title: Telmisartan prevents obesity and increases the expression of uncoupling protein 1 in diet-induced obese mice.
abstract: The aim of the present study was to clarify the effect of telmisartan, an angiotensin II receptor blocker, on the development of obesity and related metabolic disorders in diet-induced obese mice. Treatment with telmisartan dissolved in drinking water at a dosage of 5 mg/kg per day for 14 days attenuated the diet-induced weight gain without affecting food intake in diet-induced obese mice compared with controls using nontreated water. Telmisartan treatment decreased the weight of visceral adipose tissue and the triglyceride content in the liver and skeletal muscle. In addition, hyperglycemia, hyperinsulinemia, and hypertriglyceridemia in diet-induced obese mice all improved with telmisartan treatment. Furthermore, telmisartan treatment increased adiponectin mRNA in visceral white adipose tissue and was associated with a concomitant change in the serum adiponectin level. In contrast, the treatment reduced the serum level of resistin. Finally, telmisartan treatment increased the mRNA expression of uncoupling protein 1 in brown adipose tissue and was accompanied by an increase in oxygen consumption. In conclusion, telmisartan treatment might prevent the development of obesity and related metabolic disorders by altering the levels of adiponectin, resistin, and uncoupling protein 1 in diet-induced obese mice. Our results indicate that telmisartan can be used as a therapeutic tool for metabolic syndrome, including visceral obesity.
authors.affiliation: Department of Internal Medicine 1, Faculty of Medicine, Oita University, Hasama, Oita, Japan.
authors.forename: Kana
authors.initials: K
authors.lastname: Araki
authors.forename: Takayuki
authors.initials: T
authors.lastname: Masaki
authors.forename: Isao
authors.initials: I
authors.lastname: Katsuragi
authors.forename: Katsuhiro
authors.initials: K
authors.lastname: Tanaka
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Kakuma
authors.forename: Hironobu
authors.initials: H
authors.lastname: Yoshimatsu
mesh_terms: D052242:Adiponectin / Q000235:genetics / Q000378:metabolism; D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology / Q000627:therapeutic use*; D000818:Animals; D001562:Benzimidazoles / Q000494:pharmacology / Q000627:therapeutic use*; D001565:Benzoates / Q000494:pharmacology / Q000627:therapeutic use*; D001835:Body Weight / Q000187:drug effects*; D002352:Carrier Proteins / Q000096:biosynthesis* / Q000187:drug effects; D004032:Diet; D004435:Eating / Q000187:drug effects; D007473:Ion Channels; D008297:Male; D008565:Membrane Proteins / Q000096:biosynthesis* / Q000187:drug effects; D051379:Mice; D008810:Mice, Inbred C57BL; D024101:Mitochondrial Proteins; D009765:Obesity / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D010101:Oxygen Consumption; D012333:RNA, Messenger / Q000096:biosynthesis; D000077333:Telmisartan; D014280:Triglycerides / Q000032:analysis; D000071256:Uncoupling Protein 1
chemical_list: D052242:Adiponectin; D047228:Angiotensin II Type 1 Receptor Blockers; D001562:Benzimidazoles; D001565:Benzoates; D002352:Carrier Proteins; D007473:Ion Channels; D008565:Membrane Proteins; D024101:Mitochondrial Proteins; D012333:RNA, Messenger; D014280:Triglycerides; C000604372:Ucp1 protein, mouse; D000071256:Uncoupling Protein 1; D000077333:Telmisartan