Telmisartan prevents obesity and increases the expression of uncoupling protein 1 in diet-induced obese mice
Kana Araki1, Takayuki Masaki, Isao Katsuragi
1Department of Internal Medicine 1, Faculty of Medicine, Oita University, Hasama, Oita, Japan.
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.
Insights
Telmisartan, an angiotensin II receptor blocker, effectively reduced weight gain and improved metabolic disorders in obese mice. This suggests telmisartan
Area of Science:
- Pharmacology
- Metabolic Disorders
- Obesity Research
Background:
- Diet-induced obesity is linked to metabolic disorders.
- Angiotensin II receptor blockers (ARBs) are used to manage hypertension.
- The role of ARBs in obesity and metabolic syndrome requires further investigation.
Purpose of the Study:
- To investigate the effects of telmisartan on diet-induced obesity and related metabolic abnormalities in mice.
- To explore the molecular mechanisms underlying telmisartan's potential anti-obesity effects.
Main Methods:
- Administration of telmisartan (5 mg/kg/day) in drinking water for 14 days to diet-induced obese mice.
- Assessment of body weight, food intake, visceral adipose tissue weight, and triglyceride levels.
- Measurement of serum glucose, insulin, triglyceride, adiponectin, and resistin levels.
- Analysis of adiponectin and uncoupling protein 1 (UCP1) mRNA expression in adipose tissues.
- Measurement of oxygen consumption in brown adipose tissue.
Main Results:
- Telmisartan treatment attenuated diet-induced weight gain without affecting food intake.
- Reduced visceral adipose tissue weight and triglyceride content in liver and skeletal muscle.
- Improved hyperglycemia, hyperinsulinemia, and hypertriglyceridemia.
- Increased adiponectin mRNA and serum levels, decreased serum resistin levels.
- Enhanced uncoupling protein 1 mRNA expression in brown adipose tissue, leading to increased oxygen consumption.
Conclusions:
- Telmisartan may prevent obesity and metabolic disorders by modulating adiponectin, resistin, and UCP1.
- Telmisartan demonstrates potential as a therapeutic agent for metabolic syndrome, including visceral obesity.
