Flavan 3-ols improve metabolic syndrome risk factors: evidence and mechanisms

Abstract

Flavan 3-ols, a type of polyphenolic substance, are distributed in a number of plant foods. Of these foods, chocolate is very rich in flavan 3-ols as flavan 3-ol monomers, (+)-catechin and (-)-epicatechin, and the oligomers as procyanidins. There is evidence that cacao products containing flavan 3-ols have the potential to contribute to the risk reduction of cardiometabolic disorders according to recent epidemiological or intervention studies. This review focuses on recent advances in research on the ability of flavan 3-ols to reduce the risk of cardiovascular disease as a result of improving metabolic syndrome risk factors and these mechanisms.

Keywords: cardiovascular diseases; chocolate; flavan 3-ols; metabolic syndrome; risk factors.

Fig. 1

Chemical structures of flavan 3-ols in chocolate.^(–3)

Fig. 2

Relative risks for cardiovascular disease, heart failure, and stroke in adults with higher levels of chocolate consumption compared with lower levels. Reproduced from (14) with permission.

Fig. 3

Structure of (–)-epicatechin metabolites. (A) 3'-O-Methyl-(–)-epicatechin, (B) (–)-epicatechin-7-O-glucuronide, (C) 3'-O-Methyl-(–)-epicatechin-7-O-glucuronide, (D) (–)-epicatechin-3'-O-glucuronide, (E) 4'-O-Methyl-(–)-epicatechin-3'-O-glucuronide. Chemicals A, B and C were obtained from rat urine, D and E were obtained from human.

Fig. 4

VO₂ (A), VCO₂ (B) and energy expenditure (C) in rats fed control or 0.2% flavan 3-ols containing diet. Values are mean and SD. Significantly different from control, *p<0.05.

Fig. 5

The results indicated these recent reports were summarized as Table 5. Hypotensive effect was shown by oral administrated flavan 3-ols through induced endothelial nitrogen oxide synthase (eNOS) expression. In skeletal muscle, enhancement of energy expenditure was induced by oral administration of flavan 3-ols, it resulted activation of AMPK. AMPK activation enhanced both transcription and translocation of glucose transporter type 4 (GLUT4), resulting acceleration of glucose uptake. AMPK might be activated peroxisome-proliferator- activated receptor coactivator 1 (PGC1α) which was the key factor of mitochondrial biogenesis. Improvement of dyslipidemia or BMI lowering activity seen in RCT or epidemiological studies also might be induced by such mitochondria biogenesis promoting effect.