scholarly journals High Vaccenic Acid Content in Beef Fat Attenuates High Fat and High Carbohydrate Western Diet Induced Changes in Lipid Metabolism and Gut Microbiota in Pigs

2021 ◽  
Vol 9 (12) ◽  
pp. 2517
Author(s):  
Vijay P. Singh ◽  
Melanie A. Fontaine ◽  
Rabban Mangat ◽  
Janelle M. Fouhse ◽  
Abdoulaye Diane ◽  
...  

High-fat diets (HFD) have been shown to induce substantial shifts in intestinal microbial community composition and activity which are associated with adverse metabolic outcomes. Furthermore, changes in microbial composition are affected by fatty acid composition; saturated, monounsaturated (MUFA), and industrial trans fats (iTFA) adversely affect microbial diversity while polyunsaturated fats (PUFA) have been shown to have neutral effects. The effects of naturally occurring trans fats on gut microbial composition are unknown. Vaccenic acid (VA) is the most abundant naturally occurring trans fat (abundant in meat and dairy), can be elevated by altering a cow’s diet, and has been shown to have hypolipidemic effects. The aim of this study was to determine how variations of VA content in beef fat affect gut microbial composition, insulin resistance, and lipid metabolism in pigs. Low birth weight (LBW) and control pigs were fed a control or high-fat, high-carbohydrate (HFHC) diet supplemented with beef fat containing either high or low VA levels for 7 weeks. An adapted modified oral glucose tolerance test and fat challenge test were performed at 9 weeks of age following implantation of jugular catheters. Impacts on microbial composition were assessed using 16S rRNA gene amplicon sequencing. The HFHC diet containing beef fat rich in VA had a mild insulin sensitizing effect (p < 0.05, slope of curve), increased plasma HDL cholesterol (p < 0.05, +28%), reduced postprandial plasma TG (p < 0.05), and showed protection from HFHC-induced changes to gut microbial composition in LBW pigs as compared to HFHC diet containing standard beef fat. This is the first study to show effects of natural trans fats on gut dysbiosis; further studies are needed to elucidate mechanisms.

2020 ◽  
Vol 178 (2) ◽  
pp. 311-324
Author(s):  
Marisa Pfohl ◽  
Lishann Ingram ◽  
Emily Marques ◽  
Adam Auclair ◽  
Benjamin Barlock ◽  
...  

Abstract Perfluoroalkyl substances (PFAS) represent a family of environmental toxicants that have infiltrated the living world. This study explores diet-PFAS interactions and the impact of perfluorooctanesulfonic acid (PFOS) and perfluorohexanesulfonic (PFHxS) on the hepatic proteome and blood lipidomic profiles. Male C57BL/6J mice were fed with either a low-fat diet (10.5% kcal from fat) or a high fat (58% kcal from fat) high carbohydrate (42 g/l) diet with or without PFOS or PFHxS in feed (0.0003% wt/wt) for 29 weeks. Lipidomic, proteomic, and gene expression profiles were determined to explore lipid outcomes and hepatic mechanistic pathways. With administration of a high-fat high-carbohydrate diet, PFOS and PFHxS increased hepatic expression of targets involved in lipid metabolism and oxidative stress. In the blood, PFOS and PFHxS altered serum phosphatidylcholines, phosphatidylethanolamines, plasmogens, sphingomyelins, and triglycerides. Furthermore, oxidized lipid species were enriched in the blood lipidome of PFOS and PFHxS treated mice. These data support the hypothesis that PFOS and PFHxS increase the risk of metabolic and inflammatory disease induced by diet, possibly by inducing dysregulated lipid metabolism and oxidative stress.


2021 ◽  
Vol 20 (3) ◽  
pp. 6-12
Author(s):  
J. G. Birulina ◽  
V. V. Ivanov ◽  
E. E. Buyko ◽  
O. A. Trubacheva ◽  
I. V. Petrova ◽  
...  

Aim. To study the effects of a high-fat, high-carbohydrate diet on erythrocytes and platelets of rats.Materials and methods. Male Wistar rats (n = 23) were used for the study. The rats were divided into a control group and an experimental group. The rats from the control group were fed with standard rat chow. The rats from the experimental group had received a high-fat and high-carbohydrate diet for 12 weeks. In the rats, body weight and blood pressure (BP) were measured, an oral glucose tolerance test was carried out, and hematological and lipid metabolism parameters were analyzed. The conductance of erythrocyte KCa-channels was measured by the potentiometric method, and platelet aggregation was determined by the turbidimetric method.Results. Feeding the rats with a high-fat, high-carbohydrate diet for 12 weeks resulted in obesity, BP elevation, hyperglycemia, impaired glucose tolerance, and dyslipidemia with pronounced triglyceridemia. In the experimental group, a rise in the number of leukocytes, mainly due to granulocytes, and an increase in the number of platelets and their collagen-induced aggregation were observed. The red blood cell count in the rats of the experimental group did not significantly differ from that of the control group. In the experimental group, multidirectional changes in the membrane potential were observed in response to the stimulation of the KCa-channels in the erythrocyte membrane with the Ca2+ ionophore A23187 or artificial redox systems.Conclusion. The obtained data indicate that a high-fat, high-carbohydrate diet leads to metabolic and hemorheological disorders that are typical of metabolic syndrome.


Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3557
Author(s):  
Rachael G. Horne ◽  
Yijing Yu ◽  
Rianna Zhang ◽  
Nyan Abdalqadir ◽  
Laura Rossi ◽  
...  

Aim: The objective of this study was to characterize the early effects of high fructose diets (with and without high fat) on both the composition of the gut microbiota and lipid metabolism in Syrian hamsters, a reproducible preclinical model of diet-induced dyslipidemia. Methods: Eight-week-old male hamsters were fed diets consisting of high-fat/high-fructose, low-fat/high-fructose or a standard chow diet for 14 days. Stool was collected at baseline (day 0), day 7 and day 14. Fasting levels of plasma triglycerides and cholesterol were monitored on day 0, day 7 and day 14, and nonfasting levels were also assayed on day 15. Then, 16S rRNA sequencing of stool samples was used to determine gut microbial composition, and predictive metagenomics was performed to evaluate dietary-induced shifts in deduced microbial functions. Results: Both high-fructose diets resulted in divergent gut microbiota composition. A high-fat/high-fructose diet induced the largest shift in overall gut microbial composition, with dramatic shifts in the Firmicute/Bacteroidetes ratio, and changes in beta diversity after just seven days of dietary intervention. Significant associations between genus level taxa and dietary intervention were identified, including an association with Ruminococceace NK4A214 group in high-fat/high-fructose fed animals and an association with Butryimonas with the low-fat/high-fructose diet. High-fat/high-fructose feeding induced dyslipidemia with increases in plasma triglycerides and cholesterol, and hepatomegaly. Dietary-induced changes in several genus level taxa significantly correlated with lipid levels over the two-week period. Differences in microbial metabolic pathways between high-fat/high-fructose and low-fat/high-fructose diet fed hamsters were identified, and several of these pathways also correlated with lipid profiles in hamsters. Conclusions: The high-fat/high-fructose diet caused shifts in the host gut microbiota. These dietary-induced alterations in gut microbial composition were linked to changes in the production of secondary metabolites, which contributed to the development of metabolic syndrome in the host.


2014 ◽  
Vol 467 (6) ◽  
pp. 1179-1193 ◽  
Author(s):  
Loes P. M. Duivenvoorde ◽  
Evert M. van Schothorst ◽  
Davina Derous ◽  
Inge van der Stelt ◽  
Jinit Masania ◽  
...  

PLoS ONE ◽  
2014 ◽  
Vol 9 (10) ◽  
pp. e109477 ◽  
Author(s):  
Rodney Rouse ◽  
Leshuai Zhang ◽  
Katherine Shea ◽  
Hongfei Zhou ◽  
Lin Xu ◽  
...  

2012 ◽  
Vol 302 (12) ◽  
pp. E1472-E1482 ◽  
Author(s):  
Hemant Poudyal ◽  
Sunil K. Panchal ◽  
Leigh C. Ward ◽  
Jennifer Waanders ◽  
Lindsay Brown

Age-related physiological changes develop at the same time as the increase in metabolic syndrome in humans after young adulthood. There is a paucity of data in models mimicking chronic diet-induced changes in human middle age and interventions to reverse these changes. This study measured the changes during chronic consumption of a high-carbohydrate (as cornstarch), low-fat (C) diet and a high-carbohydrate (as fructose and sucrose), high-fat (H) diet in rats for 32 wk. C diet feeding induced changes without metabolic syndrome, such as disproportionate increases in total body lean and fat mass, reduced bone mineral content, cardiovascular remodeling with increased systolic blood pressure, left ventricular and arterial stiffness, and increased plasma markers of liver injury. H diet feeding induced visceral adiposity with reduced lean mass, increased lipid infiltration in the skeletal muscle, impaired glucose and insulin tolerance, cardiovascular remodeling, hepatic steatosis, and increased infiltration of inflammatory cells in the heart and the liver. Chia seed supplementation for 24 wk attenuated most structural and functional modifications induced by age or H diet, including increased whole body lean mass and lipid redistribution from the abdominal area, and normalized the chronic low-grade inflammation induced by H diet feeding; these effects may be mediated by increased metabolism of anti-inflammatory n-3 fatty acids from chia seed. These results suggest that chronic H diet feeding for 32 wk mimics the diet-induced cardiovascular and metabolic changes in middle age and that chia seed may serve as an alternative dietary strategy in the management of these changes.


2018 ◽  
Vol 314 (6) ◽  
pp. E572-E583 ◽  
Author(s):  
Ryuya Maekawa ◽  
Hidetada Ogata ◽  
Masatoshi Murase ◽  
Norio Harada ◽  
Kazuyo Suzuki ◽  
...  

Both high-fat (HFD) and high-carbohydrate (ST) diets are known to induce weight gain. Glucose-dependent insulinotropic polypeptide (GIP) is secreted mainly from intestinal K cells upon stimuli by nutrients such as fat and glucose, and it potentiates glucose-induced insulin secretion. GIP is well known to contribute to HFD-induced obesity. In this study, we analyzed the effect of ST feeding on GIP secretion and metabolic parameters to explore the role of GIP in ST-induced weight gain. Both wild-type (WT) and GIP receptor deficient ( GiprKO) mice were fed normal chow (NC), ST, or moderate (m)HFD for 22 wk. Body weight was measured, and then glucose tolerance tests were performed. Insulin secretion from isolated islets also was analyzed. WT mice fed ST or mHFD displayed weight gain concomitant with increased plasma GIP levels compared with WT mice fed NC. WT mice fed mHFD showed improved glucose tolerance due to enhanced insulin secretion during oral glucose tolerance tests compared with WT mice fed NC or ST. GiprKO mice fed mHFD did not display weight gain. On the other hand, GiprKO mice fed ST showed weight gain and did not display obvious glucose intolerance. Glucose-induced insulin secretion was enhanced during intraperitoneal glucose tolerance tests and from isolated islets in both WT and GiprKO mice fed ST compared with those fed NC. In conclusion, enhanced GIP secretion induced by mHFD-feeding contributes to increased insulin secretion and body weight gain, whereas GIP is marginally involved in weight gain induced by ST-feeding.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Tom Houben ◽  
John Penders ◽  
Yvonne Oligschlaeger ◽  
Inês A. Magro dos Reis ◽  
Marc-Jan Bonder ◽  
...  

Abstract While the link between diet-induced changes in gut microbiota and lipid metabolism in metabolic syndrome (MetS) has been established, the contribution of host genetics is rather unexplored. As several findings suggested a role for the lysosomal lipid transporter Niemann-Pick type C1 (NPC1) in macrophages during MetS, we here explored whether a hematopoietic Npc1 mutation, induced via bone marrow transplantation, influences gut microbiota composition in low-density lipoprotein receptor knockout (Ldlr−/−) mice fed a high-fat, high-cholesterol (HFC) diet for 12 weeks. Ldlr−/− mice fed a HFC diet mimic a human plasma lipoprotein profile and show features of MetS, providing a model to explore the role of host genetics on gut microbiota under MetS conditions. Fecal samples were used to profile the microbial composition by 16 s ribosomal RNA gene sequencing. The hematopoietic Npc1 mutation shifted the gut microbiota composition and increased microbial richness and diversity. Variations in plasma lipid levels correlated with microbial diversity and richness as well as with several bacterial genera. This study suggests that host genetic influences on lipid metabolism affect the gut microbiome under MetS conditions. Future research investigating the role of host genetics on gut microbiota might therefore lead to identification of diagnostic and therapeutic targets for MetS.


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