Cacao extract enriched in polyphenols prevents insulin-resistance and dyslipemia in a rat model

Cocoa-derived foods are rich in polyphenols obtained from the fermented, roasted and industrially processed seeds of Theobroma cacao L. (Sterculiaceae). Its biological activities are due to procyanidins and flavanols [1]. Administration of a sucrose rich diet (SRD) to normal rats generates insulin resistance, oxidative stress, inflammation and liver dysfunction similar to those observed in human metabolic syndrome [2]. Our objective was to evaluate the effects of a cocoa extract enriched in polyphenols (CEP) in preventing the endocrine-metabolic alterations produced by SRD.

Male Wistar rats were fed with a standard commercial diet and drinking water (Blank); 10% sucrose in water alone (SRD, negative control) or treated with CEP (250 mg/kg, all days) or N-acetyl-cysteine (NAC, 50 mg/kg, last 5 days) as positive control. At the time of sacrifice blood glucose, insulin, triglycerides and serum transaminases were determined. In liver, we measured: a) oxidative stress markers (GSH and protein carbonyls); b) glycogen content, glucokinase and glucose-6-phosphatase activities; and, d) protein levels of Akt/pAkt, eNOS/p-eNOS, iNOS and COX-2.

Insulin, triglicerides and glycogen were significantly reduced vs. control, whereas glucose-6-Pase activity was reduced. Glucose and glucokinase activity did not suffer significant changes. Serum transaminases showed no differences thus demonstrating no hepatotoxicity. SRD rats showed a decrease in GSH level, a value that increased significantly in CEP animals (36.0 vs. 12.9 mmol/g). No changes were observed in protein carbonyl levels. P-Akt and P-eNOS levels were significantly reduced in SRD animals. iNOS and COX-2 were significantly increased in these animals. CEP administration prevented the mentioned changes.

In conclusion, CEP co-administration is effective in preventing the endocrine-metabolic changes induced by a SRD. This prevention is mediated through P-Akt/P-eNOS-dependent signaling pathway.

[1] Andújar et al. Oxid Med Cell Longev. 2012, 2012, 906252.

[2] Francini et al. Life Sci. 2010; 86: 965 – 971.