The Role of Intestinal Bacteria Overgrowth in Obesity-Related Nonalcoholic Fatty Liver Disease

Ferolla, S; Armiliato, Geyza N. A.; Couto, Cláudia Alves; Ferrari, Teresa Cristina Abreu

doi:10.3390/nu6125583

Cited by 94 publications

(86 citation statements)

References 72 publications

(150 reference statements)

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“…The data from animal studies support the concept that the gut bacteria may contribute to NAFLD via multiple mechanisms (Table 1), including regulation of energy homeostasis [6, 7] with the increased fermentation of carbohydrates to short chain fatty acids (SCFAs) and subsequent stimulation of de novo synthesis of triglycerides in the liver [8, 9]; modulation of endocannabinoid system [10, 11]; modulation of choline metabolism (which is required for very-low-density lipoprotein synthesis and hepatic lipid export) [12, 13]; modulation of bile acid homeostasis [14, 15]; the ability to generate endogenous ethanol [16, 17]; and bacteria-derived toxins (e.g., lipopolysaccharides (LPS)), which may activate pro-inflammatory cytokine production in the liver macrophages resulting in hepatocellular inflammation [4]. Small intestine bacterial overgrowth (SIBO) has also been linked to NASH pathogenesis [18, 19] [20]. The gut microbiota may also contribute to hepatic fibrosis via stimulation of Toll-like receptor (TLR)-9-dependent profibrotic pathways in hepatic Kupffer cells [21].…”

Section: Introductionmentioning

confidence: 99%

Gut–liver axis, nutrition, and non-alcoholic fatty liver disease

Kirpich

Marsano

McClain

2015

Clinical Biochemistry

264

176

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Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of diseases involving hepatic fat accumulation, inflammation with the potential progression to fibrosis and cirrhosis over time. NAFLD is often associated with obesity, insulin resistance, and diabetes. The interactions between the liver and the gut, the so-called ”gut-liver axis”, play a critical role in NAFLD onset and progression. Compelling evidence links the gut microbiome, intestinal barrier integrity, and NAFLD. The dietary factors may alter the gut microbiota and intestinal barrier function, favoring the occurrence of metabolic endotoxemia and low grade inflammation, thereby contributing to the development of obesity and obesity-associated fatty liver disease. Therapeutic manipulations with prebiotics and probiotics to modulate the gut microbiota and maintain intestinal barrier integrity are potential agents for NAFLD management. This review summarizes the current knowledge regarding the complex interplay between the gut microbiota, intestinal barrier, and dietary factors in NAFLD pathogenesis. The concepts addressed in this review have important clinical implications, although more work needs to be done to understand how dietary factors affect the gut barrier and microbiota, and to comprehend how microbe-derived components may interfere with the host’s metabolism contributing to NAFLD development.

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Section: Introductionmentioning

confidence: 99%

Gut–liver axis, nutrition, and non-alcoholic fatty liver disease

Kirpich

Marsano

McClain

2015

Clinical Biochemistry

264

176

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“…The diagnosis of small intestinal bacterial overgrowth (SIBO) is applied to patients when the concentration of bacteria exceeds 10 5 organisms per milliliter in the jejunum and ileum 33, 34. Not surprisingly, patients with SIBO have increased circulating levels of bacterial endotoxin 35, 36…”

Section: Bacterial Endotoxin In Relation To Chiropractic Practicementioning

confidence: 99%

“…Third, patients who suffer from postprandial abdominal bloating that occurs within 1 hour of eating could be considered “toxic.” In the absence of gluten sensitivity, celiac disease, or other gastrointestinal tract pathologic conditions, the most common cause of such bloating is the fermentation of consumed carbohydrates by an overgrown small intestine bacterial population,32, 49 which leads to endotoxemia 35, 36. Postprandial bloating is an almost universal symptom in patients with irritable bowel syndrome 32 .…”

Section: Measuring Bacterial Endotoxin Levelsmentioning

confidence: 99%

Toxins, Toxicity, and Endotoxemia: A Historical and Clinical Perspective for Chiropractors

Seaman

2016

Journal of Chiropractic Humanities

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ObjectiveThe purpose of this commentary is to review the notion of toxicity in the context of chiropractic practice.DiscussionThe belief that body toxicity is the cause of disease has been promoted for thousands of years. Prior to the emergence of the chiropractic profession, the medical profession embraced the notion that the body becomes “toxic,” requiring detoxification interventions or surgery. The legacy of body toxicity within the chiropractic approach to patient care began with Daniel David Palmer. Today, some sectors within the medical and chiropractic professions continue to embrace the concept of body toxicity and the related need to engage in detoxifying treatments. The most common areas of focus for detoxification are the intestines and liver; however, the nature of the toxicity in these organs has yet to be defined or measured. In contrast, diet-induced systemic bacterial endotoxemia is a measureable state that is known to be promoted by a diet rich in sugar, flour, and refined oil. This suggests that bacterial endotoxin may be a candidate toxin to consider in the clinical context, as many common conditions, such as obesity, metabolic syndrome, diabetes, interstitial cystitis, depression, and migraine headache, are known to be promoted by endotoxemia.ConclusionA diet rich in refined sugar, flour, and oils may induce proinflammatory changes within intestinal microbiota that lead to systemic, low-grade endotoxemia, which is a common variety of “toxicity” that is measurable and worthy of research consideration. Introducing a diet to reduce endotoxemia, rather than attempting to target a specific organ, appears to be a rational clinical approach for addressing the issue of toxicity.

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“…The authors concluded that visceral adipose contributing to overall lipidome was secondary to that of other sources of the drainage into the hepatic portal system, for example, the gut. While this is by no means a novel suggestion in the field of NASH [5][6][7], the exact mechanism of this contribution has yet to be demonstrated.…”

mentioning

confidence: 92%

“…It is evident that the changes in the lipid profiles within the liver, the adipose tissue and the plasma, accompany NAFLD, however, the contribution of these changes to the pathogenesis of this disease remain enigmatic [5]. In the current paper titled ''Circulating phospholipid profiling identifies portal contribution to NASH signature in obesity,'' Anjani and colleagues used mass spectrometry-based lipidomic analysis to dissect this so-called Non-Alcoholic Steatohepatitis (NASH) ''signature'' in a cohort of 46 morbidly obese women.…”

mentioning

confidence: 99%