Metabolic endotoxemia with obesity: Is it real and is it relevant?

The emerging evidence on the interconnectedness between the gut microbiome and host metabolism has led to a paradigm shift in the study of metabolic diseases such as obesity and type 2 diabetes with implications on both underlying pathophysiology and potential treatment. Mounting preclinical and clinical evidence of gut microbiota shifts, increased intestinal permeability in metabolic disease, and the critical positioning of the intestinal barrier at the interface between environment and internal milieu have led to the rekindling of the "leaky gut" concept. Although increased circulation of surrogate markers and directly measurable intestinal permeability have been linked to increased systemic inflammation in metabolic disease, mechanistic models behind this phenomenon are underdeveloped. Given repeated observations of microorganisms in several tissues with congruent phylogenetic findings, we review current evidence on these unanticipated niches, focusing specifically on the interaction between gut permeability and intestinal as well as extra-intestinal bacteria and their joint contributions to systemic inflammation and metabolism. We further address limitations of current studies and suggest strategies drawing on standard techniques for permeability measurement, recent advancements in microbial culture independent techniques and computational methodologies to robustly develop these concepts, which may be of considerable value for the development of prevention and treatment strategies.

Gut Microbiome, Intestinal Permeability, and Tissue Bacteria in Metabolic Disease: Perpetrators or Bystanders?

CRIg+ Macrophages Prevent Gut Microbial DNA–Containing Extracellular Vesicle–Induced Tissue Inflammation and Insulin Resistance

An intact intestinal barrier, representing the interface between inner and outer environments, is an integral regulator of health. Among several factors, bacteria and their products have been evidenced to contribute to gut barrier impairment and its increased permeability. Alterations of tight junction integrity - caused by both external factors and host metabolic state - are important for gut barrier, since they can lead to increased influx of bacteria or bacterial components (endotoxin, bacterial DNA, metabolites) into the host circulation. Increased systemic levels of bacterial endotoxins and DNA have been associated with an impaired metabolic host status, manifested in obesity, insulin resistance, and associated cardiovascular complications. Bacterial components and cells are distributed to peripheral tissues via the blood stream, possibly contributing to metabolic diseases by increasing chronic pro-inflammatory signals at both tissue and systemic levels. This response is, along with other yet unknown mechanisms, mediated by toll like receptor (TLR) transduction and increased expression of pro-inflammatory cytokines, which in turn can further increase intestinal permeability leading to a detrimental positive feedback loop. The modulation of gut barrier function through nutritional and other interventions, including manipulation of gut microbiota, may represent a potential prevention and treatment target for metabolic diseases.

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Impaired Intestinal Barrier and Tissue Bacteria: Pathomechanisms for Metabolic Diseases.

Gut bacteria are involved in a number of host metabolic processes and have been implicated in the development of obesity and type 2 diabetes in humans. The use of antibiotics changes the composition of the gut microbiota and there is accumulating evidence from observational studies for an association between exposure to antibiotics and development of obesity and type 2 diabetes. In the present paper, we review human studies examining the effects of antibiotics on body weight regulation and glucose metabolism and discuss whether the observed findings may relate to alterations in the composition and function of the gut microbiota.

Effect of antibiotics on gut microbiota, glucose metabolism and body weight regulation: a review of the literature

The patient is a 66-year-old male, who had underdone sigmoidectomy 17 years earlier due to diverticulosis, with hypertrophic myocardiopathy and atrial fibrillation treated with Sintrom He reported having abdominal pain during the previous 4 days with nausea and vomiting The abdomen was distended and tympanic with diffuse pain and no signs of peritoneal irritation Work-up showed: 7910 L, 82% N, Quick 26%; INR 293 Computed tomography showed evidence of partial thrombosis of the superior mesenteric vein (SMV), with an arteriovenous fistula of the inferior mesenteric artery to the inferior mesenteric vein (IMV) (Fig 1) Embolization was used to completely seal the fistula in this procedure (Fig 2) Three months after embolization, re-permeabilization of the SMV was observed with complete thrombosis of the embolized IMV (Fig 3) c i r e s p  2 0 1 4 ; 9 2 ( 5 ) : e 2 3

Arteriovenous Fistula in the Inferior Mesenteric Territory

Fístula arteriovenosa de territorio mesentérico inferior

Background: Morbidly obese patients show several common comorbidities associated with immunological alterations such as a sustained low-level proinflammatory profile Bacterial product translocation is frequent in inflammation-related diseases and may aggravate patients' clinical outcome Design: Consecutively admitted morbidly obese patients who presented indications for bariatric surgery were studied Before surgery, patients were subjected to a modified fasting diet Patients underwent surgery by sleeve gastrectomy or laparoscopic Roux-en-Y gastric bypass Clinical and analytical parameters were recorded Blood samples were collected at baseline, at the end of a 3-month modified fasting period, and 3, 6, and 12 months after surgery Serum cytokine and endotoxin levels were evaluated by flow cytometry and ELISA, respectively Bacterial DNA was identified in blood by broad-range PCR of prokaryote 16SrRNA gene and partial sequencing analysis Results: Fifty-eight patients were included in the study All p

/pdf/bacterial-dna-translocation-holds-increased-insulin-2keylhpyjg.pdf

Bacterial DNA translocation holds increased insulin resistance and systemic inflammatory levels in morbid obese patients

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Arteriovenous Fistula in the Inferior Mesenteric Territory

Fístula arteriovenosa de territorio mesentérico inferior

Bacterial DNA translocation holds increased insulin resistance and systemic inflammatory levels in morbid obese patients