Monday, October 3, 2022
HomeSports MedicineDietary sugar could disrupt intestine microbiota and induce metabolic problems

Dietary sugar could disrupt intestine microbiota and induce metabolic problems

A examine revealed within the journal Cell demonstrates that dietary sugar will increase the chance of metabolic syndrome by disrupting intestine microbiota and suppressing protecting T helper 17 (Th17) cells.

Research: Microbiota imbalance induced by dietary sugar disrupts immune-mediated safety from metabolic syndrome. Picture Credit score: Alpha Tauri 3D Graphics/Shutterstock


Consumption of a high-fat weight-reduction plan will increase the chance of diabetes, weight problems, heart problems, and metabolic syndrome. Though the causative hyperlink between a high-fat weight-reduction plan and metabolic threat isn’t fully identified, it has been hypothesized that diet-induced intestinal irritation could be a potential contributor.

The intestinal immune system is considered an important regulator of metabolic homeostasis. CD4 T cells are main regulators of intestinal immune responses to dietary antigens. Research have recognized sure cell varieties that exhibit each selling and protecting results in metabolic syndrome. These cell varieties are Th17 cells and sort 3 innate lymphoid cells (ILC3).

The intestine microbiota performs an important function in regulating intestinal immune responses, together with Th17 cell and ILC3 responses. Excessive-fat diet-induced adjustments in intestine microbiota composition is understood to advertise metabolic syndrome by altering vitality metabolism and immune responses.

Within the present examine, scientists have decided the connection between microbiota-controlled intestinal immune responses and diet-induced weight problems and metabolic syndrome.

Impression of a high-fat weight-reduction plan in metabolic syndrome

The comparability of immune responses induced by commonplace weight-reduction plan and high-fat weight-reduction plan in mice revealed that high-fat weight-reduction plan induces the signs of metabolic syndrome, together with physique weight acquire, insulin resistance, and glucose intolerance.

Relating to intestinal immunity, high-fat weight-reduction plan was discovered to considerably cut back the expression and performance of Th17 cells. The weight-reduction plan additionally diminished the secretion of interleukin 17 (IL-17), a cytokine produced by Th17 cells.

Mechanistically, high-fat weight-reduction plan prompted a fast lack of commensal microbiota liable for inducing Th17 cells. This subsequently led to important depletion of Th17 cells earlier than the event of metabolic syndrome.

Additional experiments revealed that commensal microbiota-induced Th17 cells play a necessary function in guaranteeing microbiota-mediated safety towards high-fat diet-related weight problems and metabolic syndrome.

Impression of dietary sugar in metabolic syndrome

Three main dangerous elements of high-fat weight-reduction plan embrace extra fats, low dietary fiber, and excessive sugar content material. Of those elements, excessive stage of sugar was recognized as the principle causal issue of diet-induced weight problems and metabolic syndrome.

Mechanistically, dietary sugar promoted the expansion of Faecalibaculum rodentium in an ILC3-dependent method. The overgrowth of this Gram-positive bacterium displaced the commensal intestine microbiota, resulting in a depletion of intestinal commensal Th17 cells and subsequent diet-mediated induction of weight problems and metabolic syndrome in mice.

Nevertheless, the findings revealed that the elimination of dietary sugar isn’t enough to make sure safety. Restoration of Th17 expression and performance by immune therapies can be required to guard the mice towards diet-induced metabolic problems.

Th17 cell-mediated safety towards metabolic syndrome

Absorption of dietary lipid by intestinal epithelial cells is a identified regulator of metabolic syndrome. Th17 cell-secreting cytokine IL-17 is understood to keep up intestinal barrier integrity by regulating epithelial cells.

The lipid content material measurement in numerous tissues of mice fed with a high-fat weight-reduction plan revealed that within the presence of Th17 cells, intestinal epithelial cells take in a lesser quantity of dietary lipid. Mechanistically, Th-17 cell-secreted IL-17 suppressed the epithelial expression of fatty acid transporter CD36, resulting in diminished lipid uptake and absorption throughout the intestinal epithelium.  

Research significance

The examine gives an interactome of dietary elements, intestine microbiota, and intestinal immune cells that regulate the pathophysiology of high-fat diet-induced metabolic problems, resembling weight problems, sort 2 diabetes, and metabolic syndrome.

The examine identifies dietary sugar as the most important deleterious part of a high-fat weight-reduction plan to extend the chance of metabolic problems. Based mostly on the findings, dietary modifications, along with immune interventions, are required to make sure full safety towards diet-induced metabolic problems.

As talked about by the scientists, the examine solely focuses on the early levels of metabolic adjustments induced by a high-fat weight-reduction plan. Since diet-induced intestinal irritation doesn’t happen at early time factors, future research are required to decipher the long-term results and protecting mechanisms of Th17 cells in systemic illness.



Please enter your comment!
Please enter your name here

Most Popular

Recent Comments