Keto Means
Keto Means
Photo: Teona Swift
Results of epidemiological studies have suggested that consumption of green tea could lower the risk of type 2 diabetes. Intervention studies show that green tea may decrease blood glucose levels, and also increase satiety.
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Read More »The primary endpoint in this study was the effect of green tea on postprandial glucose and insulin levels. Our hypothesis was that green tea could lower postprandial glucose and insulin levels. In animal in vitro studies, green tea increased the basal and insulin-stimulated glucose uptake of rat adipocytes [5], suppressed glucose absorption in the rabbit small intestine [20], and ameliorated insulin resistance by increased expression of glucose transporter IV in rat adipocytes [21]. In addition, EGCG exhibited antidiabetic properties by suppressing gluconeogenesis in rat hepatoma cells [22]. We observed no difference in glucose levels and, contrary to what we expected, the 120 min glucose value was higher following the green tea meal. A similar observation has been reported by Park et al. [23], although they also observed significantly lower glucose levels during the first hour of an OGTT trial with green tea in healthy humans. They suggested that the catechins had a hypoglycemic effect in the intestines, but a hyperglycemic effect later when in the circulation. However, the study by Park et al. included few subjects, and it seems that a crossover design was not used. Tsuneki et al. also reported an immediate glucose-lowering effect of green tea powder after OGTT in healthy humans [10]. Although we studied the immediate effects of green tea on glucose metabolism after the ingestion of a white bread meal, in the absence of similar studies for comparison, our findings that green tea does not lower glucose or insulin levels are consistent with previous long-term intervention studies [11–13]. Previous results on the effects of green tea have been ambiguous, and the discrepancy between results from human and animal studies may reflect species-specific differences. Possible reasons for the lack of positive findings in vivo might be individual variations in the bioavailability and metabolism of catechins in humans [2]. The secondary endpoint in this study was the effect of green tea on satiety. Our hypothesis was that green tea not only lower postprandial glucose and insulin levels but also increase satiety. Flint et al. [24] concluded that scoring of sensations such as hunger, satiety, fullness, and desire by VAS can be reproduced, and can therefore be used in single-meal studies. In our study, the VAS rating revealed an overall higher sensation of satiety after the green tea meal than after the reference meal. This is supported by the fact that not only was satiety increased, but also the feeling of fullness and the feeling of having had enough to consume. However, no effect was seen on satiety during a 12-week intervention with GTE capsules in obese subjects on a standardized diet [25]. Several factors may have contributed to our positive findings: we used a crossover design, we examined different sensations of satiety at frequent intervals, and we used green tea in its natural form served as a hot beverage. The taste perception of the green tea in this study may have been responsible for the satiety-promoting effect of green tea and so contributed to a stronger satiety sensation after the green tea meal than after the reference meal. Oral exposure to food is related to an increase in satiety, and a decrease in hunger and desire to eat [26]. Measurements of taste perception of the meals in this study would have provided additional information. However, the participants did not dislike the green tea meal more than the reference meal, nor did they feel sicker during the green tea trial, so the higher level of satiety could not be explained by any unpleasantness produced by the green tea meal. The subjects experienced a stronger desire to consume their favorite food or eat another mouthful of the same food after the reference meal. Since the same kind and amount of food was ingested at both occasions, greater distension of the stomach is not likely to be the mechanism behind these findings. The postprandial glucose concentration is determined by the rates of glucose formation and clearance. Insulin mediates glucose uptake in the tissues after a meal. Gastric emptying rate (GER), together with other factors, regulates the postprandial glucose response, and a reduction in the GER leads to a lower postprandial glucose concentration. Since green tea did not lower postprandial glucose or insulin levels, we can assume that a reduction in the GER is not a likely mechanism behind increased satiety or fullness. Postprandial changes in hormones may be responsible for the satiety-promoting effect of green tea. However, we did not study changes in hormones in this study. The satiety signaling process is very complex, and involves several gastrointestinal peptides and neurotransmitters [27]. Norepinephrine has an important role in satiety signaling in the hypothalamus [28]. Green tea catechins have been shown to inhibit catechol-o-methyl-transferase, an enzyme that degrades norepinephrine in the synaptic cleft [29]. This would lead to prolonged action of norepinephrine, and is one possible explanation of the effect of increased satiety with green tea. However, it is uncertain whether polyphenols can cross the blood-brain barrier [30].
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Read More »Our study has several limitations, and the results should be considered with some caution. Since the study was not blinded, we cannot exclude the possibility that the findings of greater satiety with green tea could be biased. Furthermore, the effect of green tea on satiety was only a secondary endpoint, and the subjects included were healthy and of normal weight. We may have found more significant differences in fullness and satiety if a larger number of participants had been included in the study. To simplify the comparison of the glucose AUC calculations we present our results in terms of GI. We found no difference in GI with green tea, possibly due to large inter- and intrasubject variations in AUCs. The precision could have been improved if the test and reference meals had been repeated. Standardization of the participants' diet 24 hours prior to the trials could have ensured a more similar glucose tolerance on the two trial days.
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