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Effects of prebiotics, probiotics and synbiotics on serum creatinine in non-dialysis patients: a meta-analysis of randomized controlled trials.
Liu, F, Liu, Y, Lv, X, Lun, H
Renal failure. 2023;45(1):2152693
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Plain language summary
Creatinine is a biomarker of kidney function and is used to diagnose chronic kidney disease. The aim of this meta-analysis of randomised controlled trials was to evaluate the effect of supplementation with prebiotics, probiotics and synbiotics on serum creatinine levels in patients not receiving dialysis. 12 RCTs were included in the meta-analysis of which seven were judged to have a low risk of bias whilst 1 was judged to have a high risk of bias. Overall, there was no significant effect of supplementation on serum creatinine levels. The following three subgroup analyses also showed no significant effects on creatinine levels: 1) by probiotics, prebiotics and synbiotics separately; 2) by duration: two months or less or longer than two months, 3) subgroup of 7 studies which included patients with non-dialysis kidney disease. The authors concluded that probiotics, prebiotics and synbiotics do not decrease serum creatinine levels.
Abstract
OBJECTIVE Serum creatinine level are influenced by many factors. Although accumulated data suggested that prebiotics, probiotics and synbiotics supplements could affect serum creatinine level, the results remained controversial. The aim of the present paper was to evaluate the effects of prebiotics, probiotics and synbiotics on serum creatinine in non-dialysis patients. METHODS PubMed, EMBASE (Excerpta Medica Database) and the Cochrane Library databases were searched for eligible randomized, controlled trials (RCTs) which were limited to English language studies until 30 September 2022. A random-effects model was performed to analyze the impact of pooled trials. RESULT Twelve randomized, controlled trial studies were included in the meta-analysis. Prebiotics, probiotics or synbiotics supplementation did not significantly decrease the serum creatinine levels in non-dialysis patients compared to placebo [standardized mean difference (SMD) = 0.05; 95% confidence interval (CI): (-0.21, 0.31); p = 0.72; I2 = 61%]. CONCLUSION The present meta-analysis indicated that supplementation with prebiotics, probiotics and synbiotics could not act as promising adjuvant therapies to decrease the serum creatinine levels in non-dialysis patients.
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Role of Probiotics in Non-alcoholic Fatty Liver Disease: Does Gut Microbiota Matter?
Xie, C, Halegoua-DeMarzio, D
Nutrients. 2019;11(11)
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Non-alcoholic fatty liver disease (NAFLD) is characterised by an excessive accumulation of fat in the liver tissue, without excessive alcohol consumption, and appears to be related to metabolic syndrome. It is thought to have a prevalence of 25% globally and there are no pharmacological treatments available. This review discusses the connection between the gut microbiota (GM) and NAFLD. Various mechanisms by which the GM may be involved in the development of NAFLD are discussed. As probiotics and prebiotics can normalise GM and reverse dysbiosis their use may benefit patients with NAFLD. This has been confirmed in animal models. The authors review 26 randomised controlled trials (RCTs) of probiotics and/or prebiotics in the treatment of NAFLD which evaluate biochemical markers, as well as five meta-analyses, and found that overall there is strong evidence that probiotics and/or prebiotics can lower ALT and AST (markers of NAFLD), although results for other biochemical markers were mixed. They also reviewed RCTs assessing NAFLD by imaging and histological means, and again found benefits from probiotic and/or prebiotic supplementation.
Abstract
Non-alcoholic fatty liver disease (NAFLD) is the hepatic consequence of metabolic syndrome, which often also includes obesity, diabetes, and dyslipidemia. The connection between gut microbiota (GM) and NAFLD has attracted significant attention in recent years. Data has shown that GM affects hepatic lipid metabolism and influences the balance between pro/anti-inflammatory effectors in the liver. Although studies reveal the association between GM dysbiosis and NAFLD, decoding the mechanisms of gut dysbiosis resulting in NAFLD remains challenging. The potential pathophysiology that links GM dysbiosis to NAFLD can be summarized as: (1) disrupting the balance between energy harvest and expenditure, (2) promoting hepatic inflammation (impairing intestinal integrity, facilitating endotoxemia, and initiating inflammatory cascades with cytokines releasing), and (3) altered biochemistry metabolism and GM-related metabolites (i.e., bile acid, short-chain fatty acids, aromatic amino acid derivatives, branched-chain amino acids, choline, ethanol). Due to the hypothesis that probiotics/synbiotics could normalize GM and reverse dysbiosis, there have been efforts to investigate the therapeutic effect of probiotics/synbiotics in patients with NAFLD. Recent randomized clinical trials suggest that probiotics/synbiotics could improve transaminases, hepatic steatosis, and reduce hepatic inflammation. Despite these promising results, future studies are necessary to understand the full role GM plays in NAFLD development and progression. Additionally, further data is needed to unravel probiotics/synbiotics efficacy, safety, and sustainability as a novel pharmacologic approaches to NAFLD.