TY - JOUR
T1 - Effects of (-)-epicatechin on a diet-induced rat model of cardiometabolic risk factors
AU - Gutiérrez-Salmeán, Gabriel
AU - Ortiz-Vilchis, Pilar
AU - Vacaseydel, Claudia Maria
AU - Garduño-Siciliano, Leticia
AU - Chamorro-Cevallos, German
AU - Meaney, Eduardo
AU - Villafaña, Santiago
AU - Villarreal, Francisco
AU - Ceballos, Guillermo
AU - Ramírez-Sánchez, Israel
N1 - Funding Information:
This work was supported by CONACYT Mexico Grant ♯ 129889 to GC. GGS CONACYT fellowship ♯ 304733. NIH AT4277, P60MD001 and DK98717 to FV and by an unrestricted gift from Cardero therapeutics to GC.
PY - 2014/4/5
Y1 - 2014/4/5
N2 - Overweight and obesity have been associated with increase in cardiometabolic risk. Therapeutics include lifestyle changes and/or pharmacologic agents. However, such interventions are often limited by poor compliance and/or significant side effects. The consumption of certain dietary products, such as cocoa, exerts positive effects on cardiometabolic risk factors. (-)-Epicatechin (EPI), the most abundant flavonoid in cacao has been reported to replicate such effects. However its mechanisms of action have not been fully elucidated.In a rat model of high-fat diet-induced obesity and its associated crdiometabolic risk factors, we administered 1 mg/kg of EPI, by gavage, for 2 weeks. Endpoints included weight-gain, glycemia, triglyceridemia, and systolic blood pressure. We also assessed food intake and fecal excretion. Mitochondrial function and structure related proteins were measured by Westerns.Obesity, hyperglycemia, hypertriglyceridemia, and systolic hypertension were developed after the administration of the high-fat diet for five weeks. EPI significantly decreased the rate of weight gain, glycemia and hypertriglyceridemia. The ratio between energy intake and excretion was not significantly modified by treatment. EPI restored the obesity-induced decreases in the levels of skeletal muscle and abdominal tissue sirtuins (SIRTs), peroxisome proliferator-activated receptor coactivator (PGC-1α), mitofilin, transcription factor A mitochondrial (TFAM), uncoupling protein 1 (UCP1), and deiodinase.EPI treatment yielded beneficial effects on high fat diet-induced endpoints thus may be considered as a potential agent for the treatment of obesity and its cardiometabolic associated abnormalities. Mechanism of action may be attributed to the modulation of cellular/mitochondrial function, thus improving overall metabolism.
AB - Overweight and obesity have been associated with increase in cardiometabolic risk. Therapeutics include lifestyle changes and/or pharmacologic agents. However, such interventions are often limited by poor compliance and/or significant side effects. The consumption of certain dietary products, such as cocoa, exerts positive effects on cardiometabolic risk factors. (-)-Epicatechin (EPI), the most abundant flavonoid in cacao has been reported to replicate such effects. However its mechanisms of action have not been fully elucidated.In a rat model of high-fat diet-induced obesity and its associated crdiometabolic risk factors, we administered 1 mg/kg of EPI, by gavage, for 2 weeks. Endpoints included weight-gain, glycemia, triglyceridemia, and systolic blood pressure. We also assessed food intake and fecal excretion. Mitochondrial function and structure related proteins were measured by Westerns.Obesity, hyperglycemia, hypertriglyceridemia, and systolic hypertension were developed after the administration of the high-fat diet for five weeks. EPI significantly decreased the rate of weight gain, glycemia and hypertriglyceridemia. The ratio between energy intake and excretion was not significantly modified by treatment. EPI restored the obesity-induced decreases in the levels of skeletal muscle and abdominal tissue sirtuins (SIRTs), peroxisome proliferator-activated receptor coactivator (PGC-1α), mitofilin, transcription factor A mitochondrial (TFAM), uncoupling protein 1 (UCP1), and deiodinase.EPI treatment yielded beneficial effects on high fat diet-induced endpoints thus may be considered as a potential agent for the treatment of obesity and its cardiometabolic associated abnormalities. Mechanism of action may be attributed to the modulation of cellular/mitochondrial function, thus improving overall metabolism.
KW - Cacao
KW - Epicatechin
KW - Flavonoids
KW - Metabolic cardiovascular syndrome
KW - Mitochondria
UR - http://www.scopus.com/inward/record.url?scp=84896710212&partnerID=8YFLogxK
U2 - 10.1016/j.ejphar.2014.01.053
DO - 10.1016/j.ejphar.2014.01.053
M3 - Artículo
C2 - 24491839
SN - 0014-2999
VL - 728
SP - 24
EP - 30
JO - European Journal of Pharmacology
JF - European Journal of Pharmacology
IS - 1
ER -