Increased Colonic Permeability and Lifestyles as Contributing Factors to Obesity and Liver Steatosis

Palo, Domenica Maria Di; Garruti, Gabriella; Ciaula, Agostino Di; Molina-Molina, Emilio; Shanmugam, Harshitha; Angelis, Maria De; Portincasa, Piero

doi:10.3390/nu12020564

Cited by 37 publications

(49 citation statements)

References 86 publications

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“…We assessed urine recovery of orally administered sucrose, lactulose/mannitol, and sucralose by using triple quadrupole mass-spectrometry and high-performance liquid chromatography. We found that increased colonic (but not stomach and small intestinal) permeability was linked to obesity and liver steatosis, regardless dietary habits, age, and physical activity [ 167 ] ( Figure 6 ).…”

Section: Beyond Nafld: the Gut Liver-axis The Gut Barrier And Thmentioning

confidence: 99%

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Liver Steatosis, Gut-Liver Axis, Microbiome and Environmental Factors. A Never-Ending Bidirectional Cross-Talk

Ciaula

Baj

Garruti

et al. 2020

JCM

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117

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The prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing worldwide and parallels comorbidities such as obesity, metabolic syndrome, dyslipidemia, and diabetes. Recent studies describe the presence of NAFLD in non-obese individuals, with mechanisms partially independent from excessive caloric intake. Increasing evidences, in particular, point towards a close interaction between dietary and environmental factors (including food contaminants), gut, blood flow, and liver metabolism, with pathways involving intestinal permeability, the composition of gut microbiota, bacterial products, immunity, local, and systemic inflammation. These factors play a critical role in the maintenance of intestinal, liver, and metabolic homeostasis. An anomalous or imbalanced gut microbial composition may favor an increased intestinal permeability, predisposing to portal translocation of microorganisms, microbial products, and cell wall components. These components form microbial-associated molecular patterns (MAMPs) or pathogen-associated molecular patterns (PAMPs), with potentials to interact in the intestine lamina propria enriched in immune cells, and in the liver at the level of the immune cells, i.e., Kupffer cells and stellate cells. The resulting inflammatory environment ultimately leads to liver fibrosis with potentials to progression towards necrotic and fibrotic changes, cirrhosis. and hepatocellular carcinoma. By contrast, measures able to modulate the composition of gut microbiota and to preserve gut vascular barrier might prevent or reverse NAFLD.

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Section: Beyond Nafld: the Gut Liver-axis The Gut Barrier And Thmentioning

confidence: 99%

“…Their presence in urine, in different amounts compared to the expected, indicated impaired permeability of the stomach, small intestine, or colon. Normal values for permeability test are expressed as a percentage) adapted from Di Palo et al [ 167 ]).…”

Section: Figurementioning

confidence: 99%

Liver Steatosis, Gut-Liver Axis, Microbiome and Environmental Factors. A Never-Ending Bidirectional Cross-Talk

Ciaula

Baj

Garruti

et al. 2020

JCM

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117

112

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“…(A) Initial role of wrong lifestyles (hypercaloric, unbalanced, fructose‐ and refined carbohydrate‐enriched diet, sedentary behaviour), on a genetic/racial, ethnical and environmental background. Changes in intestinal microbiota can also govern additional metabolic changes due to biotransformation of foods, local inflammatory changes, increased intestinal permeability 112 to bacterial products (ie lypopolisaccharides). (B) Expansion of visceral fat may occur in different phenotypes, independently of simple body weight (encompassing the term 'adiposity' or 'overfat').…”

Section: Introductionmentioning

confidence: 99%

COVID‐19 and non‐alcoholic fatty liver disease: Two intersecting pandemics

Portincasa

Krawczyk

Smyk

et al. 2020

Eur J Clin Investigation

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Background: Initial evidence from China suggests that most vulnerable subjects to COVID-19 infection suffer from pre-existing illness, including metabolic abnormalities. The pandemic characteristics and high-lethality rate of COVID-19 infection have raised concerns about interactions between virus pathobiology and components of the metabolic syndrome. Methods: We harmonized the information from the recent existing literature on COVID-19 acute pandemic and mechanisms of damage in non-alcoholic fatty liver disease (NAFLD), as an example of chronic (non-communicable) metabolic pandemic. Results: COVID-19-infected patients are more fragile with underlying metabolic illness, including hypertension, cardiovascular disease, type 2 diabetes, chronic lung diseases (e.g. asthma, chronic obstructive pulmonary disease and emphysema) and metabolic syndrome. During metabolic abnormalities, expansion of metabolically active fat ('overfat condition') parallels chronic inflammatory changes, development of insulin resistance and accumulation of fat in configuring NAFLD. The deleterious interplay of inflammatory pathways chronically active in NAFLD and acutely in COVID-19-infected patients, can explain liver damage in a subgroup of patients and might condition a worse outcome in metabolically compromised NAFLD patients. In a subgroup of patients with NAFLD, the underlying liver fibrosis might represent an additional and independent risk factor for severe COVID-19 illness, irrespective of metabolic comorbidities. Conclusions: NAFLD can play a role in the outcome of COVID-19 illness due to frequent association with comorbidities. Initial evidences suggest that increased liver fibrosis in NAFLD might affect COVID-19 outcome. In addition, long-term monitoring of post-COVID-19 NAFLD patients is advisable, to document further deterioration of liver damage. Further studies are required in this field.

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“…The malabsorption and the altered intestinal microbiota might facilitate, in patients with SIBO, the diffusion of products deriving from bacterial metabolism through the blood stream, thus contributing to the dissemination of pathogen associated molecular patterns (PAMPs) [ 162 , 163 ]. This condition might also interfere with a physiological intestinal permeability [ 164 ] as well as with the bioavailability of drugs [ 165 ]. SIBO could be responsible of unresponsiveness to colchicine, while SIBO decontamination therapy with rifaximin, a non-absorbable antibiotic, contributed to a decrease in FMF attacks [ 166 ].…”

Section: Gene-bacteria Interplay and Composition Of Gut Microbiotamentioning

confidence: 99%

Gut Microbiota between Environment and Genetic Background in Familial Mediterranean Fever (FMF)

Ciaula

Stella

Bonfrate

et al. 2020

Genes

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The gastrointestinal tract hosts the natural reservoir of microbiota since birth. The microbiota includes various bacteria that establish a progressively mutual relationship with the host. Of note, the composition of gut microbiota is rather individual-specific and, normally, depends on both the host genotype and environmental factors. The study of the bacterial profile in the gut demonstrates that dominant and minor phyla are present in the gastrointestinal tract with bacterial density gradually increasing in oro-aboral direction. The cross-talk between bacteria and host within the gut strongly contributes to the host metabolism, to structural and protective functions. Dysbiosis can develop following aging, diseases, inflammatory status, and antibiotic therapy. Growing evidences show a possible link between the microbiota and Familial Mediterranean Fever (FMF), through a shift of the relative abundance in microbial species. To which extent such perturbations of the microbiota are relevant in driving the phenotypic manifestations of FMF with respect to genetic background, remains to be further investigated.

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Increased Colonic Permeability and Lifestyles as Contributing Factors to Obesity and Liver Steatosis

Cited by 37 publications

References 86 publications

Liver Steatosis, Gut-Liver Axis, Microbiome and Environmental Factors. A Never-Ending Bidirectional Cross-Talk

Liver Steatosis, Gut-Liver Axis, Microbiome and Environmental Factors. A Never-Ending Bidirectional Cross-Talk

COVID‐19 and non‐alcoholic fatty liver disease: Two intersecting pandemics

Gut Microbiota between Environment and Genetic Background in Familial Mediterranean Fever (FMF)

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