scholarly journals High fat diet induces microbiota-dependent silencing of enteroendocrine cells

2019 ◽  
Author(s):  
Lihua Ye ◽  
Olaf Mueller ◽  
Jennifer Bagwell ◽  
Michel Bagnat ◽  
Rodger A. Liddle ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Experimental System ◽  
Nutrient Sensing ◽  
Enteroendocrine Cells ◽  
Sensory Cells ◽  
High Fat ◽  
Fat Feeding

ABSTRACTEnteroendocrine cells (EECs) are specialized sensory cells in the intestinal epithelium that sense and transduce nutrient information. Consumption of dietary fat contributes to metabolic disorders, but EEC adaptations to high fat feeding were unknown. Here, we established a new experimental system to directly investigate EEC activity in vivo using a zebrafish reporter of EEC calcium signaling. Our results reveal that high fat feeding alters EEC morphology and converts them into a nutrient insensitive state that is coupled to endoplasmic reticulum (ER) stress. We called this novel adaptation “EEC silencing”. Gnotobiotic studies revealed that germ-free zebrafish are resistant to high fat diet induced EEC silencing. High fat feeding altered gut microbiota composition including enrichment ofAcinetobacterspecies, and we identified anAcinetobacterstrain sufficient to induce EEC silencing. These results establish a new mechanism by which dietary fat and gut microbiota modulate EEC nutrient sensing and signaling.

scholarly journals High fat diet induces microbiota-dependent silencing of enteroendocrine cells

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Lihua Ye ◽  
Olaf Mueller ◽  
Jennifer Bagwell ◽  
Michel Bagnat ◽  
Rodger A Liddle ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Experimental System ◽  
Nutrient Sensing ◽  
Enteroendocrine Cells ◽  
Sensory Cells ◽  
High Fat ◽  
Fat Feeding

Enteroendocrine cells (EECs) are specialized sensory cells in the intestinal epithelium that sense and transduce nutrient information. Consumption of dietary fat contributes to metabolic disorders, but EEC adaptations to high fat feeding were unknown. Here, we established a new experimental system to directly investigate EEC activity in vivo using a zebrafish reporter of EEC calcium signaling. Our results reveal that high fat feeding alters EEC morphology and converts them into a nutrient insensitive state that is coupled to endoplasmic reticulum (ER) stress. We called this novel adaptation 'EEC silencing'. Gnotobiotic studies revealed that germ-free zebrafish are resistant to high fat diet induced EEC silencing. High fat feeding altered gut microbiota composition including enrichment of Acinetobacter bacteria, and we identified an Acinetobacter strain sufficient to induce EEC silencing. These results establish a new mechanism by which dietary fat and gut microbiota modulate EEC nutrient sensing and signaling.

scholarly journals High-Fat Diet Induced Gut Microbiota Alterations Associating With Ghrelin/Jak2/Stat3 Up-Regulation to Promote Benign Prostatic Hyperplasia Development

2021 ◽  
Vol 9 ◽  
Author(s):  
Meng Gu ◽  
Chong Liu ◽  
TianYe Yang ◽  
Ming Zhan ◽  
Zhikang Cai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Benign Prostatic Hyperplasia ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Prostatic Hyperplasia ◽  
Prostate Tissue ◽  
High Fat ◽  
Ghrelin Receptor

The role of high-fat diet (HFD) induced gut microbiota alteration and Ghrelin as well as their correlation in benign prostatic hyperplasia (BPH) were explored in our study. The gut microbiota was analyzed by 16s rRNA sequencing. Ghrelin levels in serum, along with Ghrelin and Ghrelin receptor in prostate tissue of mice and patients with BPH were measured. The effect of Ghrelin on cell proliferation, apoptosis, and induction of BPH in mice was explored. Our results indicated that BPH mice have the highest ratio of Firmicutes and Bacteroidetes induced by HFD, as well as Ghrelin level in serum and prostate tissue was significantly increased compared with control. Elevated Ghrelin content in the serum and prostate tissue of BPH patients was also observed. Ghrelin promotes cell proliferation while inhibiting cell apoptosis of prostate cells. The effect of Ghrelin on enlargement of the prostate was found almost equivalent to that of testosterone propionate (TP) which may be attenuated by Ghrelin receptor antagonist YIL-781. Ghrelin could up-regulate Jak2/pJak2/Stat3/pStat3 expression in vitro and in vivo. Our results suggested that Gut microbiota may associate with Ghrelin which plays an important role in activation of Jak2/Stat3 in BPH development. Gut microbiota and Ghrelin might be pathogenic factors for BPH and could be used as a target for mediation.

Decreased responsiveness to dietary fat in Otsuka Long-Evans Tokushima fatty rats lacking CCK-A receptors

1999 ◽  
Vol 277 (4) ◽  
pp. R1144-R1151 ◽  
Author(s):  
Gary J. Schwartz ◽  
Andrew Whitney ◽  
Chris Skoglund ◽  
Thomas W. Castonguay ◽  
Timothy H. Moran
Keyword(s):  
Dietary Fat ◽  
High Fat Diet ◽  
Corn Oil ◽  
High Fat ◽  
Oletf Rats ◽  
Glucose Intake ◽  
Long Evans ◽  
Fat Feeding ◽  
Cck Release ◽  
Subsequent Intake

Adult Otsuka Long-Evans Tokushima fatty (OLETF) rats lack functional cholecystokinin A (CCK-A) receptors, are diabetic, hyperphagic, and obese, and have patterns of ingestion consistent with a satiety deficit secondary to CCK insensitivity. Because dietary fat potently stimulates CCK release, we examined how dietary fat modulates feeding in adult male OLETF rats and their lean [Long-Evans Tokushima (LETO)] controls. High-fat feeding produced sustained overconsumption of high-fat diet (30% corn oil in powdered chow) over a 3-wk period in OLETF but not LETO rats. We then assessed the ability of gastric gavage (5 ml, 1–2 kcal/ml × 15 s) or duodenal preloads (1 kcal/ml, 0.44 ml/min × 10 min) of liquid carbohydrate (glucose), protein (peptone), or fat (Intralipid) to suppress subsequent 30-min 12.5% glucose intake in both strains. In OLETF rats, gastric and duodenal fat preloads were significantly less effective in suppressing subsequent intake than were equicaloric peptone or glucose. These results demonstrate that OLETF rats fail to compensate for fat calories and suggest that their hyperphagia and obesity may stem from a reduced ability to process nutrient-elicited gastrointestinal satiety signals.

Effect of a high-fat diet on the incorporation of stored triacylglycerol into hepatic VLDL

1992 ◽  
Vol 263 (4) ◽  
pp. E615-E623 ◽  
Author(s):  
O. L. Francone ◽  
G. Griffaton ◽  
A. D. Kalopissis
Keyword(s):  
Endoplasmic Reticulum ◽  
High Fat Diet ◽  
Lipid Droplets ◽  
Control Diet ◽  
Oxidation Products ◽  
High Fat ◽  
Very Low Density Lipoproteins ◽  
Total Utilization ◽  
Fat Feeding

Triacylglycerol (TG) stored in cytoplasmic lipid droplets of hepatocytes was labeled by in vivo [1-(14)C]oleic acid injection to study the effect of a high-fat diet on its incorporation into very-low-density lipoproteins (VLDL). Compared with the control diet, hepatocytes of fat-fed rats 1) contained 7.6 times more cytoplasmic (floating fat) TG and 1.9 times more endoplasmic reticulum (microsomal) TG; 2) had 8 and 6 times lower TG specific activities in cytoplasm and endoplasmic reticulum, respectively; 3) incorporated 22% less 14C label into hepatocyte esterified lipids (TG, cholesterol, phospholipid); 4) secreted 48 and 33% less radioactive and total VLDL-TG, respectively; 5) oxidized more cytoplasmic TG-fatty acid (FA); and 6) showed a 50% decreased total utilization of stored TG-FA. With both diets, the lysosomal inhibitor chloroquine concomitantly decreased productions of labeled VLDL-TG, CO2, and acid-soluble oxidation products. The decreased incorporation of stored TG into VLDL-TG appreciably contributes to the overall inhibition of hepatic VLDL secretion by fat feeding. It appears to be related to the decreased mobilization rate of stored TG and its increased channelling toward oxidation.

scholarly journals Effect of a long-term high-protein diet on survival, obesity development, and gut microbiota in mice

2016 ◽  
Vol 310 (11) ◽  
pp. E886-E899 ◽  
Author(s):  
Pia Kiilerich ◽  
Lene Secher Myrmel ◽  
Even Fjære ◽  
Qin Hao ◽  
Floor Hugenholtz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Gut Microbiota ◽  
Dietary Fat ◽  
High Fat Diet ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Low Protein

Female C57BL/6J mice were fed a regular low-fat diet or high-fat diets combined with either high or low protein-to-sucrose ratios during their entire lifespan to examine the long-term effects on obesity development, gut microbiota, and survival. Intake of a high-fat diet with a low protein/sucrose ratio precipitated obesity and reduced survival relative to mice fed a low-fat diet. By contrast, intake of a high-fat diet with a high protein/sucrose ratio attenuated lifelong weight gain and adipose tissue expansion, and survival was not significantly altered relative to low-fat-fed mice. Our findings support the notion that reduced survival in response to high-fat/high-sucrose feeding is linked to obesity development. Digital gene expression analyses, further validated by qPCR, demonstrated that the protein/sucrose ratio modulated global gene expression over time in liver and adipose tissue, affecting pathways related to metabolism and inflammation. Analysis of fecal bacterial DNA using the Mouse Intestinal Tract Chip revealed significant changes in the composition of the gut microbiota in relation to host age and dietary fat content, but not the protein/sucrose ratio. Accordingly, dietary fat rather than the protein/sucrose ratio or adiposity is a major driver shaping the gut microbiota, whereas the effect of a high-fat diet on survival is dependent on the protein/sucrose ratio.

scholarly journals It’s the fiber, not the fat: Significant effects of dietary challenge on the gut microbiome

2019 ◽  
Author(s):  
Kathleen E. Morrison ◽  
Eldin Jašarević ◽  
Christopher D. Howard ◽  
Tracy L. Bale
Keyword(s):  
Body Weight ◽  
Gut Microbiota ◽  
Dietary Fat ◽  
Gut Microbiome ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Chow Diet ◽  
Soluble Fiber ◽  
High Fat ◽  
The Impact

AbstractBackgroundDietary effects on the gut microbiome has been shown to play a key role in the pathophysiology of behavioral dysregulation, inflammatory disorders, metabolic syndrome, and obesity. Often overlooked is that experimental diets vary significantly in the proportion and source of dietary fiber. Commonly, treatment comparisons are made between animals that are fed refined diets that lack soluble fiber and animals fed vivarium-provided chow diet that contain a rich source of soluble fiber. Despite the well-established role of soluble fiber on metabolism, immunity, and behavior via the gut microbiome, the extent to which measured outcomes may be driven by differences in dietary fiber is unclear. Further, the significant impact of sex and age in response to dietary challenge is likely important and should also be considered.ResultsWe compared the impact of transitioning young and aged male and female mice from a chow diet to a refined low soluble fiber diet on body weight and gut microbiota. Then, to determine the contribution of dietary fat, we examined the impact of transitioning a subset of animals from refined low fat to refined high fat diet. Serial tracking of body weights revealed that consumption of low fat or high fat refined diet increased body weight in young and aged adult male mice. Young adult females showed resistance to body weight gain, while high fat diet-fed aged females had significant body weight gain. Transition from a chow diet to low soluble fiber refined diet accounted for most of the variance in community structure and composition across all groups. This dietary transition was characterized by a loss of taxa within the phylum Bacteroidetes and a concurrent bloom of Clostridia and Proteobacteria in a sex- and age-specific manner. Most notably, no changes to gut microbiota community structure and composition were observed between mice consuming either low- or high-fat diet, suggesting that transition to the refined diet that lacks soluble fiber is the primary driver of gut microbiota alterations, with limited additional impact of dietary fat on gut microbiota.ConclusionCollectively, our results show that the choice of control diet has a significant impact on outcomes and interpretation related to body weight and gut microbiota. These data also have broad implications for rodent studies that draw comparisons between refined high fat diets and chow diets to examine dietary fat effects on metabolic, immune, behavioral, and neurobiological outcomes.

scholarly journals The crosstalk between the gut microbiota and lipids

OCL ◽  
2020 ◽  
Vol 27 ◽  
pp. 70
Author(s):  
Philippe Gérard
Keyword(s):  
Gut Microbiota ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Fat Intake ◽  
Human Intestine ◽  
Microbiota Composition ◽  
High Fat ◽  
Potential Health ◽  
Different Types ◽  
Total Fat

The human intestine harbours a complex and diverse bacterial community called the gut microbiota. This microbiota, stable during the lifetime, is specific of each individual despite the existence of a phylogenetic core shared by the majority of adults. The influence of the gut microbiota on host’s physiology has been largely studied using germfree animals and studies using these animal models have revealed that the effects of lipids on host physiology are microbiota-dependent. Studies in mice have also shown that a high-fat diet rapidly and reproducibly alters the gut microbiome. In humans, dietary fat interventions did not lead to strong and consistent modifications of the microbiota composition. Nevertheless, an association between total fat intake and the reduction of the microbiota richness has been repeatedly found. Interestingly, different types of fat exert different or even opposite effects on the microbiota. Concurrently, the gut microbiota is able to convert the lipids entering the colon, including fatty acids or cholesterol, leading to the production of metabolites with potential health effects.

scholarly journals A novel mechanism for gut barrier dysfunction by dietary fat: epithelial disruption by hydrophobic bile acids

2013 ◽  
Vol 304 (3) ◽  
pp. G227-G234 ◽  
Author(s):  
Lotta K. Stenman ◽  
Reetta Holma ◽  
Ariane Eggert ◽  
Riitta Korpela
Keyword(s):  
Bile Acids ◽  
Dietary Fat ◽  
Barrier Function ◽  
High Fat Diet ◽  
High Fat ◽  
Barrier Dysfunction ◽  
Gut Barrier ◽  
Epithelial Integrity

Impairment of gut barrier is associated with a fat-rich diet, but mechanisms are unknown. We have earlier shown that dietary fat modifies fecal bile acids in mice, decreasing the proportion of ursodeoxycholic acid (UDCA) vs. deoxycholic acid (DCA). To clarify the potential role of bile acids in fat-induced barrier dysfunction, we here investigated how physiological concentrations of DCA and UDCA affect barrier function in mouse intestinal tissue. Bile acid experiments were conducted in vitro in Ussing chambers using 4- and 20-kDa FITC-labeled dextrans. Epithelial integrity and inflammation were assayed by histology and Western blot analysis for cyclooxygenase-2. LPS was studied in DCA-induced barrier dysfunction. Finally, we investigated in a 10-wk in vivo feeding trial in mice the barrier-disrupting effect of a diet containing 0.1% DCA. DCA disrupted epithelial integrity dose dependently at 1–3 mM, which correspond to physiological concentrations on a high-fat diet. Low-fat diet-related concentrations of DCA had no effect. In vivo, the DCA-containing diet increased intestinal permeability 1.5-fold compared with control ( P = 0.016). Hematoxylin-eosin staining showed a clear disruption of the epithelial barrier by 3 mM DCA in vitro. A short-term treatment by DCA did not increase cyclooxygenase-2 content in colon preparations. UDCA did not affect barrier function itself, but it ameliorated DCA-induced barrier disruption at a 0.6 mM concentration. LPS had no significant effect on barrier function at 0.5–4.5 μg/ml concentrations. We suggest a novel mechanism for barrier dysfunction on a high-fat diet involving the effect of hydrophobic luminal bile acids.

scholarly journals High-Fat Diets with Differential Fatty Acids Induce Obesity and Perturb Gut Microbiota in Honey Bee

2021 ◽  
Vol 22 (2) ◽  
pp. 834
Author(s):  
Xiaofei Wang ◽  
Zhaopeng Zhong ◽  
Xiangyin Chen ◽  
Ziyun Hong ◽  
Weimin Lin ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Honey Bee ◽  
Dietary Fat ◽  
Honey Bees ◽  
High Fat Diet ◽  
Dietary Fats ◽  
High Fat ◽  
High Fat Diets ◽  
Fat Diets ◽  
Host Metabolism

HFD (high-fat diet) induces obesity and metabolic disorders, which is associated with the alteration in gut microbiota profiles. However, the underlying molecular mechanisms of the processes are poorly understood. In this study, we used the simple model organism honey bee to explore how different amounts and types of dietary fats affect the host metabolism and the gut microbiota. Excess dietary fat, especially palm oil, elicited higher weight gain, lower survival rates, hyperglycemic, and fat accumulation in honey bees. However, microbiota-free honey bees reared on high-fat diets did not significantly change their phenotypes. Different fatty acid compositions in palm and soybean oil altered the lipid profiles of the honey bee body. Remarkably, dietary fats regulated lipid metabolism and immune-related gene expression at the transcriptional level. Gene set enrichment analysis showed that biological processes, including transcription factors, insulin secretion, and Toll and Imd signaling pathways, were significantly different in the gut of bees on different dietary fats. Moreover, a high-fat diet increased the relative abundance of Gilliamella, while the level of Bartonella was significantly decreased in palm oil groups. This study establishes a novel honey bee model of studying the crosstalk between dietary fat, gut microbiota, and host metabolism.

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