolerance.
With regard to intestinal immunity, a high-fat diet was found to significantly reduce the expression and function of Th17 cells. The diet also reduced the secretion of interleukin 17 (IL-17), a cytokine produced by Th17 cells.
Mechanistically, the high-fat diet caused a rapid loss of the commensal microbes responsible for stimulating Th17 cells. This subsequently resulted in a significant depletion of Th17 cells before the development of metabolic syndrome.
Further experiments revealed that Th17 cells induced by commensal microbes play an essential role in ensuring the protection of the microorganism against high-fat diet-related obesity and metabolic syndrome.
The effect of dietary sugar on metabolic syndrome
Three main harmful components of a high-fat diet include excess fat, low dietary fiber, and high sugar content. Among these components, hyperglycemia has been identified as the main causative factor for diet-induced obesity and metabolic syndrome.
Mechanistically, dietary sugar promoted growth rodent feces in an ILC3-dependent manner. The overgrowth of these Gram-positive bacteria displaced the commensal gut microbiota, Leading to depletion of gut Th17 commensal cells and subsequent diet-mediated induction of obesity and metabolic syndrome in mice.
However, the results revealed that eliminating dietary sugar is not sufficient to ensure protection. Restoration of Th17 expression and function by immunotherapies is also required to protect mice from diet-induced metabolic complications.
Th17 cell-mediated protection against metabolic syndrome
The uptake of dietary fat by intestinal epithelial cells is a well-known regulator of the metabolic syndrome. The Th17-secreted cytokine IL-17 is known to maintain the integrity of the intestinal barrier by regulating epithelial cells.
Measurement of lipid content in different tissues of mice fed a high-fat diet showed that in the presence of Th17 cells, intestinal epithelial cells absorbed less dietary fat. Mechanistically, IL-17 secreted by the Th-17 cell suppressed the epithelial expression of the fatty acid transporter CD36, resulting in reduced uptake and uptake of lipids through the intestinal epithelium.
Study the importance
The study provides an interaction between nutritional components, gut microbes, and intestinal immune cells that regulate the pathophysiology of diet-induced high-fat metabolic complications, such as obesity, type 2 diabetes and metabolic syndrome.
The study identifies dietary sugar as the main harmful component of a high-fat diet to increase the risk of metabolic disorders. Based on the findings, dietary modifications are required, along with immunological interventions, to ensure complete protection against diet-induced metabolic disorders.
As the scientists mentioned, the study focuses only on the early stages of metabolic changes caused by a high-fat diet. Since diet-induced intestinal inflammation does not occur at early time points, future studies are required to decipher the long-term effects and protective mechanisms of Th17 cells in systemic diseases.
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