SCFAs strongly stimulate PYY production in human enteroendocrine cells

Larraufie, Pierre; Martin-Gallausiaux, Camille; Lapaque, Nicolas; Doré, Joël; Gribble, Fiona M.; Reimann, Frank; Blottière, Hervé M.

doi:10.1038/s41598-017-18259-0

Cited by 285 publications

(216 citation statements)

References 43 publications

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“…As this was seen only for low-fat dieters, we hypothesized that increased plasticity might have 228 facilitated responsiveness to the increased carbohydrates and fiber consumed on the low-fat diet 229 [24], making the transition to the new diet easier for subjects in ways that aided adherence through 230 appetite suppression [33,39,8,25,12,3,2]. Our data suggest this is true for men, as we saw positive 231 correlations between plasticity and both weight loss and dietary compliance.…”

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confidence: 76%

Gut microbiota plasticity is correlated with sustained weight loss on a low-carb or low-fat dietary intervention

Grembi¹,

Nguyen²,

Haggerty

et al. 2019

Preprint

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1Background Obesity is a complex global health challenge. Although both low-carbohydrate 2 (low-carb) and low-fat diets can lead to weight loss, there is typically substantial variability 3 in weight and related outcomes for both diet approaches among obese but otherwise healthy 4 adults. Elucidating individual characteristics that might contribute to sustained weight loss is 5 critical to developing effective dietary intervention strategies. We hypothesized that structural 6 differences in the gut microbiota explained some portion of the weight loss variability among 7 people randomized to either a low-carb or low-fat diet, possibly related to its effects on dietary 8 compliance. 9 Results Our study included two staggered cohorts of obese adults enrolled in the Diet 10 Intervention Examining The Factors Interacting with Treatment Success (DIETFITS) study -11 a randomized clinical trial of either a low-fat or low-carb diet. In the discovery cohort (n=66), 12 161 pre-diet fecal samples were sequenced in addition to 157 samples collected after 10-weeks 13 of dietary intervention. In the validation cohort (n = 56), 106 pre-diet fecal samples were 14 sequenced. Pre-diet taxonomic features, such as the Prevotella/Bacteroides ratio, correlated to 15 weight loss in the discovery cohort were not confirmed in the validation cohort. The most robust 16 finding in the discovery cohort indicated that gut microbiota plasticity was linked to 12-month 17 weight loss in a diet-dependent manner; subjects with higher sustained weight loss on a low-fat 18 diet had higher pre-diet daily plasticity, whereas those most successful on the low-carb diet 19 had greater microbiota plasticity over 10 weeks of dietary intervention. Unfortunately, because 20 sample frequency and timing was quite different in the validation cohort, the relationship 21 between plasticity and weight loss could not be studied in this group. 22 Conclusions These findings suggest the potential importance of gut microbiota plasticity 23 in sustained weight loss. We highlight the importance of evaluating kinetic trends and in 24 assessing reproducibility in studies of the gut microbiota. 25 1 Background 27The global obesity pandemic has claimed one in three American adults and prevalences continue 28 to rise in many other countries as well [46]. Obesity comorbidities (e.g. cardiovascular diseases, 29 cancer, diabetes, and other chronic conditions) cost the US 8.65 billion/yr from loss of productivity 30 due to absenteeism alone [58,65,53,55,14]. The personal, social and economic costs provide an 31 urgent need for consistently effective, and possibly more personalized, weight-reduction therapies. 32Different dietary interventions, such as low-carbohydrate (low-carb) and low-fat diets, can lead 33 to weight loss, but not always; there remains substantial variability in diet success outcomes among 34 obese, but otherwise healthy, adults [37]. Additionally, adherence to dietary intervention strategies 35 has remained a major challenge, despite the clear dose-response rel...

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mentioning

confidence: 76%

Gut microbiota plasticity is correlated with sustained weight loss on a low-carb or low-fat dietary intervention

Grembi¹,

Nguyen²,

Haggerty

et al. 2019

Preprint

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“…Interestingly, FFAR3 was found in CCK-positive cells in the duodenum and in NTSpositive cells in the ileum and colon (53). Propionate is also an inhibitor of histone deacetylases (54); therefore, it can also regulate gene expression through the increase in histone acetylation (55). To our knowledge, no study has focused on the regulation of CCK by SCFAs, likely because, until recently, the abundance of CCK in the ileum, cecum, and colon was thought to be insignificant (56).…”

Section: Discussionmentioning

confidence: 99%

Fructose malabsorption induces cholecystokinin expression in the ileum and cecum by changing microbiota composition and metabolism

et al. 2019

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Current fructose consumption levels often overwhelm the intestinal capacity to absorb fructose. We investigated the impact of fructose malabsorption on intestinal endocrine function and addressed the role of the microbiota in this process. To answer this question, a mouse model of moderate fructose malabsorption [ketohexokinase mutant (KHK)−/−] and wild‐type (WT) littermate mice were used and received a 20%‐fructose (KHK‐F and WT‐F) or 20%‐glucose diet. Cholecystokinin (Cck) mRNA and protein expression in the ileum and cecum, as well as preproglucagon (Gcg) and neurotensin (Nts) mRNA expression in the cecum, increased in KHK‐F mice. In KHK‐F mice, triple‐label immunohistochemistry showed major up‐regulation of CCK in enteroendocrine cells (EECs) that were glucagon‐like peptide‐1 (GLP‐1)+/Peptide YY (PYY−) in the ileum and colon and GLP‐1−/PYY− in the cecum. The cecal microbiota composition was drastically modified in the KHK‐F in association with an increase in glucose, propionate, succinate, and lactate concentrations. Antibiotic treatment abolished fructose malabsorption‐dependent induction of cecal Cck mRNA expression and, in mouse GLUTag and human NCI‐H716 cells, Cck mRNA expression levels increased in response to propionate, both suggesting a microbiota‐dependent process. Fructose reaching the lower intestine can modify the composition and metabolism of the microbiota, thereby stimulating the production of CCK from the EECs possibly in response to propionate.—Zhang, X., Grosfeld, A., Williams, E., Vasiliauskas, D., Barretto, S., Smith, L., Mariadassou, M., Philippe, C., Devime, F., Melchior, C., Gourcerol, G., Dourmap, N., Lapaque, N., Larraufie, P., Blottière, H. M., Herberden, C., Gerard, P., Rehfeld, J. F., Ferraris, R. P., Fritton, J. C., Ellero‐Simatos, S., Douard, V. Fructose malabsorption induces cholecystokinin expression in the ileum and cecum by changing microbiota composition and metabolism. FASEB J. 33, 7126–7142 (2019). http://www.fasebj.org

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“…L-cells in the distal small intestine appear to have a greater capacity to secrete PYY than GLP-1 [6]. In this site, short-chain fatty acids (SCFAs) produced by the microbiota, increase plasma PYY, but not GLP-1 levels, both in the fasted and fed states [29]. A high-fat diet produces less SCFAs than a high-carbohydrate diet [30].…”

Section: Discussionmentioning

confidence: 99%

Secretion of Gut Hormones and Expression of Sweet Taste Receptors and Glucose Transporters in a Rat Model of Obesity

Feng¹,

Qian²,

Liu³

et al. 2019

Obes Facts

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Objectives: This study was undertaken to compare gut hormone secretion between high-fat-fed and control rats, and to examine the corresponding changes in the expression of sweet taste receptors and glucose transporters in the small intestine and hypothalamus. Methods: Four-week-old male Sprague Dawley rats were fed a standard or high-fat diet for 8 weeks (10 in each group), followed by an oral glucose tolerance test (50% glucose solution, 2 g/kg). Blood was sampled for glucose, insulin, glucagon-like peptide-1 (GLP-1) and polypeptide YY (PYY) assays. One week later, small intestinal and hypothalamic tissue were analyzed for sweet taste receptor and glucose transporter expression by real-time PCR. Results: After oral glucose, plasma GLP-1 concentrations were higher in high-fat-fed than standard-fat-fed rats (group × time interaction, p < 0.01) with significant differences at t = 15 min (p < 0.01) and 30 min (p < 0.05). Plasma PYY concentrations were lower in high-fat-fed than control rats at t = 0, 15 min (p < 0.05, respectively) and 120 min (p < 0.01). There were no differences in the expression of sweet taste receptors or glucose transporters between high-fat-fed and control rats in the duodenum, ileum, or hypothalamus. Conclusions: Changes in GLP-1 and PYY secretion after a high-fat diet appear unrelated to any changes in the expression of sweet taste receptors or glucose transporters. Impaired PYY secretion with high-fat feeding suggests that PYY analogues may provide a potential therapy in the treatment of obesity.

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SCFAs strongly stimulate PYY production in human enteroendocrine cells

Cited by 285 publications

References 43 publications

Gut microbiota plasticity is correlated with sustained weight loss on a low-carb or low-fat dietary intervention

Gut microbiota plasticity is correlated with sustained weight loss on a low-carb or low-fat dietary intervention

Fructose malabsorption induces cholecystokinin expression in the ileum and cecum by changing microbiota composition and metabolism

Secretion of Gut Hormones and Expression of Sweet Taste Receptors and Glucose Transporters in a Rat Model of Obesity

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