Folic Acid Supplementation of High Protein - High Fat Diets

Abstract Objectives To determine how low and high folic acid (FA) intake, combined with either low or high-fat diets, affects other vitamins in mouse liver and plasma. Methods C57BL/6NHsd mice were placed on one of six diets at weaning and maintained for 16 weeks. The diets varied in their fat content and FA levels: low fat (14% kcal from fat) vs high fat (58% kcal from fat) with 3 different FA levels- 0 ppm FA (FD), 2 ppm FA (Ctrl), 12 ppm (FS). Diets were matched for all other vitamins and minerals. Untargeted metabolomics analysis of plasma and snap-frozen liver samples was conducted at Metabolon®. Results In liver, excess dietary folic acid on a low-fat diet resulted in significantly increased levels of pantothenate, α-tocopherol, FA and several folate metabolites. When FA was over-supplemented in combination with a high fat (HF) diet, α-tocopherol was increased along with several nicotinate and pantothenate metabolites. Interestingly, the HF-FD and -FS diets demonstrated similar effects. These diets resulted in significantly decreased levels of riboflavin, thiamine, vitamin A, and vitamin B6 metabolites while increasing levels of pantetheine metabolites. In plasma, fewer changes with significant differences were observed when mice were fed HF diets. Several nicotinate metabolites were significantly elevated due to the FD diet with no change due to FS. Additionally, there were no changes in pantothenate or riboflavin in the plasma. Interestingly, the HF- FD and -FS diets induced similar responses but in opposite directions in plasma vs liver. The plasma levels of thiamine, vitamin A, and vitamin B6 metabolites were all significantly increased due to both low and high FA, whereas in the liver they were decreased. Additionally, no changes in α-tocopherol were seen in plasma, but the HF-FD diet raised γ/β-tocopherol levels over 2-fold despite equal amounts of vitamin E among all diets. Conclusions Untargeted metabolomic analysis revealed that diets with too high or too low folate affect other vitamins both in liver and plasma. These effects were further modulated by dietary fat levels. The HF-FD and -FS diets had significant impact on vitamins A, B1, B2, B3, B5, B6, B9 and E, along with their related derivatives, which may have serious implications for multiple metabolic pathways. Funding Sources NIH.

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Folic acid attenuates homocysteine and enhances antioxidative capacity in atherosclerotic rats

Applied Physiology Nutrition and Metabolism ◽

10.1139/apnm-2017-0158 ◽

2017 ◽

Vol 42 (10) ◽

pp. 1015-1022 ◽

Cited By ~ 6

Author(s):

Shanshan Cui ◽

Wen Li ◽

Xin Lv ◽

Pengyan Wang ◽

Guowei Huang ◽

...

Keyword(s):

Folic Acid ◽

Antioxidant Capacity ◽

Wistar Rats ◽

Folic Acid Supplementation ◽

Plasma Homocysteine ◽

Serum Folate ◽

Antioxidative Capacity ◽

High Fat ◽

Acid Supplementation ◽

Atherosclerotic Lesions

Atherosclerosis is a chronic disease that can seriously endanger human life. Folic acid supplementation modulates several disorders, including atherosclerosis, via its antiapoptotic and antioxidative properties. This study investigated whether folic acid alleviates atherogenesis by restoring homocysteine levels and antioxidative capacity in atherosclerosis Wistar rats. To this end, 28 Wistar rats were randomly divided into 4 groups (7 rats/group) as follows: (i) wild-type group, fed only the AIN-93 semi-purified rodent diet (folic acid: 2.1 mg/kg); (ii) high-fat + folic acid-deficient group (HF+DEF) (folic acid: 0.2 mg/kg); (iii) high-fat + normal folic acid group (folic acid: 2.1 mg/kg); and (iv) high-fat + folic acid-supplemented group (folic acid: 4.2 mg/kg). After 12 weeks, histopathological changes in the atherosclerotic lesions of the aortic arch were determined. In addition, serum folate levels, plasma homocysteine levels, plasma S-adenosyl-homocysteine levels, antioxidant status, oxidant status, and lipid profiles were evaluated. The results show aggravated atherosclerotic lesions in the HF+DEF group. Folic acid supplementation increased concentrations of serum folate. Further, folic acid supplementation increased high-density lipoprotein-cholesterol, decreased plasma homocysteine levels, and improved antioxidant capacity in atherogenic rats. These findings are consistent with the hypothesis that folic acid alleviates atherogenesis by reducing plasma homocysteine levels and improving antioxidant capacity in rats fed a high-fat diet.

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Satiety related to 24 h diet-induced thermogenesis during high protein/carbohydrate vs high fat diets measured in a respiration chamber

European Journal of Clinical Nutrition ◽

10.1038/sj.ejcn.1600782 ◽

1999 ◽

Vol 53 (6) ◽

pp. 495-502 ◽

Cited By ~ 246

Author(s):

MS Westerterp-Plantenga ◽

V Rolland ◽

SAJ Wilson ◽

KR Westerterp

Keyword(s):

High Protein ◽

High Fat ◽

Respiration Chamber ◽

High Fat Diets ◽

Diet Induced Thermogenesis ◽

Fat Diets

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A high-fat/high-protein, Atkins-type diet exacerbates Clostridioides (Clostridium) difficile infection in mice, whereas a high-carbohydrate diet protects

10.1101/834903 ◽

2019 ◽

Author(s):

Chrisabelle C. Mefferd ◽

Shrikant S. Bhute ◽

Jacqueline R. Phan ◽

Jacob V. Villarama ◽

Dung M. Do ◽

...

Keyword(s):

Clostridium Difficile ◽

Antibiotic Treatment ◽

Community Dynamics ◽

High Carbohydrate Diet ◽

High Protein ◽

High Fat ◽

Carbohydrate Diet ◽

High Carbohydrate ◽

High Fat Diets ◽

Fat Diets

AbstractClostridioides difficile (formerly Clostridium difficile) infection (CDI) can result from the disruption of the resident gut microbiota. Western diets and popular weight-loss diets drive large changes in the gut microbiome; however, the literature is conflicted with regard to the effect of diet on CDI. Using the hypervirulent strain C. difficile R20291 (RT027) in a mouse model of antibiotic-induced CDI, we assessed disease outcome and microbial community dynamics in mice fed two high-fat diets in comparison with a high-carbohydrate diet and a standard rodent diet. The two high-fat diets exacerbated CDI, with a high-fat/high-protein, Atkins-like diet leading to severe CDI and 100% mortality, and a high-fat/low-protein, medium-chain triglyceride (MCT)-like diet inducing highly variable CDI outcomes. In contrast, mice fed a high-carbohydrate diet were protected from CDI, despite high refined carbohydrate and low fiber content. 28 members of the Lachnospiraceae and Ruminococcaceae decreased in abundance due to diet and/or antibiotic treatment; these organisms may compete with C. difficile for amino acids and protect healthy animals from CDI in the absence of antibiotics. Together, these data suggest that antibiotic treatment might lead to loss of C. difficile competitors and create a favorable environment for C. difficile proliferation and virulence that is intensified by high-fat/high-protein diets; in contrast, high-carbohydrate diets might be protective regardless of the source of carbohydrate.

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