Obesity is an all-too common condition, and one that poses a number of health risks. Aside from cardiovascular and joint damage, obesity also weakens our immune responses.
This study investigated the link between probiotic supplementation and the strength of invariant natural killer T cells (iNKT cells). These specialized T cells work along a wide range of duties to help keep infections at bay, and prevent weight gain. But in cases of obesity, they are depleted. Whether that is an effect of weight gain overwhelming the body’s natural ability to prevent too much adipose formation, or if the obesity is a cause of already-low iNKT is still being worked out.
In any event, in this animal study, researchers found that probiotic supplementation not only restored the levels of immune-protecting iNKT cells, it also improved metabolism and alleviated obesity in mice fed a high-fat diet.
The results of this work is another example of the wide range of probiotic activity. Generally considered important for relieving digestive disorders, replenishing probiotics may be key to almost every aspect of good health.
Wang X, Ba T, Cheng Y, Zhang P, Chang X. Probiotics alleviate adipose inflammation in high-fat diet-induced obesity by restoring adipose invariant natural killer T cells. Nutrition. Available online 25 April 2021, 111285. https://doi.org/10.1016/j.nut.2021.111285
Objective: Invariant natural killer T (iNKT) cells, which are depleted in obese individuals, play important roles in preventing diet-induced obesity and associated disorders. Probiotic supplementation can alter the gut microbiota and immunomodulation in obesity. However, it remains unclear whether probiotics can affect visceral adipose iNKT cells.
Methods: Wild-type (WT) male C57BL/6 mice and CD1d knockout (CD1dKO) mice were fed a high-fat diet (HFD) or normal-fat diet (NFD). Some mice received active or heat-killed VSL#3 probiotics. Preventative VSL#3 therapy was also administered to HFD mice. Body weight, metabolic parameters, expression of genes encoding adipose inflammatory factors (IL-4, IL-10, TNF-α, IFN-γ, and IL-6), adipose iNKT cell frequency, and sub-phenotype were evaluated.
Results: HFD induced more severe obesity in CD1dKO mice than in WT mice. VSL#3 intervention significantly improved HFD-induced weight gain, adipose iNKT cell depletion, and metabolic and adipose inflammatory profiles in WT mice, but not in CD1dKO mice. Preventative VSL#3 treatment improved HFD-induced obesity and metabolic parameters, and elevated total adipose iNKT and IL-4+ iNKT cell frequencies.
Conclusions: Probiotic intervention alleviated weight gain, improved metabolic parameters, and reduced adipose inflammation in HFD-induced obesity. These effects seem to depend on the restoration of visceral adipose iNKT cells. These findings have potential implications for the management of obesity-related diseases.
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