Fructose liquid and solid formulations differently affect gut integrity, microbiota composition and related liver toxicity: a comparative in vivo study

Mastrocola, Raffaella; Ferrocino, Ilario; Liberto, Erica; Chiazza, Fausto; Cento, Alessia Sofia; Collotta, Debora; Querio, Giulia; Nigro, Debora; Bitonto, Valeria; Cutrìn, Juan Carlos; Rantsiou, Kalliopi; Durante, Mariaconcetta; Masini, Emanuela; Aragno, Manuela; Cordero, Chiara Emilia Irma; Cocolin, Luca Simone; Collino, Massimo

doi:10.1016/j.jnutbio.2018.02.003

Cited by 59 publications

(48 citation statements)

References 71 publications

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“…Mastrocola et al showed that a fructose diet, especially in solid form, resulted in gut dysbiosis, with increased colonization by Bacteroides, Lactobacillus, Lachnospiraceae, and Dorea and the accumulation of the AGEs N (epsilon)-(carboxymethyl)lysine and N(epsilon)-(carboxyethyl)lysine in the intestinal mucosa as revealed by immunofluorescence [198]. Qu et al demonstrated that Sprague-Dawley rats exposed to a high-AGE diet showed richness of the microbiota, especially saccharolytic bacteria, such as Ruminococcaceae and Alloprevotella, although some putatively harmful bacteria (Desulfovibrio and Bacteroides) were also increased [199].…”

Section: Gut-heart Crosstalk and Inflammation In The Development Of Cvdmentioning

confidence: 99%

Gut microbiota and inflammation in chronic kidney disease and their roles in the development of cardiovascular disease

et al. 2018

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The health and proper functioning of the cardiovascular and renal systems largely depend on crosstalk in the gut-kidney-heart/vessel triangle. Recent evidence suggests that the gut microbiota has an integral function in this crosstalk. Mounting evidence indicates that the development of chronic kidney and cardiovascular diseases follows chronic inflammatory processes that are affected by the gut microbiota via various immune, metabolic, endocrine, and neurologic pathways. Additionally, deterioration of the function of the cardiovascular and renal systems has been reported to disrupt the original gut microbiota composition, further contributing to the advancement of chronic cardiovascular and renal diseases. Considering the interaction between the gut microbiota and the renal and cardiovascular systems, we can infer that interventions for the gut microbiota through diet and possibly some medications can prevent/stop the vicious cycle between the gut microbiota and the cardiovascular/renal systems, leading to a decrease in chronic cardiovascular and renal diseases.

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Section: Gut-heart Crosstalk and Inflammation In The Development Of Cvdmentioning

confidence: 99%

Gut microbiota and inflammation in chronic kidney disease and their roles in the development of cardiovascular disease

et al. 2018

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“…Previous studies have shown that different dietary regimens alter the microbial composition or dysbiosis in the gut, and can alter the development and maintenance of MeS [9]. Moreover, fructose consumption is specifically linked to gut microbial dysbiosis [10][11][12], suggesting that the metabolic changes are mediated by the microbiome [10,13,14].…”

Section: Introductionmentioning

confidence: 99%

Antibiotic Treatment Does Not Ameliorate the Metabolic Changes in Rats Presenting Dysbiosis After Consuming a High Fructose Diet

et al. 2020

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High fructose consumption is one of the hallmarks of Western diets and has been found to induce MeS symptoms in parallel to gut microbial dysbiosis. However, the causality between those two is still elusive. Here, we studied whether a significant modification of gut microbial composition by antibiotics can influence the fructose-induced metabolic changes. Male Sprague-Dawley (SD) rats were divided into four groups including controls, controls + antibiotics, high fructose diet (HFrD, 60% fructose), HFrD + antibiotics (n = 7–8 in each group) for a period of 8-weeks. The high fructose diet increased blood pressure (BP), triglyceride (TG), fatty liver and the expression of hepatic genes related to lipogenesis, and fructose transport and metabolism. In addition, fructose changed the microbial composition and increased acetic and butyric acids in fecal samples but not in the blood. Antibiotic treatment significantly reduced microbial diversity and modified the microbial composition in the samples. However, minimal or no effect was seen in the metabolic phenotypes. In conclusion, high fructose consumption (60%) induced metabolic changes and dysbiosis in rats. However, antibiotic treatment did not reverse the metabolic phenotype. Therefore, the metabolic changes are probably independent of a specific microbiome profile.

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“…Alterations in the relative abundance of other gut microbiota were also observed at different time points in Sprague-Dawley rats fed a high-fat, high-sucrose diet [37]. Another study suggests that different forms of fructose consumption can change gut microbiota, intestinal mucosa integrity, and liver homeostasis [38]. The authors found that L-Ruminococcus, Coprococcus and R-Ruminococcus were increased, and the Firmicutes/Bacteroidetes ratio was decreased, in mice fed with fructose in comparison to a standard diet [38].…”

Section: Carbohydrate Interaction With Gut Microbiotamentioning

confidence: 93%

“…Another study suggests that different forms of fructose consumption can change gut microbiota, intestinal mucosa integrity, and liver homeostasis [38]. The authors found that L-Ruminococcus, Coprococcus and R-Ruminococcus were increased, and the Firmicutes/Bacteroidetes ratio was decreased, in mice fed with fructose in comparison to a standard diet [38]. Llewellyn et al reported that different types of carbohydrates altered gut microbiota density and intestinal permeability, affecting colitis severity in mice [39].…”

Section: Carbohydrate Interaction With Gut Microbiotamentioning

confidence: 99%

Role of Gut Microbiota in Neuroendocrine Regulation of Carbohydrate and Lipid Metabolism via the Microbiota-Gut-Brain-Liver Axis

2020

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Gut microbiota play an important role in maintaining intestinal health and are involved in the metabolism of carbohydrates, lipids, and amino acids. Recent studies have shown that the central nervous system (CNS) and enteric nervous system (ENS) can interact with gut microbiota to regulate nutrient metabolism. The vagal nerve system communicates between the CNS and ENS to control gastrointestinal tract functions and feeding behavior. Vagal afferent neurons also express receptors for gut peptides that are secreted from enteroendocrine cells (EECs), such as cholecystokinin (CCK), ghrelin, leptin, peptide tyrosine tyrosine (PYY), glucagon-like peptide-1 (GLP-1), and 5-hydroxytryptamine (5-HT; serotonin). Gut microbiota can regulate levels of these gut peptides to influence the vagal afferent pathway and thus regulate intestinal metabolism via the microbiota-gut-brain axis. In addition, bile acids, short-chain fatty acids (SCFAs), trimethylamine-N-oxide (TMAO), and Immunoglobulin A (IgA) can also exert metabolic control through the microbiota-gut-liver axis. This review is mainly focused on the role of gut microbiota in neuroendocrine regulation of nutrient metabolism via the microbiota-gut-brain-liver axis.2 of 21 formate, acetate, propionate, and butyrate, which are related to maintaining intestinal epithelium and permeability [11]. Further, SCFAs regulate glucose and lipid metabolism as well as immune and inflammatory responses [12,13]. Hence, gut microbiota also plays an important role in immune systems, inflammation, and cancer prevention of the host [14,15]. The enteric nervous system (ENS) is reported to be involved in intestinal metabolic regulation, and enteric neurons and intestinal neurotransmitters play an important role in ENS regulation [16][17][18]. The gut contains full ENS reflex circuits, such as motor neurons, interneurons, and sensory neurons, and these neurons transfer information between the ENS and central nervous system (CNS). The vagal nerve pathway communicates between the CNS and ENS, which has remarkable impact on regulating gastrointestinal tract functions and feeding behavior [19,20]. Thus, the vagal nerve system is also involved in intestinal metabolic regulation through the gut-brain axis. Vagal afferent neurons express receptors for gut peptides, such as cholecystokinin (CCK), ghrelin, leptin, peptide tyrosine tyrosine (PYY), glucagon-like peptide-1 (GLP-1), 5-hydroxytryptamine (5-HT) and so on, which are secreted from enteroendocrine cells (EECs) [20][21][22]. When vagal afferent neurons sense these types of gut peptides, the corresponding gut information will transfer to the CNS and exert various reactions. At the same time, gut microbiota can regulate these gut peptides, such as CCK, ghrelin, leptin, PYY, GLP-1, 5-HT levels to influence vagal afferent pathway, and then regulated intestinal metabolic metabolism via the microbiota-gut-brain axis [23][24][25].The importance of the gut-brain axis in human health and disease has been known for a long period. However, it has only been re...

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Fructose liquid and solid formulations differently affect gut integrity, microbiota composition and related liver toxicity: a comparative in vivo study

Cited by 59 publications

References 71 publications

Gut microbiota and inflammation in chronic kidney disease and their roles in the development of cardiovascular disease

Gut microbiota and inflammation in chronic kidney disease and their roles in the development of cardiovascular disease

Antibiotic Treatment Does Not Ameliorate the Metabolic Changes in Rats Presenting Dysbiosis After Consuming a High Fructose Diet

Role of Gut Microbiota in Neuroendocrine Regulation of Carbohydrate and Lipid Metabolism via the Microbiota-Gut-Brain-Liver Axis

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