scholarly journals Soluble Fiber Inulin Consumption Limits Alterations of the Gut Microbiota and Hepatic Fatty Acid Metabolism Caused by High-Fat Diet

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 1037
Author(s):  
Mayssa Albouery ◽  
Alexis Bretin ◽  
Bénédicte Buteau ◽  
Stéphane Grégoire ◽  
Lucy Martine ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Gut Microbiota ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Liver Fat ◽  
Soluble Fiber ◽  
High Fat ◽  
Total N ◽  
Hepatic Fatty Acid ◽  
Two Parameters

Diet shapes the gut microbiota which impacts hepatic lipid metabolism. Modifications in liver fat content are associated with metabolic disorders. We investigated the extent of dietary fat and fiber-induced alterations in the composition of gut microbiota and hepatic fatty acids (FAs). Mice were fed a purified low-fat diet (LFD) or high-fat diet (HFD) containing non-soluble fiber cellulose or soluble fiber inulin. HFD induced hepatic decreases in the amounts of C14:0, C16:1n-7, C18:1n-7 and increases in the amounts of C17:0, C20:0, C16:1n-9, C22:5n-3, C20:2n-6, C20:3n-6, and C22:4n-6. When incorporated in a LFD, inulin poorly affected the profile of FAs. However, when incorporated in a HFD, it (i) specifically led to an increase in the amounts of hepatic C18:0, C22:0, total polyunsaturated FAs (PUFAs), total n-6 PUFAs, C18:3n-3, and C18:2n-6, (ii) exacerbated the HFD-induced increase in the amount of C17:0, and (iii) prevented the HFD-induced increases in C16:1n-9 and C20:3n-6. Importantly, the expression/activity of some elongases and desaturases, as well as the gut microbiota composition, were impacted by the dietary fat and fiber content. To conclude, inulin modulated gut microbiota and hepatic fatty acid composition, and further investigations will determine whether a causal relationship exists between these two parameters.

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 Impact of Dietary Fat on the Progression of Liver Fibrosis: Lessons from Animal and Cell Studies

2021 ◽  
Vol 22 (19) ◽  
pp. 10303
Author(s):  
Fangping Jia ◽  
Xiao Hu ◽  
Takefumi Kimura ◽  
Naoki Tanaka
Keyword(s):  
Fatty Acid ◽  
Hepatitis C ◽  
Liver Fibrosis ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Core Gene ◽  
High Fat ◽  
Virus Core ◽  
Liver Fibrogenesis ◽  
Isocaloric Diets

Previous studies have revealed that a high-fat diet is one of the key contributors to the progression of liver fibrosis, and increasing studies are devoted to analyzing the different influences of diverse fat sources on the progression of non-alcoholic steatohepatitis. When we treated three types of isocaloric diets that are rich in cholesterol, saturated fatty acid (SFA) and trans fatty acid (TFA) with hepatitis C virus core gene transgenic mice that spontaneously developed hepatic steatosis without apparent fibrosis, TFA and cholesterol-rich diet, but not SFA-rich diet, displayed distinct hepatic fibrosis. This review summarizes the recent advances in animal and cell studies regarding the effects of these three types of fat on liver fibrogenesis.

RS4-type resistant starch prevents high-fat diet-induced obesity via increased hepatic fatty acid oxidation and decreased postprandial GIP in C57BL/6J mice

2010 ◽  
Vol 298 (3) ◽  
pp. E652-E662 ◽  
Author(s):  
Akira Shimotoyodome ◽  
Junko Suzuki ◽  
Daisuke Fukuoka ◽  
Ichiro Tokimitsu ◽  
Tadashi Hase
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Resistant Starch ◽  
High Fat Diet ◽  
Acid Oxidation ◽  
High Fat ◽  
Fat Utilization ◽  
Hepatic Fatty Acid ◽  
Diet Induced Obesity ◽  
Hepatic Fatty Acid Oxidation

Chemically modified starches (CMS) are RS4-type resistant starch, which shows a reduced availability, as well as high-amylose corn starch (HACS, RS2 type), compared with the corresponding unmodified starch. Previous studies have shown that RS4 increases fecal excretion of bile acids and reduces zinc and iron absorption in rats. The aim of this study was to investigate the effects of dietary RS4 supplementation on the development of diet-induced obesity in mice. Weight- and age-matched male C57BL/6J mice were fed for 24 wk on a high-fat diet containing unmodified starch, hydroxypropylated distarch phosphate (RS4), or HACS (RS2). Those fed the RS4 diet had significantly lower body weight and visceral fat weight than those fed either unmodified starch or the RS2 diet. Those fed the RS4 diet for 4 wk had a significantly higher hepatic fatty acid oxidation capacity and related gene expression and lower blood insulin than those fed either unmodified starch or the RS2 diet. Indirect calorimetry showed that the RS4 group exhibited higher energy expenditure and fat utilization compared with the RS2 group. When gavaged with fat (trioleate), RS4 stimulated a lower postprandial glucose-dependent insulinotropic polypeptide (GIP; incretin) response than RS2. Higher blood GIP levels induced by chronic GIP administration reduced fat utilization in high-fat diet-fed mice. In conclusion, dietary supplementation with RS4-type resistant starch attenuates high-fat diet-induced obesity more effectively than RS2 in C57BL/6J mice, which may be attributable to lower postprandial GIP and increased fat catabolism in the liver.

Differential effects of short- and long-term high-fat diet feeding on hepatic fatty acid metabolism in rats

2011 ◽  
Vol 1811 (7-8) ◽  
pp. 441-451 ◽  
Author(s):  
Jolita Ciapaite ◽  
Nicole M. van den Broek ◽  
Heleen te Brinke ◽  
Klaas Nicolay ◽  
Jeroen A. Jeneson ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
High Fat Diet ◽  
Acid Metabolism ◽  
High Fat ◽  
Differential Effects ◽  
Hepatic Fatty Acid ◽  
Short And Long Term

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 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 Elevated hepatic fatty acid elongase‐5 (Elovl5) attenuates fatty liver in high fat diet induced obese mice

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Sasmita Tripathy ◽  
Robert D Stevens ◽  
James R Bain ◽  
Christopher B Newgard ◽  
Donald B Jump
Keyword(s):  
Fatty Acid ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Obese Mice ◽  
High Fat ◽  
Fatty Acid Elongase ◽  
Hepatic Fatty Acid

scholarly journals The PPARβ/δ Activator GW501516 Prevents the Down-Regulation of AMPK Caused by a High-Fat Diet in Liver and Amplifies the PGC-1α-Lipin 1-PPARα Pathway Leading to Increased Fatty Acid Oxidation

Endocrinology ◽  
2011 ◽  
Vol 152 (5) ◽  
pp. 1848-1859 ◽  
Author(s):  
Emma Barroso ◽  
Ricardo Rodríguez-Calvo ◽  
Lucía Serrano-Marco ◽  
Alma M. Astudillo ◽  
Jesús Balsinde ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
High Fat Diet ◽  
Plasma Lipoproteins ◽  
Acid Oxidation ◽  
Mrna Levels ◽  
High Fat ◽  
Hepatic Fatty Acid ◽  
Lipin 1 ◽  
Hepatic Fatty Acid Oxidation

Metabolic syndrome-associated dyslipidemia is mainly initiated by hepatic overproduction of the plasma lipoproteins carrying triglycerides. Here we examined the effects of the peroxisome proliferator-activated receptors (PPAR)-β/δ activator GW501516 on high-fat diet (HFD)-induced hypertriglyceridemia and hepatic fatty acid oxidation. Exposure to the HFD caused hypertriglyceridemia that was accompanied by reduced hepatic mRNA levels of PPAR-γ coactivator 1 (PGC-1)-α and lipin 1, and these effects were prevented by GW501516 treatment. GW501516 treatment also increased nuclear lipin 1 protein levels, leading to amplification in the PGC-1α-PPARα signaling system, as demonstrated by the increase in PPARα levels and PPARα-DNA binding activity and the increased expression of PPARα-target genes involved in fatty acid oxidation. These effects of GW501516 were accompanied by an increase in plasma β-hydroxybutyrate levels, demonstrating enhanced hepatic fatty acid oxidation. Moreover, GW501516 increased the levels of the hepatic endogenous ligand for PPARα, 16:0/18:1-phosphatidilcholine and markedly enhanced the expression of the hepatic Vldl receptor. Interestingly, GW501516 prevented the reduction in AMP-activated protein kinase (AMPK) phosphorylation and the increase in phosphorylated levels of ERK1/2 caused by HFD. In addition, our data indicate that the activation of AMPK after GW501516 treatment in mice fed HFD might be the result of an increase in the AMP to ATP ratio in hepatocytes. These findings indicate that the hypotriglyceridemic effect of GW501516 in HFD-fed mice is accompanied by an increase in phospho-AMPK levels and the amplification of the PGC-1α-lipin 1-PPARα pathway.

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.

scholarly journals The effect of dietary fat on lipogenesis in mammary gland and liver from lactating and virgin mice

1969 ◽  
Vol 115 (4) ◽  
pp. 807-815 ◽  
Author(s):  
Stuart Smith ◽  
Harriet T. Gagné ◽  
Dorothy R. Pitelka ◽  
S. Abraham
Keyword(s):  
Mammary Gland ◽  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Corn Oil ◽  
Acid Synthesis ◽  
High Fat ◽  
C3h Mice ◽  
Parenchymal Cells

1. Virgin and lactating C3H mice maintained on laboratory chow were transferred to a high-fat (15% corn oil) or a fat-free diet 3 days before being killed. 2. The linoleate content of liver, mammary gland and milk was decreased in lactating mice given the fat-free diet but was increased in those fed on the high-fat diet. Changes in linoleate content and mammary gland followed a similar but much less marked trend in virgin animals. 3. Hepatic fatty acid synthesis in lactating and virgin mice fed on the fat-free diet was higher than in corresponding animals fed on either the chow or the high-fat diet. The lipogenic capacity of livers from mice fed on either the chow or the high-fat diet was greater in lactating than in virgin animals. These changes in hepatic lipogenic capacity were accompanied by alterations in the specific activities of certain enzymes involved in fat synthesis. 4. Mammary gland from virgin and lactating animals showed no such adaptation to dietary fat. Results indicate that fatty acid synthesis in neither mammary-gland parenchymal cells nor mammary-gland adipose cells can be influenced by dietary fat in the same way as in the hepatocyte.

Sign in / Sign up

Export Citation Format

Share Document