What is it about?
The bacteria in our gut convert nutrients from food into specific metabolites, and these are absorbed into our blood and supplied to the rest of the body, including skeletal muscle. To further our understanding of the relationship between gut bacteria and muscle, we examined the effect of phenolic metabolites derived from gut bacteria on the ability of human muscle cells to take up and metabolize glucose. As a model, we used differentiated human skeletal muscle cells, from the cell line LHCN-M2, which behave similarly to the muscle fibres in our body. We selected a panel of phenolic metabolites to test and found that several of them increased glucose uptake and metabolism, notably in muscle cells grown in high glucose and insulin (which mimics the conditions in the body of a type 2 diabetic). One of the most effective compounds was isovanillic acid 3-O-sulfate (IVAS), a metabolite that is converted by gut bacteria from cyanidin 3-O-glucoside, which is a major compound in berries. IVAS stimulated an increase in glucose transport through mechanisms that are also stimulated by insulin, and increased the levels of glucose transporters and insulin signalling pathway proteins, as well as activation of the insulin signalling pathway.
Photo by Devin Rajaram on Unsplash
Why is it important?
Our findings that the stimulation of glucose uptake and metabolism by a unique gut bacteria metabolite provides a novel link between diet, gut microbes and skeletal muscle energy source utilization. This is significant because it means that eating berries and such plant-derived foods could help to regulate blood glucose levels, which is especially important to those at risk of type 2 diabetes. Knowing that the foods we eat and our gut bacteria have an effect on metabolism in muscle also has implications for sporting performance and other aspects of health and disease involving skeletal muscle.
Read the Original
This page is a summary of: Gut microbiome catabolites as novel modulators of muscle cell glucose metabolism, The FASEB Journal, February 2019, Federation of American Societies For Experimental Biology (FASEB), DOI: 10.1096/fj.201801209r.
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Quercetin preserves redox status and stimulates mitochondrial function in metabolically-stressed HepG2 cells.
Another publication that came from my PhD, which explores the effects of quercetin on high glucose-induced oxidative stress, with associated mitochondrial damage and increased risk of insulin resistance and type 2 diabetes, in liver cells. Our results suggest that quercetin may protect mitochondrial function from high glucose-induced stress and enhance respiration, which is beneficial in certain metabolic diseases.
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