Different host-specific responses in thyroid function and gut microbiota modulation between diet-induced obese and normal mice given the same dose of iodine
“…Iodine supplementation decreased Faecalibacterium prausnizii, Lactobacillus, and Bifidobacterium in high-fat fed mice. These findings demonstrate that iodine supplementation can alter host metabolism and the composition of the gut microbiome, where obesity or dietary lipids influence the effect of iodine (Shen et al 2019).…”
Section: Iodinementioning
confidence: 71%
“…Excess iodine in obese high-fat diet mice resulted in weight loss, reduced adiposity and liver weight, and increased circulating thyroid hormone concentrations. Oral iodine supplementation altered the gut flora in obese high-fat fed and lean mice (Shen et al 2019). Iodine supplementation increased the relative abundance of Oscillibacter and Allobaculum and decreased Blautia in both lean and obese mice.…”
Section: Iodinementioning
confidence: 97%
“…Excess iodine in mice can increase adiposity, body weight, and liver weight, with variability in circulating thyroid hormones, including decreased total T4 and thyroid-stimulating hormone and increased free T3 and T4 (Shen et al 2019). However, obesity may influence the effects of iodine supplementation.…”
Micronutrients influence hormone action and host metabolism. Dietary minerals, trace elements and vitamins can alter blood glucose and cellular glucose metabolism and several micronutrients are associated with risk and progression of type 2 diabetes. Dietary components, microbes and host immune, endocrine, and metabolic responses all interact in the intestine. There has been a focus on macronutrients modifying the host-microbe relationship in metabolic disease. Micronutrients are positioned to alter host-microbe symbiosis that participates in host endocrine control of glucose metabolism. Minerals and trace elements can alter the composition of the intestinal microbiota, gut barrier function, compartmentalized metabolic inflammation, cellular glucose transport and endocrine control of glucose metabolism, including insulin and thyroid hormones. Dietary vitamins also influence the composition of the intestinal microbiota and vitamins can be biotransformed by gut microbes. Host-microbe regulation of vitamins can alter immunity, lipid and glucose metabolism, and cell fate and function of pancreatic beta cells. Causal effects of micronutrients in host-microbe metabolism are still emerging and the mechanisms linking dietary excess or deficiency of specific micronutrients to changes in gut microbes directly linked to metabolic disease risk are not yet clear. Dietary fiber, fat, protein, and carbohydrates are key dietary factors that impact how microbes participate in host glucose metabolism. It is possible that micronutrient and microbiota-derived factors also participate in host-microbe responses that tip the balance in endocrine control of host glucose metabolism. Dietary micronutrients should be considered, tested, and controlled in preclinical and clinical studies investigating host-microbe factors in metabolic diseases.
“…Iodine supplementation decreased Faecalibacterium prausnizii, Lactobacillus, and Bifidobacterium in high-fat fed mice. These findings demonstrate that iodine supplementation can alter host metabolism and the composition of the gut microbiome, where obesity or dietary lipids influence the effect of iodine (Shen et al 2019).…”
Section: Iodinementioning
confidence: 71%
“…Excess iodine in obese high-fat diet mice resulted in weight loss, reduced adiposity and liver weight, and increased circulating thyroid hormone concentrations. Oral iodine supplementation altered the gut flora in obese high-fat fed and lean mice (Shen et al 2019). Iodine supplementation increased the relative abundance of Oscillibacter and Allobaculum and decreased Blautia in both lean and obese mice.…”
Section: Iodinementioning
confidence: 97%
“…Excess iodine in mice can increase adiposity, body weight, and liver weight, with variability in circulating thyroid hormones, including decreased total T4 and thyroid-stimulating hormone and increased free T3 and T4 (Shen et al 2019). However, obesity may influence the effects of iodine supplementation.…”
Micronutrients influence hormone action and host metabolism. Dietary minerals, trace elements and vitamins can alter blood glucose and cellular glucose metabolism and several micronutrients are associated with risk and progression of type 2 diabetes. Dietary components, microbes and host immune, endocrine, and metabolic responses all interact in the intestine. There has been a focus on macronutrients modifying the host-microbe relationship in metabolic disease. Micronutrients are positioned to alter host-microbe symbiosis that participates in host endocrine control of glucose metabolism. Minerals and trace elements can alter the composition of the intestinal microbiota, gut barrier function, compartmentalized metabolic inflammation, cellular glucose transport and endocrine control of glucose metabolism, including insulin and thyroid hormones. Dietary vitamins also influence the composition of the intestinal microbiota and vitamins can be biotransformed by gut microbes. Host-microbe regulation of vitamins can alter immunity, lipid and glucose metabolism, and cell fate and function of pancreatic beta cells. Causal effects of micronutrients in host-microbe metabolism are still emerging and the mechanisms linking dietary excess or deficiency of specific micronutrients to changes in gut microbes directly linked to metabolic disease risk are not yet clear. Dietary fiber, fat, protein, and carbohydrates are key dietary factors that impact how microbes participate in host glucose metabolism. It is possible that micronutrient and microbiota-derived factors also participate in host-microbe responses that tip the balance in endocrine control of host glucose metabolism. Dietary micronutrients should be considered, tested, and controlled in preclinical and clinical studies investigating host-microbe factors in metabolic diseases.
“…Although the evidence is limited to only one animal study, it suggests that iodine supplementation is dependent on the levels of fat in the diet and results in differential effects on the gut microbiome [159]. Iodine supplementation in an HFD mouse model improved the thyroid hormone status, but resulted in a gut dysbiosis characterized by an increased abundance of pathogenic microbes and a depletion of beneficial microbes, such as Fecalibacterium prausnizii [159]. Alternatively, when the diet was low in fat, the same dose of iodine had beneficial effects on gut microbiota by increasing Bifidobacterium, Lactobacillus, Fecalibacterium, and Allobaculuum in the control group [159].…”
Understanding how dietary nutrients modulate the gut microbiome is of great interest for the development of food products and eating patterns for combatting the global burden of non-communicable diseases. In this narrative review we assess scientific studies published from 2005 to 2019 that evaluated the effect of micro- and macro-nutrients on the composition of the gut microbiome using in vitro and in vivo models, and human clinical trials. The clinical evidence for micronutrients is less clear and generally lacking. However, preclinical evidence suggests that red wine- and tea-derived polyphenols and vitamin D can modulate potentially beneficial bacteria. Current research shows consistent clinical evidence that dietary fibers, including arabinoxylans, galacto-oligosaccharides, inulin, and oligofructose, promote a range of beneficial bacteria and suppress potentially detrimental species. The preclinical evidence suggests that both the quantity and type of fat modulate both beneficial and potentially detrimental microbes, as well as the Firmicutes/Bacteroides ratio in the gut. Clinical and preclinical studies suggest that the type and amount of proteins in the diet has substantial and differential effects on the gut microbiota. Further clinical investigation of the effect of micronutrients and macronutrients on the microbiome and metabolome is warranted, along with understanding how this influences host health.
“…Administration of KIO3 in these animals led to weight reduction, increased concentration of thyroid hormones, alteration in the expression of the genes involved in thyroid biosynthesis, and cause various effects on the gut microbiota, changing the composition of the intestinal microenvironment, resulting in an imbalance of gut microbes: increases in pathogenic bacteria (Enterococcus, Clostridium, Fusobacterium nucleatum, Burkholderiales, Helicobacter), decrease in beneficial ones (Lactobacilli, Bifidobacteria), quite the contrary to what has been observed in non-obese hosts (p < 0.05). Therefore, even with iodine dosages considered safe, obesity and quantitative and qualitative changes in the microbiota can increase the risk of thyroid dysfunction (10). Frohlich and Wahl concluded in their review that the composition of the microbiota and the different representation of its individual components in the various parts of the gastrointestinal system influence the absorption of I − , also modifying the enterohepatic circulation of thyroid hormones.…”
The human microbiota is an integral component in the maintenance of health and of the immune system. Microbiome-wide association studies have found numerous diseases associated to dysbiosis. Studies are needed to move beyond correlations and begin to address causation. Autoimmune thyroid diseases (ATD) are one of the most common organ-specific autoimmune disorders with an increasing prevalence, higher than 5% worldwide. Most frequent manifestations of ATD are Hashimoto’s thyroiditis and Graves’ disease. The exact etiology of ATD remains unknown. Until now it is not clear whether bacterial infections can trigger ATD or modulate the efficacy of treatment and prognosis. The aim of our review is to characterize the microbiota and in ATD and to evaluate the impact of dysbiosis on treatment and prognosis. Moreover, variation of gut microbiome has been associated with thyroid cancer and benign nodules. Here we will characterize the microbioma in benign thyroid nodules, and papillary thyroid cancer to evaluate their implications in the pathophysiology and progression.
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