Bile acid receptors as targets for the treatment of dyslipidemia and cardiovascular disease

Porez, Geoffrey; Prawitt, Janne; Gross, Barbara; Staels, Bart

doi:10.1194/jlr.r024794

Cited by 247 publications

(176 citation statements)

References 172 publications

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“…FGF inhibits CYP7A1 expression, the first step in the conversion of cholesterol to bile acids. Chenodeoxycholic acid for example increases LDL through this pathway [11] .…”

Section: Bile Acid-activated Receptorsmentioning

confidence: 99%

Obesity diabetes and the role of bile acids in metabolism

Tomkin

Owens

2016

Journal of Translational Internal Medicine

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Bile acids have many activities over and above their primary function in aiding absorption of fat and fat soluble vitamins. Bile acids are synthesized from cholesterol, and thus are involved in cholesterol homeostasis. Bile acids stimulate glucagon-like peptide 1 (GLP1) production in the distal small bowel and colon, stimulating insulin secretion, and therefore, are involved in carbohydrate and fat metabolism. Bile acids through their insulin sensitising effect play a part in insulin resistance and type 2 diabetes. Bile acid metabolism is altered in obesity and diabetes. Both dietary restriction and weight loss due to bariatric surgery, alter the lipid carbohydrate and bile acid metabolism. Recent research suggests that the forkhead transcription factor FOXO is a central regulator of bile, lipid, and carbohydrate metabolism, but conflicting studies mean that our understanding of the complexity is not yet complete.

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“…FGF inhibits CYP7A1 expression, the first step in the conversion of cholesterol to bile acids. Chenodeoxycholic acid for example increases LDL through this pathway [11] .…”

Section: Bile Acid-activated Receptorsmentioning

confidence: 99%

Obesity diabetes and the role of bile acids in metabolism

Tomkin

Owens

2016

Journal of Translational Internal Medicine

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“…Moreover, the transcriptional regulation of cholesterol transporters by bile acids either through farnesoid X receptor (FXR), fibroblast growth factor (FGF) receptors or the G-protein coupled receptor TGR5 (GPBAR1) would seem meaningful. Such data are relevant especially given the recent interest in FXR or TGR5 agonists for the treatment of metabolic disease [20]. The tissue expressing the highest levels of TGR5 is the gallbladder; interestingly, TGR5 knockout mice are protected from cholesterol gallstone development [21].…”

mentioning

confidence: 99%

The Neglected Cousin of the Hepatocyte: How Gallbladder Epithelial Cells Might Contribute to Cholesterol Gallstone Formation

Dikkers

Tietge

2013

Dig Dis Sci

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“…The mechanisms by which vitamin B6 affects bile acid metabolism under HF diet conditions are currently unknown. Lithocholic acid strongly activates pregnane X receptor (PXR) and farnesoid X receptor (FXR), but deoxycholic acid has weak effects (37,38). Therefore, a question was raised if the altered ratio of lithocholic acid to deoxycholic acid leads to modulation of the signaling of these receptors in the intestine.…”

Section: Resultsmentioning

confidence: 99%

Consumption of Vitamin B6 Reduces Fecal Ratio of Lithocholic Acid to Deoxycholic Acid, a Risk Factor for Colon Cancer, in Rats Fed a High-Fat Diet

Okazaki

Utama

Suidasari

et al. 2012

J Nutr Sci Vitaminol

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SummaryTo examine the effect of supplemental dietary vitamin B6 on the colonic luminal environment, growing male rats were fed a high-fat diet containing 1, 7, or 35 mg pyridoxine HCl/kg diet for 6 wk. Food intake and growth were unaffected by the dietary treatment. Supplemental dietary vitamin B 6 signifi cantly reduced the production of a fecal secondary bile acid, lithocholic acid (the most toxic secondary bile acid and a risk factor for colon cancer), and markedly reduced the ratio of lithocholic acid to deoxycholic acid (a less toxic secondary bile acid) in feces (pϽ0.05). Increasing dietary vitamin B6 increased fecal mucin levels (a marker of intestinal barrier function) in a dose-dependent manner (pϽ0.05) but did not affect fecal immunoglobulin A levels (an index of intestinal immune function). Cecal levels of organic acids were not signifi cantly affected by supplemental dietary vitamin B6. These results suggest the possibility that dietary vitamin B6 affects the colonic luminal environment by altering the production of secondary bile acids and mucins.

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Bile acid receptors as targets for the treatment of dyslipidemia and cardiovascular disease

Cited by 247 publications

References 172 publications

Obesity diabetes and the role of bile acids in metabolism

Obesity diabetes and the role of bile acids in metabolism

The Neglected Cousin of the Hepatocyte: How Gallbladder Epithelial Cells Might Contribute to Cholesterol Gallstone Formation

Consumption of Vitamin B6 Reduces Fecal Ratio of Lithocholic Acid to Deoxycholic Acid, a Risk Factor for Colon Cancer, in Rats Fed a High-Fat Diet

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