![Measures of glucose tolerance and insulin sensitivity. A . Blood glucose from the oral glucose tolerance test (OGTT) from 0– 120 min. B . Total area under the curve for OGTT over 120 min. C . Blood glucose following an insulin tolerance test (ITT). D . Total area under the curve for the ITT over 120 min. Data represents means 6 SE, n = 9–12 per treatment. { p , 0.05 for fluid (water vs.aspartame) within diet (chow, high fat). Statistics ( p values) for area under the curve data (diet, fluid) and their interactions are also shown, p , 0.05 being considered significant. Data from the water controls (chow, high fat) were part of a shared control group that has been previously published [15]. Permission to reuse the data in this figure was obtained from Elsevier. Abbreviations are as follows; CHW, chow water; CHA, chow aspartame; HFW, high fat water; HFA, high fat aspartame. doi:10.1371/journal.pone.0109841.g001](https://www.researchgate.net/profile/Dustin-Hittel/publication/264417584/figure/fig1/AS:296002553696259@1447583916248/Measures-of-glucose-tolerance-and-insulin-sensitivity-A-Blood-glucose-from-the-oral_Q320.jpg)
![Gut microbiota analyses of diet and fluid treatments.
A. Graphical representation of the absolute changes in the Firmicutes:Bacteroidetes ratio in fresh fecal matter resulting from dietary (chow or high fat) or fluid (water or aspartame) treatment. HFW has elevated levels in comparison to the other groups, with the data representing absolute number (106) of 16S rRNA gene copies per 20 ng DNA. The numerical value above each bar represents the Firmicutes:Bacteroidetes value. B. Relative bacterial abundance within the Firmicutes phyla. Data is based on 16S rRNA gene copies (106/20 ng DNA), on a relative (100%) scale. Consistent with the absolute results (Table 2), APM treatment within HF (HFA) increased the relative proportion of Clostridium leptum and attenuated high fat- increased in Clostridium cluster XI. Data from the water controls (chow, high fat) were part of a shared control group that has been previously published [15]. Permission to reuse the data in this figure was obtained from Elsevier. Abbreviations are as follows: CHW, chow water; CHA, chow aspartame; HFW, high fat water; HFA, high fat aspartame. Data represents means ± SE, n = 9–12 per treatment.](https://www.researchgate.net/profile/Dustin-Hittel/publication/264417584/figure/fig3/AS:339893206175757@1458048263356/Gut-microbiota-analyses-of-diet-and-fluid-treatments-A-Graphical-representation-of-the_Q320.jpg)
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Low-Dose Aspartame Consumption Differentially Affects Gut Microbiota-Host Metabolic Interactions in the Diet- Induced Obese Rat
PLOS One
Abstract and Figures
Aspartame consumption is implicated in the development of obesity and metabolic disease despite the intention of limiting caloric intake. The mechanisms responsible for this association remain unclear, but may involve circulating metabolites and the gut microbiota. Aims were to examine the impact of chronic low-dose aspartame consumption on anthropometric, metabolic and microbial parameters in a diet-induced obese model. Male Sprague-Dawley rats were randomized into a standard chow diet (CH, 12% kcal fat) or high fat (HF, 60% kcal fat) and further into ad libitum water control (W) or low-dose aspartame (A, 5–7 mg/kg/d in drinking water) treatments for 8 week (n = 10–12 animals/treatment). Animals on aspartame consumed fewer calories, gained less weight and had a more favorable body composition when challenged with HF compared to animals consuming water. Despite this, aspartame elevated fasting glucose levels and an insulin tolerance test showed aspartame to impair insulin-stimulated glucose disposal in both CH and HF, independently of body composition. Fecal analysis of gut bacterial composition showed aspartame to increase total bacteria, the abundance of Enterobacteriaceae and Clostridium leptum. An interaction between HF and aspartame was also observed for Roseburia ssp wherein HF-A was higher than HF-W (P,0.05). Within HF, aspartame attenuated the typical HF-induced increase in the Firmicutes:Bacteroidetes ratio. Serum metabolomics analysis revealed aspartame to be rapidly metabolized and to be associated with elevations in the short chain fatty acid propionate, a bacterial end product and highly gluconeogenic substrate, potentially explaining its negative affects on insulin tolerance. How aspartame influences gut microbial composition and the implications of these changes on the development of metabolic disease require further investigation.
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... Multiple studies examining the physiological effects of NNS have identified the gut microbiota as a key mediator, raising questions about the long-term safety and hostmicrobiome dynamics of these compounds [3,[60][61][62][63][64]. With advancements in sequencing technologies and computational tools-alongside decreasing costs associated with microbiome analysis-interest in understanding the gut microbiome's role in human health has expanded significantly [65]. ...
... Palmnäs et al. [63] investigated the impact of chronic low-dose aspartame ingestion on microbiome profile and metabolic parameters in a diet-induced obese rat model. Aspartame was supplied in conjunction with a high-fat (60% kcal fat) diet in this study. ...
Background and Aim: The human gut microbiome plays a crucial role in maintaining health. Artificial sweeteners, also known as non-nutritive sweeteners (NNS), have garnered attention for their potential to disrupt the balance of the gut microbiome. This review explores the complex relationship between NNS and the gut microbiome, highlighting their potential benefits and risks. By synthesizing current evidence, we aim to provide a balanced perspective on the role of AS in dietary practices and health outcomes, emphasizing the need for targeted research to guide their safe and effective use. Methods: A comprehensive literature review was conducted through searches in PubMed and Google Scholar, focusing on the effects of artificial sweeteners on gut microbiota. The search utilized key terms including “Gut Microbiome”, “gut microbiota”, “Eubiosis”, “Dysbiosis”, “Artificial Sweeteners”, and “Nonnutritive Sweeteners”. Results: NNS may alter the gut microbiome, but findings remain inconsistent. Animal studies often report a decrease in beneficial bacteria like Bifidobacterium and Lactobacillus, and an increase in harmful strains such as Clostridium difficile and E. coli, potentially leading to inflammation and gut imbalance. Disruptions in short-chain fatty acid (SCFA) production and gut hormone signaling have also been observed. However, human studies generally show milder or no significant changes, highlighting the limitations in translating animal model findings directly to humans. Differences in study design, dosage, exposure time, and sweetener type likely contribute to these varied outcomes. Conclusions: While NNS offer certain benefits, including reduced caloric intake and improved blood sugar regulation, their impact on gut microbiome health raises important concerns. The observed reduction in beneficial bacteria and the rise in pathogenic strains underscore the need for caution in NNS consumption. Furthermore, the disruption of SCFA production and metabolic pathways illustrates the intricate relationship between diet and gut health.
... Non-nutritive sweeteners (NNS) aim to combat obesity and diabetes by providing zero-calorie alternatives to sugar. Several studies have shown that NNS change the composition of the microbiome, and a subset of these studies have demonstrated that NNS may impair glucose tolerance via their induced changes in the gut microbiome (111)(112)(113). However, there are inconsistencies across studies. ...
The gut microbiome has been linked to everything from human behavior to athletic performance to disease pathogenesis. And yet, few universal truths have emerged regarding how the microbiome exerts its effects or responds to the host environment except for one: gut microbiota are exquisitely sensitive to human diets. What we eat from birth onward shapes our gut microbiome composition and function, and this is likely an evolutionarily conserved interaction that benefits the microbe and often the host. However, modern diets and lifestyles have created discordance between our slowly evolving human genome and rapidly adaptable microbiome, and have been implicated in the rise of chronic diseases over the past 75 years. Diet and microbiome interactions have been reviewed extensively, so here we focus on areas of microbiome research that have most illuminated natural and disruptive dietary forces over time in humans, and where we may have opportunities to restore the natural balance of host with microbes in our modern world.
... Alterations in gut microbiota induced by AS, have been linked to impaired glucose tolerance and insulin resistance [47]. The expression of sodium dependent glucose transporter-1 was reported to be enhanced by certain AS, that elevated fasting blood sugars in rats under study leading to increased risk of Type-2 diabetes [48]. Chronic consumption of AS make cells less responsive to insulin signalling, thereby increasing the risk of metabolic disorders. ...
Artificial Sweeteners are used world-wide as sugar substitutes, and are found in various food products and pharmaceuticals. However, their increasing occurrence in the aquatic ecosystems has raised concerns about their environmental persistence, possible bioaccumulation and potential toxicity. This review emphasises on the occurrence and toxicity mechanism of AS with special focus to metabolism, gut and neurological health and carcinogenic potential in humans. Additionally, it exhibits the ecotoxicological effects of AS on aquatic and terrestrial systems. This review also identifies and presents critical research gaps by thorough bibliometric analysis. A One Health Approach which integrates human, environmental and wild life health is essential for assessing AS risks and developing sustainable solutions to mitigate AS pollution and its long-lasting consequences.
... Several studies have reported their effects on human health and their interactions with the microbiota. [42][43][44] Moreover, a recently published clinical study suggests that non-nutritive sweeteners may induce glycaemic alterations that are person-specific and dependent on the composition of the microbiome. 45 Our recent findings, along with other studies using in vitro microbiota systems, highlight the potential of MBRA to predict sensitivity to such compounds. ...
Background: Non-absorbed dietary emulsifiers, including carboxymethylcellulose (CMC), directly disturb intestinal microbiota, thereby promoting chronic intestinal inflammation in mice. A randomised controlled-feeding study (Functional Research on Emulsifiers in Humans, FRESH) found that CMC also detrimentally impacts intestinal microbiota in some, but not all, healthy individuals.
Objectives: This study aimed to establish an approach for predicting an individual's sensitivity to dietary emulsifiers via their baseline microbiota.
Design: We evaluated the ability of an in vitro microbiota model (MiniBioReactor Arrray, MBRA) to reproduce and predict an individual donor's sensitivity to emulsifiers. Metagenomes were analysed to identify signatures of emulsifier sensitivity.
Results: Exposure of human microbiotas, maintained in the MBRA, to CMC recapitulated the differential CMC sensitivity previously observed in FRESH subjects. Furthermore, select FRESH control subjects (ie, not fed CMC) had microbiotas that were highly perturbed by CMC exposure in the MBRA model. CMC-induced microbiota perturbability was associated with a baseline metagenomic signature, suggesting the possibility of using one's metagenome to predict sensitivity to dietary emulsifiers. Transplant of human microbiotas that the MBRA model deemed CMC-sensitive, but not those deemed insensitive, into IL-10-/- germfree mice resulted in overt colitis following CMC feeding.
Conclusion: These results suggest that an individual's sensitivity to emulsifier is a consequence of, and can thus be predicted by, examining their baseline microbiota, paving the way to microbiota-based personalised nutrition.
... Estas enfermedades están mediadas por mecanismos específicos, uno de los mecanismos más discutidos es la alteración de la microbiota intestinal, un conjunto de microorganismos que desempeñan un papel crucial en la salud metabólica y el sistema inmunológico. Los edulcorantes como la sucralosa y el aspartamo han demostrado modificar la composición de la microbiota (36,37), promoviendo un estado de disbiosis que puede desencadenar inflamación crónica y alterar el metabolismo de la glucosa. Este desequilibrio en la microbiota podría contribuir al desarrollo de resistencia a la insulina, lo que a su vez aumenta el riesgo de diabetes tipo II (38). ...
Introducción: el consumo de bebidas energéticas se ha convertido en un tema de preocupación en la salud pública, dado a su relación con desenlaces fatales, asociados con el sistema cardiovascular; tales como arritmias, infartos de miocardio, miocardiopatías y muerte súbita. Objetivos: establecer, mediante una revisión sistemática de la literatura, los posibles efectos adversos del consumo de bebidas energéticas en estudiantes universitarios. Métodos: se realizó una búsqueda sistemática de la literatura en Scopus, Science Direcct, Nature, Scielo, Redalyc, PubMed and LILACS. La búsqueda arrojó un total de 3142 artículos, de los cuales 65 fueron seleccionados para esta revisión. Resultados: existe una asociación positiva entre el consumo de bebidas energéticas y el consumo de alcohol, la prevalencia en el consumo de bebidas energéticas entre los estudiantes colombianos de pregrado fue entre el 35 y el 81,7 %. Siendo los estudiantes de los programas de ciencias de la salud e ingeniería los que más consumen estas bebidas. Entre las razones para el alto consumo de bebidas energéticas se encuentran: la carga académica, aumento de la vigilia, rendimiento en la actividad física y consumo de alcohol. Conclusiones: el consumo excesivo de bebidas energéticas combinado con actividad física o alcohol en estudiantes universitarios aumenta significativamente los riesgos cardiovasculares y otros efectos adversos para la salud.
... Although NNS were once considered inert due to containing no or few calories, NNS have metabolic effects in rodents [3][4][5][6][7][8] and humans [9,10], and positive associations between NNS consumption and body weight [11,12], metabolic syndrome [13,14], cardiovascular disease [15,16], and stroke [15,17] are reported in observational studies. In some studies, NNS consumption is also positively associated with cancer risk [18,19], although findings of studies linking NNS to cancer outcomes are mixed [20,21]. ...
... While a considerable number of studies indicate that the ASs can have positive effects, such as preventing caries [60,61], aiding in weight regulation [62], and reducing the risk of cardiovascular and metabolic diseases [24,63], there are also studies that challenge these claims and disprove the benefits. Critics argue that the potential risks of ASs may outweigh their benefits, highlighting concerns that include possible negative impacts on health [24,25,29,30,[64][65][66][67]. ...
Background/objectives:
Artificial sweeteners (ASs) are food additives used to impart sweetness to various food products. Common sweeteners used individually or in combination include acesulfame-K, aspartame, cyclamate, saccharin, sucralose, and neotame. While traditionally considered harmless, emerging research suggest potential health implications. This study aims to analyze commonly consumed food products in Croatia for ASs presence, quantify four ASs, and estimate daily intake of ASs. Additionally, product labeling was assessed for compliance with Regulation 1169/2011 on food information to consumers.
Methods:
This study assessed the presence of acesulfame-K, aspartame, cyclamate, and saccharin dihydrate in 121 frequently consumed food products from the Croatian market using a high-performance liquid chromatography method. Based on obtained concentrations, data from a parallel consumption study, and existing literature on acceptable daily intake (ADI), we assessed exposure to ASs.
Results:
ASs were found in a substantial proportion of analyzed products, with multiple sweeteners often present in a single product. Specifically, ASs were detected in 74% of carbonated drinks, 54% of fruit juices, 86% of energy drinks, 70% of high-protein milk products, and 66% of chewing gums. Hypothetical consumption scenarios demonstrated that children, due to their low body mass, are at the highest risk of exceeding ADI values.
Conclusions:
The widespread presence of ASs in food products raises concerns about excessive intake, particularly among children who frequently consume soft drinks, instant beverages, and protein drinks. These findings highlight the need for further research into cumulative ASs exposure and its potential health effects, as well as the importance of public health strategies to regulate ASs consumption.
... However, recent research suggests that artificial sweetener intake is associated with obesity (7; 8) , and the World Health Organization now advises against the use of non-nutritive sweeteners (including both artificial sweeteners and natural sweeteners such as steviol glycosides) for weight loss purposes (9) . Some studies have shown impairment in insulin tolerance in aspartame-exposed rats independently of body fat composition (10) and increased glucose intolerance in both mice and humans exposed to artificial sweeteners, partly mediated by changes in the gut microbiome (11; 12) . ...
Artificial sweeteners are used to reduce energy intake, but studies suggest that consumption during pregnancy may impact the offspring’s risk of overweight. In this longitudinal cohort study, we aimed to examine the association between consumption of artificially sweetened or sugar-sweetened beverages during pregnancy and offspring overweight from birth to 18 years in the Danish National Birth Cohort (DNBC). 101,042 pregnancies were enrolled in the DNBC from 1996-2002. Follow-up was conducted throughout pregnancy, childhood, and adolescence. 72,821 women completed a Food Frequency Questionnaire during pregnancy reporting intake of beverages sweetened with artificial sweeteners or sugar. Offspring height and weight were obtained during childhood and adolescence. Multivariate logistic regression was performed to estimate the odds ratio (OR) for overweight concerning maternal beverage consumption. Analyses were adjusted for risk factors for childhood overweight, including maternal age, pre-pregnancy body mass index (BMI), physical activity and smoking in pregnancy, healthy eating index, paternal BMI, socioeconomic status, and duration of breastfeeding. We found increased odds of overweight in 7, 11, 14, and 18-year-old offspring, whose mothers reported drinking ≥1 artificially sweetened beverages daily during pregnancy compared to no consumption (18 years: adjusted OR 1.26 (95% confidence interval 1.12, 1.42)). We found decreased adjusted odds of overweight in 11 and 18-year-old offspring, whose mothers reported drinking ≥1 sugar-sweetened beverages daily during pregnancy compared to no consumption. We found that consumption of artificially sweetened beverages during pregnancy was associated with an increased risk of overweight in childhood and adolescence. Adjustment for risk factors for overweight and total energy intake did not explain the association. Further studies are warranted to establish the mechanism of the association.
Metabolic syndrome is associated with alterations in the structure of the gut microbiota leading to low-grade inflammatory responses. An increased penetration of the impaired gut membrane by bacterial components is believed to induce this inflammation, possibly involving epigenetic alteration of inflammatory molecules such as Toll-like receptors (TLRs). We evaluated changes of the gut microbiota and epigenetic DNA methylation of TLR2 and TLR4 in three groups of subjects: type 2 diabetics under glucagon-like peptide-1 agonist therapy, obese individuals without established insulin resistance, and a lean control group. Clostridium cluster IV, Clostridium cluster XIVa, lactic acid bacteria, Faecalibacterium prausnitzii and Bacteroidetes abundances were analysed by PCR and 454 high-throughput sequencing. The epigenetic methylation in the regulatory region of TLR4 and TLR2 was analysed using bisulfite conversion and pyrosequencing. We observed a significantly higher ratio of Firmicutes/ Bacteroidetes in type 2 diabetics compared to lean controls and obese. Major differences were shown in lactic acid bacteria, with the highest abundance in type 2 diabetics, followed by obese and lean participants. In comparison, F. prausnitzii was least abundant in type 2 diabetics, and most abundant in lean controls. Methylation analysis of four CpGs in the first exon of TLR4 showed significantly lower methylation in obese individuals, but no significant difference between type 2 diabetics and lean controls. Methylation of seven CpGs in the promoter region of TLR2 was significantly lower in type 2 diabetics compared to obese subjects and lean controls. The methylation levels of both TLRs were significantly correlated with body mass index. Our data suggest that changes in gut microbiota and thus cell wall components are involved in the epigenetic regulation of inflammatory reactions. An improved diet targeted to induce gut microbial balance and in the following even epigenetic changes of pro-inflammatory genes may be effective in the prevention of metabolic syndrome.
Alterations in the composition of the gut microbiome and/or immune system function may have a role in the development of autism spectrum disorders (ASD). The current study examined the effects of prenatal and early life administration of lipopolysaccharide (LPS), a bacterial mimetic, and the short chain fatty acid, propionic acid (PPA), a metabolic fermentation product of enteric bacteria, on developmental milestones, locomotor activity, and anxiety-like behavior in adolescent male and female offspring. Pregnant Long-Evans rats were subcutaneously injected once a day with PPA (500 mg/kg) on gestation days G12-16, LPS (50 µg/kg) on G15-16, or vehicle control on G12-16 or G15-16. Male and female offspring were injected with PPA (500 mg/kg) or vehicle twice a day, every second day from postnatal days (P) 10-18. Physical milestones and reflexes were monitored in early life with prenatal PPA and LPS inducing delays in eye opening. Locomotor activity and anxiety were assessed in adolescence (P40-42) in the elevated plus maze (EPM) and open-field. Prenatal and postnatal treatments altered behavior in a sex-specific manner. Prenatal PPA decreased time spent in the centre of the open-field in males and females while prenatal and postnatal PPA increased anxiety behavior on the EPM in female rats. Prenatal LPS did not significantly influence those behaviors. Evidence for the double hit hypothesis was seen as females receiving a double hit of PPA (prenatal and postnatal) displayed increased repetitive behavior in the open-field. These results provide evidence for the hypothesis that by-products of enteric bacteria metabolism such as PPA may contribute to ASD, altering development and behavior in adolescent rats similar to that observed in ASD and other neurodevelopmental disorders.
The conflict of interest statement was omitted from the version of this article that was published online ahead of the issue. The conflict of interest statement is now included in the article, published in this issue.
Objectives:
We examined national patterns in adult diet-beverage consumption and caloric intake by body-weight status.
Methods:
We analyzed 24-hour dietary recall with National Health and Nutrition Examination Survey 1999-2010 data (adults aged ≥ 20 years; n = 23 965).
Results:
Overall, 11% of healthy-weight, 19% of overweight, and 22% of obese adults drink diet beverages. Total caloric intake was higher among adults consuming sugar-sweetened beverages (SSBs) compared with diet beverages (2351 kcal/day vs 2203 kcal/day; P = .005). However, the difference was only significant for healthy-weight adults (2302 kcal/day vs 2095 kcal/day; P < .001). Among overweight and obese adults, calories from solid-food consumption were higher among adults consuming diet beverages compared with SSBs (overweight: 1965 kcal/day vs 1874 kcal/day; P = .03; obese: 2058 kcal/day vs 1897 kcal/day; P < .001). The net increase in daily solid-food consumption associated with diet-beverage consumption was 88 kilocalories for overweight and 194 kilocalories for obese adults.
Conclusions:
Overweight and obese adults drink more diet beverages than healthy-weight adults and consume significantly more solid-food calories and a comparable total calories than overweight and obese adults who drink SSBs. Heavier US adults who drink diet beverages will need to reduce solid-food calorie consumption to lose weight.
New approaches are needed to examine the diverse symptoms and comorbidities of the growing family of neurodevelopmental disorders known as autism spectrum disorder (ASD). ASD originally was thought to be a static, inheritable neurodevelopmental disorder, and our understanding of it is undergoing a major shift. It is emerging as a dynamic system of metabolic and immune anomalies involving many organ systems, including the brain, and environmental exposure. The initial detailed observation and inquiry of patients with ASD and related conditions and the histories of their caregivers and families have been invaluable. How gastrointestinal (GI) factors are related to ASD is not yet clear. Nevertheless, many patients with ASD have a history of previous antibiotic exposure or hospitalization, GI symptoms, abnormal food cravings, and unique intestinal bacterial populations, which have been proposed to relate to variable symptom severity.
In addition to traditional scientific inquiry, detailed clinical observation and recording of exacerbations, remissions, and comorbidities are needed. This article reviews the role that enteric short-chain fatty acids, particularly propionic (also called propanoic) acid, produced from ASD-associated GI bacteria, may play in the etiology of some forms of ASD. Human populations that are partial metabolizers of propionic acid are more common than previously thought. The results from pre-clinical laboratory studies show that propionic acid-treated rats display ASD-like repetitive, perseverative, and antisocial behaviors and seizure. Neurochemical changes, consistent and predictive with findings in ASD patients, including neuroinflammation, increased oxidative stress, mitochondrial dysfunction, glutathione depletion, and altered phospholipid/acylcarnitine profiles, have been observed. Propionic acid has bioactive effects on (1) neurotransmitter systems, (2) intracellular acidification and calcium release, (3) fatty acid metabolism, (4) gap junction gating, (5) immune function, and (6) alteration of gene expression that warrant further exploration. Traditional scientific experimentation is needed to verify the hypothesis that enteric short-chain fatty acids may be a potential environmental trigger in some forms of ASD. Novel collaborative developments in systems biology, particularly examining the role of the microbiome and its effects on host metabolism, immune and mitochondrial function, and gene expression, hold great promise in ASD.
Soluble dietary fibers promote metabolic benefits on body weight and glucose control, but underlying mechanisms are poorly understood. Recent evidence indicates that intestinal gluconeogenesis (IGN) has beneficial effects on glucose and energy homeostasis. Here, we show that the short-chain fatty acids (SCFAs) propionate and butyrate, which are generated by fermentation of soluble fiber by the gut microbiota, activate IGN via complementary mechanisms. Butyrate activates IGN gene expression through a cAMP-dependent mechanism, while propionate, itself a substrate of IGN, activates IGN gene expression via a gut-brain neural circuit involving the fatty acid receptor FFAR3. The metabolic benefits on body weight and glucose control induced by SCFAs or dietary fiber in normal mice are absent in mice deficient for IGN, despite similar modifications in gut microbiota composition. Thus, the regulation of IGN is necessary for the metabolic benefits associated with SCFAs and soluble fiber.
Evidence suggests that short-chain fatty acids (SCFAs) derived from microbial metabolism in the gut play a central role in host homeostasis. The present review describes the current understanding and physiological implications of SCFAs derived from microbial metabolism of nondigestible carbohydrates.
Recent studies indicate a role for SCFAs, in particular propionate and butyrate, in metabolic and inflammatory disorders such as obesity, diabetes and inflammatory bowel diseases, through the activation of specific G-protein-coupled receptors and modification of transcription factors. Established prebiotics, such as fructooligosaccharides and galactooligosaccharides, which support the growth of Bifidobacteria, mainly mediate acetate production. Thus, recent identification of prebiotics which are able to stimulate the production of propionate and butyrate by benign saccharolytic populations in the colon is of interest.
Manipulation of saccharolytic fermentation by prebiotic substrates is beginning to provide information on structure-function relationships relating to the production of SCFAs, which have multiple roles in host homeostasis.
Objective:
Prebiotics and probiotics may be able to modify an obesity-associated gut microbiota. The aim of this study was to examine the individual and combined effects of the prebiotic oligofructose (OFS) and the probiotic Bifidobacterium animalis subsp. lactis BB-12 (BB-12) on gut microbiota and host metabolism in obese rats.
Methods:
Adult male, diet-induced obese Sprague Dawley rats were randomized to: (1) Control (C); (2) 10% OFS; (3) BB-12; (4) OFS + BB-12 for 8 weeks (n = 9-10 rats/group). Body composition, glycemia, gut permeability, satiety hormones, cytokines, and gut microbiota were examined.
Results:
Prebiotic, but not probiotic reduced energy intake, weight gain, and fat mass (P < 0.01). OFS, BB-12, and the combined OFS + BB-12 improved glycemia (P < 0.05). Individually, OFS and BB-12 reduced insulin levels (P < 0.05). Portal GLP-1 was increased with OFS, whereas probiotic increased GLP-2 (P < 0.05). There was a marked increase in bifidobacteria and lactobacilli (P < 0.01) with OFS that was not observed with probiotic alone.
Conclusions:
The impact of prebiotic intake on body composition and gut microbiota was of greater magnitude than the probiotic BB-12. Despite this, an improvement in glucose AUC with both prebiotic or probiotic demonstrates the beneficial role of each of these "biotic" agents in glycemic control.