Many researchers have reported that obesity is a major risk factor for diabetes, cardiovascular diseases, several forms of cancer (such as breast, colon and prostate), pulmonary, osteoarticular and metabolic diseases in the past decades. Recently, the hypolipidemic and anti-obesity effects of green tea in animals and humans have slowly become a hot topic in nutritional and food science research. This review will up-date the information of the anti-obesity effects of green tea in human intervention and animal studies. During recent years, an increasing number of clinical trials have confirmed the beneficial effects of green tea on obesity. However, the optimal dose has not yet been established owing to the very different results from studies with a similar design, which may be caused by differences in the extent of obesity, dietary intake, physical activity intensity, the strength of subjects’ compliance to test instruction, the genetic background of populations, body composition and dietary habits. Therefore, further investigations on a larger scale and with longer periods of observation and tighter controls are needed to define optimal doses in subjects with varying degrees of metabolic risk factors and to determine differences in beneficial effects among diverse populations. Moreover, data from laboratory studies have shown that green tea has important roles in fat metabolism by reducing food intake, interrupting lipid emulsification and absorption, suppressing adipogenesis and lipid synthesis and increasing energy expenditure via thermogenesis, fat oxidation and fecal lipid excretion. However, the exact molecular mechanisms remain elusive.

Procyanidins (PAs) are polyphenols in plant food that have many health benefits, including cancer prevention, cardiovascular protection and diabetes prevention. PAs have been known to have low oral bioavilability. In this review, we summarize the published results on the ADME (absorption, distribution, metabolism and excretion) of PAs in vivo and in vitro. After oral administration, in the stomach the decomposition of PAs is highly dependent on the pH value of gastric juice, which is also affected by food intake. In the small intestine, PA polymers and oligomers with DP > 4 are not directly absorbed in vivo, but minor PA monomers and dimers could be detected in the plasma. Methylated and glucuronidated PA dimers and monomers are the main metabolites of PAs in plasma. In the colon, PAs are catabolized by colonic microflora into a series of low molecular weight phenolic acids, such as phenyl valerolactone, phenylacetic acids and phenylpropionic acids. We reviewed the degradation of PAs in gastric digestion, the absorption of PAs in the small intestine and the metabolic pathway of PAs by colonic microflora. To clearly explain the in vivo pharmacokinetics of PAs, a systematic comparative analysis on previously published data on PAs was conducted.