scholarly journals Changes in gut microbiome as important risk- factor for development of metabolic diseases

2017 ◽  
Vol 0 (1(57)) ◽  
pp. 17-27
Author(s):  
С. М. Ткач ◽  
О. С. Ларін ◽  
А. В. Підаєв
Author(s):  
Sunmin Park ◽  
Sunna Kang ◽  
Da Sol Kim

Abstract. Folate and vitamin B12(V-B12) deficiencies are associated with metabolic diseases that may impair memory function. We hypothesized that folate and V-B12 may differently alter mild cognitive impairment, glucose metabolism, and inflammation by modulating the gut microbiome in rats with Alzheimer’s disease (AD)-like dementia. The hypothesis was examined in hippocampal amyloid-β infused rats, and its mechanism was explored. Rats that received an amyloid-β(25–35) infusion into the CA1 region of the hippocampus were fed either control(2.5 mg folate plus 25 μg V-B12/kg diet; AD-CON, n = 10), no folate(0 folate plus 25 μg V-B12/kg diet; AD-FA, n = 10), no V-B12(2.5 mg folate plus 0 μg V-B12/kg diet; AD-V-B12, n = 10), or no folate plus no V-B12(0 mg folate plus 0 μg V-B12/kg diet; AD-FAB12, n = 10) in high-fat diets for 8 weeks. AD-FA and AD-VB12 exacerbated bone mineral loss in the lumbar spine and femur whereas AD-FA lowered lean body mass in the hip compared to AD-CON(P < 0.05). Only AD-FAB12 exacerbated memory impairment by 1.3 and 1.4 folds, respectively, as measured by passive avoidance and water maze tests, compared to AD-CON(P < 0.01). Hippocampal insulin signaling and neuroinflammation were attenuated in AD-CON compared to Non-AD-CON. AD-FAB12 impaired the signaling (pAkt→pGSK-3β) and serum TNF-α and IL-1β levels the most among all groups. AD-CON decreased glucose tolerance by increasing insulin resistance compared to Non-AD-CON. AD-VB12 and AD-FAB12 increased insulin resistance by 1.2 and 1.3 folds, respectively, compared to the AD-CON. AD-CON and Non-AD-CON had a separate communities of gut microbiota. The relative counts of Bacteroidia were lower and those of Clostridia were higher in AD-CON than Non-AD-CON. AD-FA, but not V-B12, separated the gut microbiome community compared to AD-CON and AD-VB12(P = 0.009). In conclusion, folate and B-12 deficiencies impaired memory function by impairing hippocampal insulin signaling and gut microbiota in AD rats.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Christophe Lay ◽  
Collins Wenhan Chu ◽  
Rikky Wenang Purbojati ◽  
Enzo Acerbi ◽  
Daniela I. Drautz-Moses ◽  
...  

Abstract Background The compromised gut microbiome that results from C-section birth has been hypothesized as a risk factor for the development of non-communicable diseases (NCD). In a double-blind randomized controlled study, 153 infants born by elective C-section received an infant formula supplemented with either synbiotic, prebiotics, or unsupplemented from birth until 4 months old. Vaginally born infants were included as a reference group. Stool samples were collected from day 3 till week 22. Multi-omics were deployed to investigate the impact of mode of delivery and nutrition on the development of the infant gut microbiome, and uncover putative biological mechanisms underlying the role of a compromised microbiome as a risk factor for NCD. Results As early as day 3, infants born vaginally presented a hypoxic and acidic gut environment characterized by an enrichment of strict anaerobes (Bifidobacteriaceae). Infants born by C-section presented the hallmark of a compromised microbiome driven by an enrichment of Enterobacteriaceae. This was associated with meta-omics signatures characteristic of a microbiome adapted to a more oxygen-rich gut environment, enriched with genes associated with reactive oxygen species metabolism and lipopolysaccharide biosynthesis, and depleted in genes involved in the metabolism of milk carbohydrates. The synbiotic formula modulated expression of microbial genes involved in (oligo)saccharide metabolism, which emulates the eco-physiological gut environment observed in vaginally born infants. The resulting hypoxic and acidic milieu prevented the establishment of a compromised microbiome. Conclusions This study deciphers the putative functional hallmarks of a compromised microbiome acquired during C-section birth, and the impact of nutrition that may counteract disturbed microbiome development. Trial registration The study was registered in the Dutch Trial Register (Number: 2838) on 4th April 2011.


2008 ◽  
Vol 21 (9) ◽  
pp. 873-878 ◽  
Author(s):  
Juan Torres ◽  
Jose María Aguado ◽  
Rafael San Juan ◽  
Amado Andrés ◽  
Prado Sierra ◽  
...  

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Aleksei Zulkarnaev ◽  
Andrey Vatazin ◽  
Vadim Stepanov ◽  
Ekaterina Parshina ◽  
Mariya Novoseltseva

Abstract Background and Aims The prevalence of central vein stenosis (CVS) in patients on hemodialysis (HD) is difficult to be assessed directly. This is mainly caused by the variety of clinical signs and the high frequency of asymptomatic CVS. Aim: to assess the frequency of occurrence of various CVS forms in HD patients. Method The retrospective observational study is based on the results of treatment of 1865 HD patients who underwent diagnostic and therapeutic procedures on vascular access in our center. In case of vascular access dysfunction, patients were examined according to a local protocol: ultrasound of the peripheral (to exclude lesion of peripheral AVF segments) and central veins (over the available length), followed with CT-angiography or percutaneous angiography, if necessary. Results AVF/AVG dysfunction was observed in 29.4% of patients (549 of 1865). 211 patients were diagnosed with CVS. The prevalence of CVS was 11.3% (211 of 1865) among all HD patients and 38.4% (211 of 549) in patients with AVF dysfunction. Among patients with CVS, 37% (78 of 211) had vein lesions without clinical symptoms or with minimal manifestations (a tendency to decrease KT/V). The prevalence of asymptomatic CVS was 4.2% (78 of 1865) in the general population of HD patients and 14.2% (78 of 549) in patients with AVF dysfunction. In case of asymptomatic CVS it was detected by an ultrasound examination during CVC implantation (N=38), during unsuccessful attempts to implant CVC (N=29), in the case of recurrent AVF thrombosis without underlying peripheral segments lesion (N=9) or during echocardiography (N=2). The prevalence of asymptomatic CVS among patients without AVF dysfunction was 5.9% (78 of 1316). True prevalence of subclinical CVS among HD patients without obvious signs of AVF dysfunction may vary widely. A total of 48.8% (103 of 211) of all CVS cases were treated. At the same time, in 10.7% (11 of 103) of cases, patients did not present symptoms of CVS, and surgery was performed due to recurrent AVF thrombosis without damage of the peripheral parts of AVF. Patients with clinically manifest CVS who received endovascular interventions had a significantly higher risk of AVF loss compared to patients with asymptomatic CVS: HR=2.566 [95% CI 1.706; 3.86], log rank p&lt;0.0001. However, patients with an asymptomatic CVS had a higher risk of AVF function loss compared to the general HD population (HR=2,051 [95% CI 1,243; 3,384], log rank p= 0.0004) – fig. 1. The use of CVC is a known risk factor of CVS development. We analyzed the relationship of CVS risk with multiply CVC placements and catheter dwell time using the Cox proportional hazards regression model (fig. 2). In the univariate model, a greater No of CVCs as well as longer time in place increased the risk of CVS. In the multivariate model (χ2=105.516, df=2, p&lt;0.0001), catheter dwell time was no longer associated with an increased risk of CVC, while the mean number of inserted catheters remained an important risk factor. Conclusion The prevalence of both symptomatic and asymptomatic forms of CVS in HD patients is high. Patients with vascular access dysfunction should be carefully examined to identify the asymptomatic CVS. The mean No of catheterizations is a more important risk factor of CVS than longer catheter dwell time.


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