title: Inhibition of intestinal cholesterol absorption might explain cholesterol-lowering effect of telmisartan.
abstract: OBJECTIVE
  Telmisartan, an angiotensin II type 1 receptor blocker (ARB), acts as a partial agonist for peroxisome proliferator-activated receptor-γ, and thus improves abnormalities of glucose metabolism and hypertriglyceridaemia in addition to its documented blood pressure-lowering effects. Recently, it has been demonstrated that telmisartan also lowers the levels of total cholesterol and low-density lipoprotein (LDL) cholesterol levels. This study was designed to investigate the mechanism of cholesterol reduction.
  
  
  METHODS
  We measured serum levels of cholestanol, a cholesterol absorption marker, and lathosterol, a cholesterol synthesis marker, in 20 patients with both hypercholesterolaemia and hypertension. Ten patients were treated with telmisartan and the remaining 10 with fluvastatin.
  
  
  RESULTS
  After 3 months of treatment, total and LDL cholesterol levels decreased in the telmisartan group (P<0.01 for both total and LDL cholesterol levels) and the fluvastatin group (P<0.001 for both total and LDL cholesterol levels). The change in cholestanol level after 3 months of treatment was positively correlated with the levels of total (R=0.72, P<0.05) and LDL cholesterol (R=0.81, P<0.01) in the telmisartan group. The change in lathosterol level was positively correlated with the levels of total (R=0.88, P=0.001) and LDL cholesterol (R=0.89, P=0.001) in the fluvastatin group.
  
  
  CONCLUSIONS
  Our results suggest that the cholesterol-lowering effect of telmisartan might be caused by inhibition of cholesterol absorption, whereas that of statins is by inhibition of cholesterol synthesis. If confirmed, co-treatment with the two agents may be useful for synergistically lowering cholesterol in hypertensive patients.
authors.affiliation: Department of Cardiovascular Medicine, Dokkyo Medical University, Mibu, Tochigi, Japan. inouet@dokkyomed.ac.jp
authors.forename: T
authors.initials: T
authors.lastname: Inoue
authors.forename: I
authors.initials: I
authors.lastname: Taguchi
authors.forename: S
authors.initials: S
authors.lastname: Abe
authors.forename: S
authors.initials: S
authors.lastname: Toyoda
authors.forename: M
authors.initials: M
authors.lastname: Sakuma
authors.forename: K
authors.initials: K
authors.lastname: Node
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D000924:Anticholesteremic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001562:Benzimidazoles / Q000494:pharmacology / Q000627:therapeutic use*; D001565:Benzoates / Q000494:pharmacology / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D004083:Cholestanol / Q000097:blood; D002784:Cholesterol / Q000097:blood* / Q000378:metabolism; D008078:Cholesterol, LDL / Q000097:blood; D005229:Fatty Acids, Monounsaturated / Q000494:pharmacology / Q000627:therapeutic use; D005260:Female; D000077340:Fluvastatin; D005765:Gastrointestinal Agents / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D006937:Hypercholesterolemia / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D006973:Hypertension / Q000097:blood / Q000150:complications / Q000188:drug therapy; D007211:Indoles / Q000494:pharmacology / Q000627:therapeutic use; D007408:Intestinal Absorption / Q000187:drug effects*; D008297:Male; D008875:Middle Aged; D047495:PPAR gamma / Q000819:agonists; D000077333:Telmisartan
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000924:Anticholesteremic Agents; D001562:Benzimidazoles; D001565:Benzoates; D015415:Biomarkers; D008078:Cholesterol, LDL; D005229:Fatty Acids, Monounsaturated; D005765:Gastrointestinal Agents; D007211:Indoles; D047495:PPAR gamma; D000077340:Fluvastatin; C001521:lathosterol; D004083:Cholestanol; D002784:Cholesterol; D000077333:Telmisartan