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The effects of probiotic and synbiotic supplementation on metabolic syndrome indices in adults at risk of type 2 diabetes: study protocol for a randomized controlled trial.
Kassaian, N, Aminorroaya, A, Feizi, A, Jafari, P, Amini, M
Trials. 2017;(1):148
Abstract
BACKGROUND The incidence of type 2 diabetes, cardiovascular diseases, and obesity has been rising dramatically; however, their pathogenesis is particularly intriguing. Recently, dysbiosis of the intestinal microbiota has emerged as a new candidate that may be linked to metabolic diseases. We hypothesize that selective modulation of the intestinal microbiota by probiotic or synbiotic supplementation may improve metabolic dysfunction and prevent diabetes in prediabetics. In this study, a synthesis and study of synbiotics will be carried out for the first time in Iran. METHODS/DESIGN In a randomized triple-blind controlled clinical trial, 120 adults with impaired glucose tolerance based on the inclusion criteria will be selected by a simple random sampling method and will be randomly allocated to 6 months of 6 g/d probiotic, synbiotic or placebo. The fecal abundance of bacteria, blood pressure, height, weight, and waist and hip circumferences will be measured at baseline and following treatment. Also, plasma lipid profiles, HbA1C, fasting plasma glucose, and insulin levels, will be measured and insulin resistance (HOMA-IR) and beta-cell function (HOMA-B) will be calculated at baseline and will be repeated at months 3, 6, 12, and 18. The data will be compared within and between groups using statistical methods. DISCUSSION The results of this trial could contribute to the evidence-based clinical guidelines that address gut microbiota manipulation to maximize health benefits in prevention and management of metabolic syndrome in prediabetes. TRIAL REGISTRATION Iranian Registry of Clinical Trials: IRCT201511032321N2 . Registered on 27 February 2016.
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Microbial enterotypes, inferred by the prevotella-to-bacteroides ratio, remained stable during a 6-month randomized controlled diet intervention with the new nordic diet.
Roager, HM, Licht, TR, Poulsen, SK, Larsen, TM, Bahl, MI
Applied and environmental microbiology. 2014;(3):1142-9
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Abstract
It has been suggested that the human gut microbiota can be divided into enterotypes based on the abundance of specific bacterial groups; however, the biological significance and stability of these enterotypes remain unresolved. Here, we demonstrated that subjects (n = 62) 18 to 65 years old with central obesity and components of metabolic syndrome could be grouped into two discrete groups simply by their relative abundance of Prevotella spp. divided by Bacteroides spp. (P/B ratio) obtained by quantitative PCR analysis. Furthermore, we showed that these groups remained stable during a 6-month, controlled dietary intervention, where the effect of consuming a diet in accord with the new Nordic diet (NND) recommendations as opposed to consuming the average Danish diet (ADD) on the gut microbiota was investigated. In this study, subjects (with and without stratification according to P/B ratio) did not reveal significant changes in 35 selected bacterial taxa quantified by quantitative PCR (ADD compared to NND) resulting from the dietary interventions. However, we found higher total plasma cholesterol within the high-P/B group than in the low-P/B group after the intervention. We propose that stratification of humans based simply on their P/B ratio could allow better assessment of possible effects of interventions on the gut microbiota and physiological biomarkers.
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Gut microbioma population: an indicator really sensible to any change in age, diet, metabolic syndrome, and life-style.
Annalisa, N, Alessio, T, Claudette, TD, Erald, V, Antonino, de L, Nicola, DD
Mediators of inflammation. 2014;:901308
Abstract
Obesity has become a pandemic threat in the latest 30 years. The trend of the prevalence of overweight and obesity has got an overall increase in every part of the world, regardless of ethnicity, life-style and social ties. High food intake, genetic, and sedentary have been related to obesity; it has been also hypothesized that gut microbiota could have an impact on the complex mechanism underlying the weight gain. This review aims to illustrate the actual literature about gut microbiota and its relation with obesity and to analyze the possible implications of factors such as diet and life-style onto the composition of gut microbiota, that can lead to overweight/obesity condition.
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Diabetes, obesity and gut microbiota.
Everard, A, Cani, PD
Best practice & research. Clinical gastroenterology. 2013;(1):73-83
Abstract
The gut microbiota composition has been associated with several hallmarks of metabolic syndrome (e.g., obesity, type 2 diabetes, cardiovascular diseases, and non-alcoholic steatohepatitis). Growing evidence suggests that gut microbes contribute to the onset of the low-grade inflammation characterising these metabolic disorders via mechanisms associated with gut barrier dysfunctions. Recently, enteroendocrine cells and the endocannabinoid system have been shown to control gut permeability and metabolic endotoxaemia. Moreover, targeted nutritional interventions using non-digestible carbohydrates with prebiotic properties have shown promising results in pre-clinical studies in this context, although human intervention studies warrant further investigations. Thus, in this review, we discuss putative mechanisms linking gut microbiota and type 2 diabetes. These data underline the advantage of investigating and changing the gut microbiota as a therapeutic target in the context of obesity and type 2 diabetes.
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Prebiotics, faecal transplants and microbial network units to stimulate biodiversity of the human gut microbiome.
Van den Abbeele, P, Verstraete, W, El Aidy, S, Geirnaert, A, Van de Wiele, T
Microbial biotechnology. 2013;(4):335-40
Abstract
Accumulating evidence demonstrates the intimate association between human hosts and the gut microbiome. Starting at birth, the sterile gut of the newborn acquires a diverse spectrum of microbes, needed for immunological priming. However, current practices (caesarean sections, use of formula milk) deprive newborns from being exposed to this broad spectrum of microbes. Unnecessary use of antibiotics and excessive hygienic precautions (e.g. natural versus chlorinated drinking water) together with the Western diet further contribute to a decreased microbial diversity in the adult gut. This has been correlated with recurrent Clostridium difficile infection, inflammatory bowel diseases and obesity, among others. A healthy gut microbiome is thus characterized by a diverse network of metabolically interacting microbial members. In this context, we review several existing and novel approaches to manage the gut microbiome. First, prebiotic compounds should be re-defined in the sense that they should enhance the ecological biodiversity rather than stimulating single species. Recent studies highlight that structurally different polysaccharides require specific primary degraders but also enhance a similar network of secondary degraders that benefit from cross-feeding. A faecal transplantation is a second approach to restore biodiversity when the microbiota is severely dysbiosed, with promising results regarding C. difficile-associated disease and obesity-related metabolic syndromes. A final strategy is the introduction of key microbial network units, i.e. pre-organized microbial associations, which strengthen the overall microbial network of the gut microbiome that supports human health.
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Neuroendocrine body weight regulation: integration between fat tissue, gastrointestinal tract, and the brain.
Boguszewski, CL, Paz-Filho, G, Velloso, LA
Endokrynologia Polska. 2010;(2):194-206
Abstract
Human body weight is maintained at a fairly stable level regardless of changes in energy intake and energy expenditure. Compensatory mechanisms within the central nervous system (CNS), which regulate food intake and energy expenditure, are triggered by other central and peripheral signals. Peripherally, the main sources of those signals are the adipose tissue, gastrointestinal tract, and pancreas. The main signal originating from the adipose tissue is leptin, which promotes the activation of anorexigenic pathways in the CNS. Similarly, the central action of insulin also reduces food intake and stimulates catabolic pathways. The gastrointestinal tract contributes with several peptides that influence food intake, such as ghrelin, glucagon-like peptide 1 (GLP-1), peptide YY (PYY), oxyntomodulin (OXM), and cholecystokinin (CCK). Other substances secreted by the pancreas, such as pancreatic polypeptide (PP) and amylin, a hormone co-secreted with insulin, also affect energy balance. More recently, the endocannabinoid system has also been identified as a contributor in the maintenance of energy balance. Better understanding of these mechanistic systems involved in the regulation of energy metabolism will hopefully lead to the development of new therapeutic approaches against obesity, metabolic syndrome, and other nutritional disorders.
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Dietary fiber supplements: effects in obesity and metabolic syndrome and relationship to gastrointestinal functions.
Papathanasopoulos, A, Camilleri, M
Gastroenterology. 2010;(1):65-72.e1-2
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Abstract
Dietary fiber is a term that reflects a heterogeneous group of natural food sources, processed grains, and commercial supplements. Several forms of dietary fiber have been used as complementary or alternative agents in the management of manifestations of the metabolic syndrome, including obesity. Not surprisingly, there is a great variation in the biological efficacy of dietary fiber in the metabolic syndrome and body weight control. Diverse factors and mechanisms have been reported as mediators of the effects of dietary fiber on the metabolic syndrome and obesity. Among this array of mechanisms, the modulation of gastric sensorimotor influences appears to be crucial for the effects of dietary fiber but also quite variable. This report focuses on the role, mechanism of action, and benefits of different forms of fiber and supplements on obesity and the metabolic syndrome, glycemia, dyslipidemia, and cardiovascular risk and explores the effects of dietary fiber on gastric sensorimotor function and satiety in mediating these actions of dietary fiber.
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A carbohydrate-restricted diet alters gut peptides and adiposity signals in men and women with metabolic syndrome.
Hayes, MR, Miller, CK, Ulbrecht, JS, Mauger, JL, Parker-Klees, L, Gutschall, MD, Mitchell, DC, Smiciklas-Wright, H, Covasa, M
The Journal of nutrition. 2007;(8):1944-50
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Abstract
Carbohydrate-restricted diets have been shown to enhance satiation- and other homeostatic-signaling pathways controlling food intake and energy balance, which may serve to reduce the incidence of obesity and metabolic syndrome. This study was designed as a correlational, observational investigation of the effects of a carbohydrate-restricted diet on weight loss and body fat reduction and associated changes in circulating leptin, insulin, ghrelin, and cholecystokinin (CCK) concentrations in overweight/obese patients (4 men and 16 women) with metabolic syndrome. Subjects received clinical instruction on the initiation and maintenance of the commercial South Beach Diet, consisting of 2 phases: Phase I (initial 2 wk of the study) and Phase II (remaining 10 wk). Participants showed a decrease (P < 0.05) in body weight (93.5 +/- 3.6 kg vs. 88.3 +/- 3.4 kg), BMI (33.9 +/- 1.3 kg/m(2) vs. 32.0 +/- 1.3 kg/m(2)), waist circumference (112.8 +/- 2.8 cm vs. 107.7 +/- 3.0 cm), and total percent body fat (40.2 +/- 1.5% vs. 39.2 +/- 1.5%) by study completion. Plasma fasting insulin and leptin concentrations decreased significantly from baseline concentrations (139.1 +/- 12.2 pmol/L and 44.1 +/- 4.5 microg/L, respectively) by the end of Phase I (98.6 +/- 2.6 pmol/L and 33.3 +/- 4.1 microg/L, respectively). Plasma fasting ghrelin concentrations significantly increased from baseline (836.7 +/- 66.7 ng/L) by Phase II (939.9 +/- 56.8 ng/L). The postprandial increase in plasma CCK concentrations (difference in plasma CCK concentrations from fasting to postprandial) after Phase I (2.4 +/- 0.3 pmol/L) and Phase II (2.5 +/- 0.4 pmol/L) was significantly greater than the postprandial increase at baseline (1.1 +/- 0.5 pmol/L). Collectively, these results suggest that in patients with metabolic syndrome, improved adiposity signaling and increased postprandial CCK concentrations may act together as a possible compensatory control mechanism to maintain low intakes and facilitate weight loss, despite an increase in fasting ghrelin concentrations and subjective measures of hunger.