The interrelationship between bile acid and vitamin A homeostasis

Saeed, Ali; Hoekstra, Mark; Hoeke, Martijn O.; Heegsma, Janette; Faber, Klaas Nico

doi:10.1016/j.bbalip.2017.01.007

Cited by 64 publications

(55 citation statements)

References 227 publications

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“…Bile acid synthesis is controlled by overlapping feedback mechanisms in enterocytes and hepatocytes, ensuring that the rate of BA synthesis is inversely proportional to BA absorption, preventing BA synthesis beyond physiologic requirements . Interestingly, vitamins A and D contribute to the regulation of BA synthesis by interactions between their nuclear receptors and specific regulatory gene elements . Their effect is to increase expression of fibroblast growth factor‐19, a potent antagonist of cholesterol 7‐alpha‐hydroxylase, the enzyme responsible for BA synthesis.…”

Section: Discussionmentioning

confidence: 99%

Serum concentrations of lipid‐soluble vitamins in dogs with exocrine pancreatic insufficiency treated with pancreatic enzymes

Barko

Williams

2018

Veterinary Internal Medicne

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BackgroundIn humans, exocrine pancreatic insufficiency (EPI) is associated with deficiencies in lipid‐soluble vitamins. Little is reported regarding lipid‐soluble vitamin status in dogs with EPI.Hypothesis/ObjectivesCompare serum concentrations of retinol, 25‐hydrocholecalciferol (25OHD), and α‐tocopherol among dogs with EPI, those with subclinical EPI (sEPI), and healthy dogs. Detect associations between serum concentrations of lipid‐soluble vitamins and residual clinical signs in treated dogs with EPI and sEPI.AnimalsTwenty dogs with EPI and five dogs with sEPI receiving pancreatic enzyme replacement therapy. Ten healthy dogs sampled before and after 10 days of pancreatic enzyme supplementation.MethodsCase‐control study. Serum retinol and α‐tocopherol concentrations were measured by high‐performance liquid chromatography. Serum 25OHD concentrations were measured by radioimmunoassay.ResultsSerum retinol concentration was significantly lower in dogs with EPI (median, 490 ng/mL; range, 322‐990 ng/mL) and serum α‐tocopherol concentration was significantly lower in dogs with EPI (median, 11.51 μg/L; range, 4.8‐27.1 μg/L) and sEPI (median, 12.66 μg/L; range, 10.21‐21.03 μg/L) compared with healthy dogs (median, 1203 ng/mL; range, 637‐1768 ng/mL and median, 43.54 μg/L; range, 34.26‐53.97 μg/L, respectively). Dogs with weight loss had significantly lower 25OHD (mean, 243.50 nmol/L; standard deviation [SD], 3.54 nmol/L) than dogs with stable weight (314.0 nmol/L; SD, 138.38 nmol/L).Conclusions and Clinical ImportanceAltered homeostasis of lipid‐soluble vitamins is present in dogs with EPI and sEPI, despite enzyme replacement therapy. Additional studies are needed to determine the clinical relevance of these findings and the therapeutic potential of lipid‐soluble vitamin supplementation in dogs with EPI and sEPI.

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Section: Discussionmentioning

confidence: 99%

Serum concentrations of lipid‐soluble vitamins in dogs with exocrine pancreatic insufficiency treated with pancreatic enzymes

Barko

Williams

2018

Veterinary Internal Medicne

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“…p53, vitamin D receptor (VDR), and bile acid receptor farnesoid x receptor (FXR) have been implicated in inducing miR-22 level (1,2,14). Because retinoic acid (RA) and bile acids share common metabolic and anticancer effects (16)(17)(18)(19)(20), it would be of interest to study whether miR-22 can be induced by RA-regulated signaling.…”

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confidence: 99%

RARβ acts as both an upstream regulator and downstream effector of miR‐22 , which epigenetically regulates NUR77 to induce apoptosis of colon cancer cells

et al. 2018

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This study investigates the mechanism and consequences of microRNA‐22 (miR‐22) induction. Our data revealed for the first time that retinoic acid (RA) and histone deacetylase (HDAC) inhibitors, including short‐chain fatty acids and suberanilohydroxamic acid (SAHA), could individually or in combination induce miR‐22. This induction was mediated via RA receptor β (RARβ) binding to a direct repeat 5 (DR5) motif. In addition, we uncovered HDAC1 as a novel miR‐22 target. In an miR‐22–dependent manner, HDAC inhibitors and RA reduced HDAC1, HDAC4, and sirtuin 1 (SIRT1), which were involved in chromatin remodeling of the RARβ and nerve growth factor IB (NUR77). Thus, HDAC inhibitors and RA‐induced miR‐22 resulted in simultaneous induction of cytoplasmic RARβ and NUR77, leading to apoptosis of colon cancer cells. In mice, miR‐22 and its inducers inhibited the growth of xenograft colon cancer. Moreover, tumor size reduction was accompanied by elevated miR‐22, NUR77, and RARβ and by reduced HDACs. In human colon polyps and adenocarcinomas, miR‐22 and RARβ were consistently reduced, which was associated with elevated HDAC1, HDAC4, and SIRT1 in colon adenocarcinomas. Results from this study revealed a novel anticancer mechanism of RARβ via miR‐22 induction to epigenetically regulate itself and NUR77, providing a promising cancer treatment modality using miR‐22 and its inducers.—Hu, Y., French, S. W., Chau, T., Liu, H.‐X., Sheng, L., Wei, F., Stondell, J., Garcia, J. C., Du, Y., Bowlus, C. L., Wan, Y.‐J. Y. RARβ acts as both an upstream regulator and downstream effector of miR‐22, which epigenetically regulates NUR77 to induce apoptosis of colon cancer cells. FASEB J. 33, 2314–2326 (2019). http://www.fasebj.org

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“…Vitamin A plays a crucial role in eye health, epithelial cell growth, wound healing, and immune response. Deficiency is common in PBC, PSC, and CCA because of decreased bile acid secretion, which causes fat and fat‐soluble vitamin malabsorption . Additional risk factors in liver disease include compromised production of retinol binding protein (RBP), which is likely as a consequence of zinc deficiency, and reduced vitamin A storage capacity within the hepatic stellate cells in the liver that differentiate into collagen‐ and fibronectin‐producing myofibroblast cells .…”

Section: Fat‐soluble Vitamin Deficienciesmentioning

confidence: 99%

Micronutrients in Liver Disease: Roles, Risk Factors for Deficiency, and Recommendations for Supplementation

et al. 2019

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Micronutrients are essential components of the diet and are required to maintain fundamental bodily functions. Liver disease has a profound effect on nutrient intake, metabolism of nutrients, and nutrition status, often resulting in some degree of malnutrition, including micronutrient deficiency. Vitamin and mineral deficiencies can impair metabolic processes at the cellular and biochemical level even before clinical and physical alterations are seen. It is essential that micronutrient status is evaluated as part of a comprehensive nutrition assessment for all patients with chronic or advanced liver disease. Early intervention to correct suspected or confirmed deficiencies may minimize symptoms and improve clinical outcomes and quality of life. In this narrative review, different types of liver disease and associated micronutrient abnormalities are outlined, and methods of micronutrient assessment and supplementation are discussed. (Nutr Clin Pract. 2020;35:50-62)

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The interrelationship between bile acid and vitamin A homeostasis

Cited by 64 publications

References 227 publications

Serum concentrations of lipid‐soluble vitamins in dogs with exocrine pancreatic insufficiency treated with pancreatic enzymes

Serum concentrations of lipid‐soluble vitamins in dogs with exocrine pancreatic insufficiency treated with pancreatic enzymes

RARβ acts as both an upstream regulator and downstream effector of miR‐22 , which epigenetically regulates NUR77 to induce apoptosis of colon cancer cells

Micronutrients in Liver Disease: Roles, Risk Factors for Deficiency, and Recommendations for Supplementation

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