Circulating microbiota-derived metabolites: a “liquid biopsy?

Aragonès, Gemma; Colom‐Pellicer, Marina; Aguilar, Carmen; Guiu‐Jurado, Esther; Martínez, Salomé; Sabench, Fàtima; Porras, José Antonio; Riesco, David; Castillo, Daniel Del; Richart, C; Auguet, Teresa

doi:10.1038/s41366-019-0430-0

Cited by 58 publications

(53 citation statements)

References 47 publications

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“…Moreover, the jejunal HTR expression was analyzed for the first time in women with NAFLD in the present study. In a previous work of our group, we reported that the intestine–liver axis is very important in NAFLD [ 8 ]. As stated previously, intestinal dysbiosis disrupts gut homeostasis and may affect serotonin synthesis [ 57 ].…”

Section: Discussionmentioning

confidence: 99%

“…In this sense, the gut–liver axis plays a key role in the progression of NAFLD. Changes in the microbial composition generated by a high-fat diet (HFD) or high-carbohydrate diet (HCD) give rise to a release of metabolites derived from the microbiota that have a negative impact on liver metabolism, promoting the development of metabolic diseases such as NAFLD [ 8 ]. On the other hand, the release into the bloodstream of histamine synthesized by intestinal mast cells [ 9 ], or enterochromaffin (EC) cell-derived serotonin [ 10 ] also promote liver metabolic dysregulation, leading to steatosis and liver inflammation.…”

Section: Introductionmentioning

confidence: 99%

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Deregulated Serotonin Pathway in Women with Morbid Obesity and NAFLD

Binetti

Bertran

Riesco

et al. 2020

Life

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Non-alcoholic fatty liver disease (NAFLD) extends from simple steatosis (SS) to non-alcoholic steatohepatitis (NASH). Peripheral serotonin (5-HT) has become as an important regulator of different metabolic pathways. 5-HT has been related to obesity and lipid accumulation in the liver. The objective of this study was to assess the relationship between the 5-HT signaling pathway and the degree of NAFLD, as well as to investigate whether peripheral 5-HT levels are related to the hepatic and jejunal mRNA abundance of serotonin receptors (HTR) in a cohort of women with morbid obesity (MO) and NAFLD. ELISA was used to quantify the serum 5-HT from normal-weight subjects (n = 26) and patients with MO (n = 58). We used RTq-PCR analysis to evaluate the relative expression of HTR in women with MO with normal liver (n = 22), SS (n = 21), and NASH (n = 15). The 5-HT was diminished in women with MO under a hypocaloric diet, regardless of the presence of NAFLD. Additionally, we report a negative correlation of 5-HT levels with metabolic syndrome criteria, suggesting that serotonin may have a protective role in obesity. Additionally, the hepatic expression of HTR2A and HTR2B were decreased in women with MO and NAFLD, but no significant differences in the HTR jejunal expression according to the presence of NAFLD were found.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Deregulated Serotonin Pathway in Women with Morbid Obesity and NAFLD

Binetti

Bertran

Riesco

et al. 2020

Life

Self Cite

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“…Inflammasome key protein complexes when activated induce cell apoptosis and proinflammatory cells release and are essential in host defences mechanism. NLRP3 inflammasome contributes through gut microbiota to control the NAFLD/obesity progression via overproduction of leptin, downregulation of adiponectin generation, and promotion of fibrosis [101]. Circulating microbiota-derived metabolites could be used for NAFLD diagnosis [102].…”

Section: Adipokinesmentioning

confidence: 99%

The Intricate Relationship between Type 2 Diabetes Mellitus (T2DM), Insulin Resistance (IR), and Nonalcoholic Fatty Liver Disease (NAFLD)

Tănase

Gosav

Costea

et al. 2020

Journal of Diabetes Research

276

180

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Nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes mellitus (T2DM) remain as one of the most global problematic metabolic diseases with rapidly increasing prevalence and incidence. Epidemiological studies noted that T2DM patients have by two-fold increase to develop NAFLD, and vice versa. This complex and intricate association is supported and mediated by insulin resistance (IR). In this review, we discuss the NAFLD immunopathogenesis, connection with IR and T2DM, the role of screening and noninvasive tools, and mostly the impact of the current antidiabetic drugs on steatosis liver and new potential therapeutic targets.

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“…As expected, in the NAFLD patients, mRNA expression of fatty acid synthase (FAS, a key enzyme in the hepatic de novo lipogenesis) increased, together with the LPS receptors TLR2 and TLR4. Consequently, the circulating levels of gut microbiota-derived metabolites were analyzed observing that TMAO, glycocholic acid and deoxycholic acid plasma levels were significantly increased in NAFLD patients, suggesting the use of circulating microbiota-derived metabolites as a scoring system for the clinical diagnosis of NAFLD [45]. The up-regulation of lipogenic genes due to a high intake of saturated fatty acids (SFAs) triggers triglyceride (TG) formation [46].…”

Section: Role Of Diet In Nafld Progression and Gut Microbiota Dysbiosismentioning

confidence: 99%

Diet, Gut Microbiota and Non-Alcoholic Fatty Liver Disease: Three Parts of the Same Axis

Quesada-Vázquez

Aragonès

Bas

et al. 2020

Cells

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Non-Alcoholic Fatty Liver Disease (NAFLD) is the most common liver disease in the world. NAFLD is principally characterized by an excessive fat accumulation in the hepatocytes. Diet is considered as one of the main drivers to modulate the composition of gut microbiota, which participate in different processes, affecting human metabolism. A disruption in the homeostasis of gut microbiota may lead to dysbiosis, which is commonly reflected by a reduction of the beneficial species and an increment in pathogenic microbiota. Gut and liver are in close relation due to the anatomical and functional interactions led by the portal vein, thus altered intestinal microbiota might affect liver functions, promoting inflammation, insulin resistance and steatosis, which is translated into NAFLD. This review will highlight the association between diet, gut microbiota and liver, and how this axis may promote the development of NAFLD progression, discussing potential mechanisms and alterations due to the dysbiosis of gut microbiota. Finally, it will revise the variations in gut microbiota composition in NAFLD, and it will focus in specific species, which directly affect NAFLD progression.

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Circulating microbiota-derived metabolites: a “liquid biopsy?

Cited by 58 publications

References 47 publications

Deregulated Serotonin Pathway in Women with Morbid Obesity and NAFLD

Deregulated Serotonin Pathway in Women with Morbid Obesity and NAFLD

The Intricate Relationship between Type 2 Diabetes Mellitus (T2DM), Insulin Resistance (IR), and Nonalcoholic Fatty Liver Disease (NAFLD)

Diet, Gut Microbiota and Non-Alcoholic Fatty Liver Disease: Three Parts of the Same Axis

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