Beyond cholesterol lowering: pleiotropic effects of bile acid binding resins against cardiovascular disease risk factors in patients with metabolic syndrome.
Prospective epidemiologic studies have shown that dyslipidemia and hyperglycemia are major risk factors for atherosclerotic cardiovascular diseases. Undesirable metabolic conditions are observed to coexist in patients with metabolic syndrome, which is an important risk factor for cardiovascular disease. To prevent cardiovascular disease, a pleiotropic agent is needed to improve the metabolic disorder in patients with metabolic syndrome. Bile acid binding resins increase the fecal excretion of bile acids. The decrease in bile acids returned to the liver leads to an up-regulation of hepatic low-density lipoprotein (LDL) receptor activity, which decreases LDL cholesterol (LDL-C) in the circulation and increases high-density lipoprotein cholesterol. On the other hand, bile acids can also regulate the transcription of genes involved in LDL-C synthesis and cholesterol homeostasis via nuclear hormone receptors. Consequently, these receptors may represent novel therapeutic targets for dyslipidemia and provide insight into the role of the bile acid pathway in other metabolic processes. This review focuses on the recent findings on bile acid binding resins and cardiovascular disease risk factors. Moreover, known and proposed mechanisms of how bile acid binding resins may improve glucose and energy metabolism are discussed; these effects may help to explain the mechanisms by which bile acid binding resins may reduce cardiovascular disease.
Yamaoka-Tojo
Minako
M
Department of Cardioangiology, Kitasato University School of Medicine, 1-15-1 Kitasato, Sagamihara, Kanagawa 228-8555, Japan. myamaoka@med.kitasato-u.ac.jp
Tojo
Taiki
T
Izumi
Tohru
T
D000837:Anion Exchange Resins / Q000009:adverse effects / Q000266:history / Q000627:therapeutic use*; D001647:Bile Acids and Salts / Q000378:metabolism*; D001786:Blood Glucose / Q000187:drug effects; D002318:Cardiovascular Diseases / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D002784:Cholesterol / Q000097:blood*; D015536:Down-Regulation; D004734:Energy Metabolism / Q000187:drug effects; D004764:Enterohepatic Circulation / Q000187:drug effects; D049673:History, 20th Century; D006801:Humans; D000960:Hypolipidemic Agents / Q000009:adverse effects / Q000266:history / Q000627:therapeutic use*; D007249:Inflammation / Q000150:complications / Q000378:metabolism / Q000517:prevention & control; D050356:Lipid Metabolism / Q000187:drug effects; D024821:Metabolic Syndrome / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D012307:Risk Factors; D015398:Signal Transduction / Q000187:drug effects; D016896:Treatment Outcome
D000837:Anion Exchange Resins; D001647:Bile Acids and Salts; D001786:Blood Glucose; D000960:Hypolipidemic Agents; D002784:Cholesterol