Skip to main content Accessibility help
×
Home
Hostname: page-component-55597f9d44-pgkvd Total loading time: 0.641 Render date: 2022-08-18T19:41:40.385Z Has data issue: true Feature Flags: { "shouldUseShareProductTool": true, "shouldUseHypothesis": true, "isUnsiloEnabled": true, "useRatesEcommerce": false, "useNewApi": true } hasContentIssue true

Gut microbiota and metabolic disorders: how prebiotic can work?

Published online by Cambridge University Press:  29 January 2013

Nathalie M. Delzenne*
Affiliation:
Université catholique de Louvain, Louvain Drug Research Institute, Metabolism and Nutrition Research Group, Avenue Mounier 73, Box B1.73.11, B-1200Brussels, Belgium
Audrey M. Neyrinck
Affiliation:
Université catholique de Louvain, Louvain Drug Research Institute, Metabolism and Nutrition Research Group, Avenue Mounier 73, Box B1.73.11, B-1200Brussels, Belgium
Patrice D. Cani
Affiliation:
Université catholique de Louvain, Louvain Drug Research Institute, Metabolism and Nutrition Research Group, Avenue Mounier 73, Box B1.73.11, B-1200Brussels, Belgium
*
*Corresponding author: N. M. Delzenne, fax +32 2 764 73 59; email email nathalie.delzenne@uclouvain.be
Rights & Permissions[Opens in a new window]

Abstract

Experimental data in animals, but also observational studies in obese patients, suggest that the composition of the gut microbiota differs in obese v. lean individuals, in diabetic v. non-diabetic patients or in patients presenting other diseases associated with obesity or nutritional dysbalance, such as non-alcoholic steatohepatitis. In the present review, we will describe how changes in the gut microbiota composition and/or activity by dietary fibres with prebiotic properties, can modulate host gene expression and metabolism. We will evaluate their potential relevance in the management of obesity and related metabolic disturbances, in view of the experimental data and intervention studies published up to date.

Type
Full Papers
Copyright
Copyright © The Authors 2013

The worldwide epidemic of obesity is a crucial problem of public health, as it is associated with a cluster of metabolic disorders such as insulin resistance, type 2 diabetes and fatty liver disease(Reference Hotamisligil1). The cause of obesity is basically linked to ‘nutritional disequilibrium’ in an individual who consumes an excess of fat and calories v. energy expenditure, over a relatively long period of time. In addition, overfeeding is often associated with inadequate nutrition, leading namely to a low intake of n-3 PUFA and of dietary fibres. In that respect, some dietary habits related to an increase in bioactive food components present in whole grain cereals could be helpful in prevention of chronic diseases(Reference Gil, Ortega and Maldonado2). In recent years, there has been increased attention focused on the bacteria that colonise our gut, which in ideal conditions live in symbiosis with the host(Reference Qin, Li and Raes3, Reference Diamant, Blaak and de Vos4). Novel culture-independent technologies based on the analysis of the bacterial gene 16SrRNA (e.g., pyrosequensing) allowed significant progress in the knowledge of our microbial partners(Reference Hsiao and Fraser-Liggett5, Reference Turnbaugh, Ley and Hamady6). Even if most of the function of the microbial genes remains unknown until now, and if we are conditioned at birth with a ‘personal’ profile of gut microbes, several recent papers and reviews support the idea that ‘dysbiosis’ (inadequate change of gut microbiota composition and/or activity related to host disease) characterises obese or overweight individuals(Reference Ley, Backhed and Turnbaugh7Reference Munukka, Wiklund and Pekkala11).

The first studies reporting changes in gut microbiota composition in obese individuals have focused on changes in phyla proportion (decreased Bacteroides:Firmicutes ratio). Recently, Arumugam et al. (Reference Arumugam, Raes and Pelletier12) have identified, in individuals from different countries and continents, three robust clusters of gut microbial communities defined as ‘enterotypes’ by the authors. They found that these enterotypes were identified by the variation at the level of one of the three following genera: Bacteroides, Prevotella and Ruminococcus. Wu et al. (Reference Wu, Chen and Hoffmann10) have shown that enterotypes were strongly associated with long-term diet, namely protein and animal fat (associated with Bacteroides) v. carbohydrates (Prevotella). Experiments performed in a model of mice colonised with the human gut microbiota reveals that changes in the diet composition (from high carbohydrates to western diet) allows a rapid switch of the microbial community, which can be transferred to germ-free mice(Reference Turnbaugh, Ridaura and Faith13). Interestingly, the transfer of this modified gut microbiota to germ-free mice also transfers the obese phenotype(Reference Turnbaugh, Ridaura and Faith13). Those data suggest that the gut microbiota composition/activity associated with nutritional imbalance might contribute to obesity and related disorders(Reference Ley8, Reference Caesar, Fak and Backhed14Reference Kau, Ahern and Griffin17). If dysbiosis exists, is there a means to favourably change the microbial environment, and thereby to improve host health? This idea fits with the concept of prebiotic, originally described in the 90s, referring to dietary compounds that modulate the composition and activity of the gastrointestinal microbiota to improve health and well-being(Reference Gibson and Roberfroid18Reference Brownawell, Caers and Gibson20). The main purpose of the present paper is to report how nutrients with potential prebiotic properties are interacting with host metabolism in the context of obesity. We will refer to both mechanistic approaches in animals and to the lower number of intervention studies performed with prebiotics in human subjects.

Selection of nutrients with prebiotic properties: the bifidogenic effect as a starting point

Wu et al. (Reference Wu, Chen and Hoffmann10) have shown that microbiome composition may change 24 h after initiating a high-fat/low-fibre or a high-fibre/low-fat diet, but that enterotype identity remained stable during a 10 d nutritional intervention. They suggest that nutrients like dietary fibres, which are not digested by host enzymes, could modulate the gut microbiome in a relatively short period of time, independent of the effect of changes in transit time. Would it be possible to link the properties of dietary fibres, which specifically modulate the gut microbiota, with host functions related to obesity and overfeeding? Fermentable carbohydrates have initially been recognised as prebiotics, because they were preferentially fermented by specific types of bacteria, generally recognised as beneficial for host. Indeed, Bifidobacterium spp. represent an important and complex group of bacteria whose presence is often associated with interesting health effects(Reference Boesten and de Vos21Reference Turroni, Marchesi and Foroni23). In the context of obesity, several studies reported that a low number of Bifidobacterium spp. correlated with the development of obesity and/or diabetes(Reference Kalliomaki, Collado and Salminen24Reference Wu, Ma and Han26). We have previously demonstrated that diet-induced obesity (high-fat–low-carbohydrate diet) in mice markedly affects the gut microbial community, where the levels of Bifidobacterium spp. were significantly reduced, in accordance with the observation in human subjects(Reference Cani, Neyrinck and Fava27, Reference Cani, Amar and Iglesias28). Several fermentable carbohydrates (glucans, galactans, fructans, etc.) are easily and widely fermented by Bifidobacteria. Several data have shown the bifidogenic effect of dietary fructans or arabinoxylans added in the diet of obese mice or rats(Reference Cani, Neyrinck and Fava27, Reference Everard, Lazarevic and Derrien29Reference Anastasovska, Arora and Sanchez Canon35).

In fact, promoting Bifidobacteria is not the sole consequence of the prebiotic treatment. By pyrosequencing and microarray analysis of the caecal 16SrDNA of ob/ob mice treated or not with prebiotics, we were able to point out more than 100 taxa that were different upon prebiotic treatment, some bacteria being particularly increased and some of them decreased by more than 10-fold(Reference Everard, Lazarevic and Derrien29). This allowed for the identification of interesting bacteria which are promoted with a prebiotic approach in this particular context, such as Faecalibacterium prausnitzii, exhibiting interesting anti-inflammatory properties and potentially involved in diabetes-related inflammation, or Akkermansia muciniphila, which has been shown to be inversely correlate with weight gain(Reference Everard, Lazarevic and Derrien29, Reference Santacruz, Collado and Garcia-Valdes36, Reference Furet, Kong and Tap37). Other studies have also shown that the prebiotic fibres decreased the Firmicutes:Bacteroidetes ratio in obese rats(Reference Parnell and Reimer34). Concerning human data, we have recently confirmed, in an intervention study with prebiotics v. placebo in obese women that even if the increase in Bifidobacteria remains the major and common signature of the prebiotic approach, a complex modulation of the gut microbial ecology also occurs upon prebiotic treatment in obese individuals(Reference Dewulf, Cani and Claus38).

Effect of prebiotic on host metabolism in obesity: relation with the modulation of the microbial ecosystem

Effect on body weight and adiposity

In obese animals (ob/ob mice, diet-induced obesity, obese Zucker or JCR:LA-cp rats), the dietary supplementation with non-digestible/fermentable carbohydrates – such as inulin-type fructans or arabinoxylans – is able to lessen adiposity(Reference Delzenne and Cani16, Reference Neyrinck, Possemiers and Druart30, Reference Parnell and Reimer33, Reference Parnell and Reimer34, Reference Cani and Delzenne39Reference Delzenne, Neyrinck and Backhed41). Prebiotic treatment changes the gene expression pattern in the white adipose tissue of obese mice (by acting on PPARγ and G-coupled receptors protein 43), leading to an increased lipolysis, a decreased adipogenesis and an increased metabolic response to hormones such as leptin, all those phenomenon contributing to a lower adiposity(Reference Everard, Lazarevic and Derrien29, Reference Neyrinck, Possemiers and Druart30, Reference Dewulf, Cani and Neyrinck42). In human subjects, treating obese individuals with fructan-type prebiotics has been tried in a limited number of intervention studies. Ingestion of inulin-type fructans prebiotic for 1 year has a significant benefit in the maintenance of BMI and fat mass in non-obese young adolescents(Reference Abrams, Griffin and Hawthorne43). Three months of treatment with fructans also decreases body weight gain and fat mass in adult obese subjects(Reference Parnell and Reimer44). The daily intake of yacon syrup, which contributed to an intake of 0·14 g fructans/kg per d over 120 d, decreases body weight, waist circumference and BMI in obese pre-menopausal women(Reference Genta, Cabrera and Habib45). Even if those data are significant, the weight loss remains modest (a few kg). None of those studies have reported the link between the changes in host adiposity and gut microbial composition.

Effect on gut peptides and appetite regulation

In obese animal fed inulin-type fructans, an increase in anorexigenic peptides (peptide YY and glucagon-like peptide 1 (7–36) amide) and a decrease in the orexigenic peptide ghrelin occurs, which contributes to the satietogenic effect of the peptide (for review see Cani & Delzenne(Reference Cani and Delzenne15)). In addition, the supplementation with fructans in high-fat diet-fed mice modulates the neuronal activation within the arcuate nucleus, which can contribute to the control of food intake(Reference Anastasovska, Arora and Sanchez Canon35). In human subjects, the satietogenic effect related to prebiotic interventions (assessed after 2 weeks to 3 months of treatment) is also being related to an increase in satietogenic and/or a decrease in orexigenic (ghrelin) peptides(Reference Parnell and Reimer44, Reference Cani, Lecourt and Dewulf46Reference Verhoef, Meyer and Westerterp48).

The modulation of the gut endocrine function by prebiotics in obese mice involves an increase in the number of L endocrine cells in the intestine, an effect which is correlated to bacterial changes in the gut(Reference Everard, Lazarevic and Derrien29). It is rather difficult to know by which mechanism the gut microbial environment influences L cells' differentiation. However, the production of SCFA (namely acetate, propionate) upon prebiotic fermentation could be part of the increase in secretion of gut peptides by the endocrine cells(Reference Tolhurst, Heffron and Lam49).

Effect on inflammation and gut barrier integrity

The gut microbiota can be involved in the development of a low-grade inflammation, classically associated with the metabolic disorders related to obesity(Reference Cani, Amar and Iglesias28, Reference de Lartigue, de La Serre and Raybould50, Reference Reigstad, Lunden and Felin51). The serum level of lipopolysaccharides (LPS), the main component of the Gram-negative bacteria, is approximately doubled in obese, diabetic or high-fat diet-fed individuals, a phenomenon that contributes to proinflammatory processes. The increase in LPS may occur by processes involving an increase in chylomicron formation (upon high-fat diet feeding), a decrease in gut barrier integrity and/or a decrease in alkaline phosphatase activity, which is the enzyme responsible for the cleavage of LPS in the intestine (for review see Cani & Delzenne(Reference Cani and Delzenne15) and Cani et al. (Reference Cani, Osto and Geurts52)). Several prebiotics (glucans, fructans) are able to counteract the increase in LPS level in animal models of obesity(Reference Cani, Neyrinck and Fava27, Reference Neyrinck, Van Hée and Piront31, Reference Cani, Possemiers and Van de32, Reference Serino, Luche and Gres53). The decrease in LPS absorption occurs in prebiotic-treated animals through an improvement of the expression and activity of proteins involved in gut barrier function, including glucagon-like peptide 2, which is co-secreted with glucagon-like peptide 1 by endocrine L cells. In addition, a drop in endocannabinoid system activation in the intestinal cells also participates in the gut barrier function by prebiotics in obese animals(Reference Cani, Neyrinck and Fava27, Reference Cani, Possemiers and Van de32, Reference Cani and Delzenne39, Reference Cani, Lecourt and Dewulf46, Reference Cani and Delzenne54Reference Muccioli, Naslain and Backhed58). Further mechanistic studies are needed in order to better understand how prebiotic nutrients may interact with the host immune response in the context of obesity and related disorders. Moreover, the relevance of those effects remains to be studied in human subjects.

Effect on glucose and lipid metabolism

In the majority of studies, the administration of prebiotics lead to an improvement of fasting and/or post-oral glucose load glycaemia (for review see Roberfroid et al. (Reference Roberfroid, Gibson and Hoyles19)). The mechanisms could involve the secretion of gut peptides with incretin function, such as glucagon-like peptide 1, which participates in the improvement of hepatic insulin resistance(Reference Cani, Knauf and Iglesias57). Several studies in human subjects also show an improvement in postprandial glycaemia, or, in some studies, in triglyceridaemia, upon prebiotic treatment, but those data are really not numerous enough to draw any conclusion on a potential benefit for diabetic or dyslipidaemic patients (for review see Delzenne et al. (Reference Delzenne, Neyrinck and Backhed41)). In most experimental studies, prebiotics are able to decrease the hepatic accumulation of TAG and/or cholesterol in the liver tissue, defined as steatosis. This effect could be particularly interesting, as the occurrence of non-alcoholic fatty liver disease is present in 25–75 % of the obese individuals. There again, mechanistic studies in animals reveal changes in hepatic host gene expression upon prebiotic treatment that could implicate, depending on the experimental conditions, a decrease in sterol-response-element-binding protein-dependent cholesterogenesis and/or lipogenesis, and/or of changes in PPARα-driven fatty acid oxidation (for review see Delzenne et al. (Reference Delzenne, Neyrinck and Backhed41), Delzenne & Cani(Reference Delzenne and Cani59)and Pachikian et al. (Reference Pachikian, Essaghir and Demoulin60)). Once again, research is needed to discover which microbial-derived metabolite could interfere with those metabolic processes. Only two intervention studies with prebiotics (fructans) have been reported in patients exhibiting hepatic diseases, suggesting an improvement of markers such as LPS or aminotransferases, without referring to the modulation of the gut microbiota(Reference Daubioul, Horsmans and Lambert61, Reference Malaguarnera, Vacante and Antic62).

Conclusion and perspectives

Highly fermentable carbohydrates, such as prebiotics, are able to counteract several metabolic alterations linked to obesity, including hyperglycaemia, inflammation and hepatic steatosis, at least in animal models (Fig. 1). The mechanistic studies suggest that the changes in the gut microbiota occurring upon prebiotic treatment, which appear much wider than the single increase in Bifidobacteria initially described, can be related to an improvement of gut bacterial functions implicated in the regulation of host energy homoeostasis. The promotion of gut hormones' release, changes in the gut barrier integrity and/or the release of bacterial-derived metabolites could all participate in the improvement of host health in the particular context of overfeeding and obesity. Appropriate human intervention studies with ‘colonic’ nutrients (dietary fibres, prebiotics and others) able to selectively promote beneficial bacteria, or with food containing colonic nutrients, are essential to confirm the relevance of those nutrients in the nutritional management of overweight and obesity.

Fig. 1 Effect of dietary carbohydrates with prebiotic properties on host pathophysiology related to obesity. In view of the experimental data obtained in intervention studies in animals, it has been shown that dietary carbohydrates with prebiotic properties change the gut microbiota composition by favouring bacteria involved in the control of gut barrier function and host immunity. In the gut, prebiotics help reinforcing the gut barrier and promote gut hormones that control appetite, glucose homoeostasis and systemic inflammation. The prebiotic approach also counteracts hepatic steatosis, hepatic insulin resistance and adiposity by modifying gene expression at the tissue level. F. prausnitzii, Faecalibacterium prausnitzii; SREBP, sterol-regulatory-element-binding protein; GPR43, G-coupled receptors protein 43; GLP, glucagon-like peptide; PYY, peptide YY. ITF, inulin-type fructans; AX, arabinoxylans.

Acknowledgements

P. D. C. is a research associate from the FRS-FNRS (Fonds de la Recherche Scientifique, Belgique). N. M. D. and P. D. C. are recipients of subsides from the Fonds National de la Recherche Scientifique (FNRS/FRSM) and from the ‘fonds spéciaux de recherche’, Université catholique de Louvain (UCL). The authors declare no conflict of interest related to the content of the present paper. All authors contributed equally to all aspects of the article.

References

1Hotamisligil, GS (2006) Inflammation and metabolic disorders. Nature 444, 860867.CrossRefGoogle ScholarPubMed
2Gil, A, Ortega, RM & Maldonado, J (2011) Wholegrain cereals and bread: a duet of the Mediterranean diet for the prevention of chronic diseases. Public Health Nutr 14, 23162322.CrossRefGoogle ScholarPubMed
3Qin, J, Li, R, Raes, J, et al. (2010) A human gut microbial gene catalogue established by metagenomic sequencing. Nature 464, 5965.CrossRefGoogle ScholarPubMed
4Diamant, M, Blaak, EE & de Vos, WM (2011) Do nutrient–gut–microbiota interactions play a role in human obesity, insulin resistance and type 2 diabetes? Obes Rev 12, 272281.CrossRefGoogle ScholarPubMed
5Hsiao, WW & Fraser-Liggett, CM (2009) Human microbiome project – paving the way to a better understanding of ourselves and our microbes. Drug Discov Today 14, 331333.CrossRefGoogle ScholarPubMed
6Turnbaugh, PJ, Ley, RE, Hamady, M, et al. (2007) The human microbiome project. Nature 449, 804810.CrossRefGoogle ScholarPubMed
7Ley, RE, Backhed, F, Turnbaugh, P, et al. (2005) Obesity alters gut microbial ecology. Proc Natl Acad Sci U S A 102, 1107011075.CrossRefGoogle ScholarPubMed
8Ley, RE (2010) Obesity and the human microbiome. Curr Opin Gastroenterol 26, 511.CrossRefGoogle ScholarPubMed
9Ley, RE, Turnbaugh, PJ, Klein, S, et al. (2006) Microbial ecology: human gut microbes associated with obesity. Nature 444, 10221023.CrossRefGoogle ScholarPubMed
10Wu, GD, Chen, J, Hoffmann, C, et al. (2011) Linking long-term dietary patterns with gut microbial enterotypes. Science 334, 105108.CrossRefGoogle ScholarPubMed
11Munukka, E, Wiklund, P, Pekkala, S, et al. (2012) Women with and without metabolic disorder differ in their gut microbiota composition. Obesity (Silver Spring) 20, 10821087.CrossRefGoogle ScholarPubMed
12Arumugam, M, Raes, J, Pelletier, E, et al. (2011) Enterotypes of the human gut microbiome. Nature 473, 174180.CrossRefGoogle ScholarPubMed
13Turnbaugh, PJ, Ridaura, VK, Faith, JJ, et al. (2009) The effect of diet on the human gut microbiome: a metagenomic analysis in humanized gnotobiotic mice. Sci Transl Med 1, 6ra14.CrossRefGoogle ScholarPubMed
14Caesar, R, Fak, F & Backhed, F (2010) Effects of gut microbiota on obesity and atherosclerosis via modulation of inflammation and lipid metabolism. J Intern Med 268, 320328.CrossRefGoogle ScholarPubMed
15Cani, PD & Delzenne, NM (2011) The gut microbiome as therapeutic target. Pharmacol Ther 130, 202212.CrossRefGoogle ScholarPubMed
16Delzenne, NM & Cani, PD (2010) Nutritional modulation of gut microbiota in the context of obesity and insulin resistance: potential interest of prebiotics. Int Dairy J 20, 277280.CrossRefGoogle Scholar
17Kau, AL, Ahern, PP, Griffin, NW, et al. (2011) Human nutrition, the gut microbiome and the immune system. Nature 474, 327336.CrossRefGoogle ScholarPubMed
18Gibson, GR & Roberfroid, MB (1995) Dietary modulation of the human colonic microbiota: introducing the concept of prebiotics. J Nutr 125, 14011412.Google ScholarPubMed
19Roberfroid, M, Gibson, GR, Hoyles, L, et al. (2010) Prebiotic effects: metabolic and health benefits. Br J Nutr 104, Suppl. 2, S1S63.CrossRefGoogle ScholarPubMed
20Brownawell, AM, Caers, W, Gibson, GR, et al. (2012) Prebiotics and the health benefits of fiber: current regulatory status, future research, and goals. J Nutr 142, 962974.CrossRefGoogle ScholarPubMed
21Boesten, RJ & de Vos, WM (2008) Interactomics in the human intestine: Lactobacilli and Bifidobacteria make a difference. J Clin Gastroenterol 42, S163S167.CrossRefGoogle Scholar
22Boesten, RJ, Schuren, FH & de Vos, WM (2009) A Bifidobacterium mixed-species microarray for high resolution discrimination between intestinal bifidobacteria. J Microbiol Methods 76, 269277.CrossRefGoogle ScholarPubMed
23Turroni, F, Marchesi, JR, Foroni, E, et al. (2009) Microbiomic analysis of the bifidobacterial population in the human distal gut. ISME J 3, 745751.CrossRefGoogle ScholarPubMed
24Kalliomaki, M, Collado, MC, Salminen, S, et al. (2008) Early differences in fecal microbiota composition in children may predict overweight. Am J Clin Nutr 87, 534538.CrossRefGoogle ScholarPubMed
25Collado, MC, Isolauri, E, Laitinen, K, et al. (2008) Distinct composition of gut microbiota during pregnancy in overweight and normal-weight women. Am J Clin Nutr 88, 894899.CrossRefGoogle ScholarPubMed
26Wu, X, Ma, C, Han, L, et al. (2010) Molecular characterisation of the faecal microbiota in patients with type II diabetes. Curr Microbiol 61, 6978.CrossRefGoogle ScholarPubMed
27Cani, PD, Neyrinck, AM, Fava, F, et al. (2007) Selective increases of bifidobacteria in gut microflora improve high-fat-diet-induced diabetes in mice through a mechanism associated with endotoxaemia. Diabetologia 50, 23742383.CrossRefGoogle ScholarPubMed
28Cani, PD, Amar, J, Iglesias, MA, et al. (2007) Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes 56, 17611772.CrossRefGoogle ScholarPubMed
29Everard, A, Lazarevic, V, Derrien, M, et al. (2011) Responses of gut microbiota and glucose and lipid metabolism to prebiotics in genetic obese and diet-induced leptin-resistant mice. Diabetes 60, 27752786.CrossRefGoogle ScholarPubMed
30Neyrinck, AM, Possemiers, S, Druart, C, et al. (2011) Prebiotic effects of wheat arabinoxylan related to the increase in bifidobacteria, Roseburia and Bacteroides/Prevotella in diet-induced obese mice. PLoS One 6, e20944.CrossRefGoogle ScholarPubMed
31Neyrinck, AM, Van Hée, VF, Piront, N, et al. (2012) Wheat-derived arabinoxylan oligosaccharides with prebiotic effect increase satietogenic gut peptides and reduce metabolic endotoxemia in diet-induced obese mice. Nutr Diabetes 2, e28.CrossRefGoogle ScholarPubMed
32Cani, PD, Possemiers, S, Van de, WT, et al. (2009) Changes in gut microbiota control inflammation in obese mice through a mechanism involving GLP-2-driven improvement of gut permeability. Gut 58, 10911103.CrossRefGoogle ScholarPubMed
33Parnell, JA & Reimer, A (2012) Prebiotic fiber modulation of the gut microbiota improves risk factors for obesity and the metabolic syndrome. Gut Microbes 3, 2934.CrossRefGoogle ScholarPubMed
34Parnell, JA & Reimer, RA (2012) Prebiotic fibres dose-dependently increase satiety hormones and alter Bacteroidetes and Firmicutes in lean and obese JCR:LA-cp rats. Br J Nutr 107, 601613.CrossRefGoogle ScholarPubMed
35Anastasovska, J, Arora, T, Sanchez Canon, GJ, et al. (2012) Fermentable carbohydrate alters hypothalamic neuronal activity and protects against the obesogenic environment. Obesity (Silver Spring) 20, 10161023.CrossRefGoogle ScholarPubMed
36Santacruz, A, Collado, MC, Garcia-Valdes, L, et al. (2010) Gut microbiota composition is associated with body weight, weight gain and biochemical parameters in pregnant women. Br J Nutr 104, 8392.CrossRefGoogle ScholarPubMed
37Furet, JP, Kong, LC, Tap, J, et al. (2010) Differential adaptation of human gut microbiota to bariatric surgery-induced weight loss: links with metabolic and low-grade inflammation markers. Diabetes 59, 30493057.CrossRefGoogle ScholarPubMed
38Dewulf, EM, Cani, PD, Claus, SP, et al. (2012) Inulin-type fructans with prebiotic properties lessen endotoxemia and modulate host metabolism by changing gut microbiota composition in obese women. Obes Facts Eur J Obes 5, 200.Google Scholar
39Cani, PD & Delzenne, NM (2009) The role of the gut microbiota in energy metabolism and metabolic disease. Curr Pharm Des 15, 15461558.CrossRefGoogle ScholarPubMed
40Neyrinck, AM & Delzenne, NM (2010) Potential interest of gut microbial changes induced by non-digestible carbohydrates of wheat in the management of obesity and related disorders. Curr Opin Clin Nutr Metab Care 13, 722728.CrossRefGoogle ScholarPubMed
41Delzenne, NM, Neyrinck, AM, Backhed, F, et al. (2011) Targeting gut microbiota in obesity: effects of prebiotics and probiotics. Nat Rev Endocrinol 7, 639646.CrossRefGoogle ScholarPubMed
42Dewulf, EM, Cani, PD, Neyrinck, AM, et al. (2011) Inulin-type fructans with prebiotic properties counteract GPR43 overexpression and PPARgamma-related adipogenesis in the white adipose tissue of high-fat diet-fed mice. J Nutr Biochem 22, 712722.CrossRefGoogle ScholarPubMed
43Abrams, SA, Griffin, IJ, Hawthorne, KM, et al. (2007) Effect of prebiotic supplementation and calcium intake on body mass index. J Pediatr 151, 293298.CrossRefGoogle ScholarPubMed
44Parnell, JA & Reimer, RA (2009) Weight loss during oligofructose supplementation is associated with decreased ghrelin and increased peptide YY in overweight and obese adults. Am J Clin Nutr 89, 17511759.CrossRefGoogle ScholarPubMed
45Genta, S, Cabrera, W, Habib, N, et al. (2009) Yacon syrup: beneficial effects on obesity and insulin resistance in humans. Clin Nutr 28, 182187.CrossRefGoogle ScholarPubMed
46Cani, PD, Lecourt, E, Dewulf, EM, et al. (2009) Gut microbiota fermentation of prebiotics increases satietogenic and incretin gut peptide production with consequences for appetite sensation and glucose response after a meal. Am J Clin Nutr 90, 12361243.CrossRefGoogle ScholarPubMed
47Cani, PD, Joly, E, Horsmans, Y, et al. (2006) Oligofructose promotes satiety in healthy human: a pilot study. Eur J Clin Nutr 60, 567572.CrossRefGoogle ScholarPubMed
48Verhoef, SP, Meyer, D & Westerterp, KR (2011) Effects of oligofructose on appetite profile, glucagon-like peptide 1 and peptide YY3-36 concentrations and energy intake. Br J Nutr 106, 17571762.CrossRefGoogle ScholarPubMed
49Tolhurst, G, Heffron, H, Lam, YS, et al. (2012) Short-chain fatty acids stimulate glucagon-like peptide-1 secretion via the G-protein-coupled receptor FFAR2. Diabetes 61, 364371.CrossRefGoogle ScholarPubMed
50de Lartigue, G, de La Serre, CB & Raybould, HE (2011) Vagal afferent neurons in high fat diet-induced obesity; intestinal microflora, gut inflammation and cholecystokinin. Physiol Behav 105, 100105.CrossRefGoogle ScholarPubMed
51Reigstad, CS, Lunden, GO, Felin, J, et al. (2009) Regulation of serum amyloid A3 (SAA3) in mouse colonic epithelium and adipose tissue by the intestinal microbiota. PLoS One 4, e5842.CrossRefGoogle ScholarPubMed
52Cani, PD, Osto, M, Geurts, L, et al. (2012) Involvement of gut microbiota in the development of low-grade inflammation and type 2 diabetes associated with obesity. Gut Microbes 1; 3(4). http://dx.doi.org/10.4161/gmic.19625.Google Scholar
53Serino, M, Luche, E, Gres, S, et al. (2012) Metabolic adaptation to a high-fat diet is associated with a change in the gut microbiota. Gut 61, 543553.CrossRefGoogle ScholarPubMed
54Cani, PD & Delzenne, NM (2009) Interplay between obesity and associated metabolic disorders: new insights into the gut microbiota. Curr Opin Pharmacol 9, 737743.CrossRefGoogle ScholarPubMed
55Delzenne, NM, Cani, PD & Neyrinck, AM (2007) Modulation of glucagon-like peptide 1 and energy metabolism by inulin and oligofructose: experimental data. J Nutr 137, 2547S2551S.CrossRefGoogle ScholarPubMed
56Cani, PD & Delzenne, NM (2007) Gut microflora as a target for energy and metabolic homeostasis. Curr Opin Clin Nutr Metab Care 10, 729734.CrossRefGoogle ScholarPubMed
57Cani, PD, Knauf, C, Iglesias, MA, et al. (2006) Improvement of glucose tolerance and hepatic insulin sensitivity by oligofructose requires a functional glucagon-like peptide 1 receptor. Diabetes 55, 14841490.CrossRefGoogle ScholarPubMed
58Muccioli, GG, Naslain, D, Backhed, F, et al. (2010) The endocannabinoid system links gut microbiota to adipogenesis. Mol Syst Biol 6, 392.CrossRefGoogle ScholarPubMed
59Delzenne, NM & Cani, PD (2011) Interaction between obesity and the gut microbiota: relevance in nutrition. Annu Rev Nutr 31, 1531.CrossRefGoogle ScholarPubMed
60Pachikian, BD, Essaghir, A, Demoulin, JB, et al. (2011) Prebiotic approach improves hepatic steatosis associated with n-3 polyunsaturated fatty acid depletion in mice. Ann Nutr Metab 58, S3, 76.Google Scholar
61Daubioul, CA, Horsmans, Y, Lambert, P, et al. (2005) Effects of oligofructose on glucose and lipid metabolism in patients with nonalcoholic steatohepatitis: results of a pilot study. Eur J Clin Nutr 59, 723726.CrossRefGoogle ScholarPubMed
62Malaguarnera, M, Vacante, M, Antic, T, et al. (2012) Bifidobacterium longum with fructo-oligosaccharides in patients with non alcoholic steatohepatitis. Dig Dis Sci 57, 545553.CrossRefGoogle ScholarPubMed
Figure 0

Fig. 1 Effect of dietary carbohydrates with prebiotic properties on host pathophysiology related to obesity. In view of the experimental data obtained in intervention studies in animals, it has been shown that dietary carbohydrates with prebiotic properties change the gut microbiota composition by favouring bacteria involved in the control of gut barrier function and host immunity. In the gut, prebiotics help reinforcing the gut barrier and promote gut hormones that control appetite, glucose homoeostasis and systemic inflammation. The prebiotic approach also counteracts hepatic steatosis, hepatic insulin resistance and adiposity by modifying gene expression at the tissue level. F. prausnitzii, Faecalibacterium prausnitzii; SREBP, sterol-regulatory-element-binding protein; GPR43, G-coupled receptors protein 43; GLP, glucagon-like peptide; PYY, peptide YY. ITF, inulin-type fructans; AX, arabinoxylans.

You have Access
109
Cited by

Save article to Kindle

To save this article to your Kindle, first ensure coreplatform@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

Gut microbiota and metabolic disorders: how prebiotic can work?
Available formats
×

Save article to Dropbox

To save this article to your Dropbox account, please select one or more formats and confirm that you agree to abide by our usage policies. If this is the first time you used this feature, you will be asked to authorise Cambridge Core to connect with your Dropbox account. Find out more about saving content to Dropbox.

Gut microbiota and metabolic disorders: how prebiotic can work?
Available formats
×

Save article to Google Drive

To save this article to your Google Drive account, please select one or more formats and confirm that you agree to abide by our usage policies. If this is the first time you used this feature, you will be asked to authorise Cambridge Core to connect with your Google Drive account. Find out more about saving content to Google Drive.

Gut microbiota and metabolic disorders: how prebiotic can work?
Available formats
×
×

Reply to: Submit a response

Please enter your response.

Your details

Please enter a valid email address.

Conflicting interests

Do you have any conflicting interests? *