L-Arabinose selectively inhibits intestinal sucrase activity in vitro and suppresses the glycemic response in a dose-dependent manner in experimental animals. In the present study, we investigated the effect of L-arabinose on the glycemic response of healthy volunteers and patients with type 2 diabetes. In the first experiment using a cross-over design, eight fasted normal volunteers were each given 50g of sucrose with and without 2g of L-arabinose. The increases of plasma glucose and serum insulin were significantly lower in the individuals given both L-arabinose and sugar. In the second experiment, the dose-dependency of L-arabinose was evaluated. Forty normal volunteers over 40 years old were given a jelly containing 30g of sucrose with added L-arabinose in ratios of 0%, 2%, 3% and 4% (w/w)(n=10). L-Arabinose at 3% and 4% significantly suppressed the increase of plasma glucose at 30min after ingestion. In the third experiment, patients with type 2 diabetes (n=10) were given the jelly with 3% (w/w) added L-arabinose using a cross-over design. L-Arabinose suppressed the maximal increase of plasma glucose after sucrose ingestion. These results demonstrate that L-arabinose attenuates sucrose-induced hyperglycemia both in normal subjects and diabetic patients, presumably through inhibition of intestinal sucrase activity.

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We previously found that dietary polyunsaturated fatty acids (PUFA) was quickly (starting within 1h) and preferentially incorporated into tissue lipids and suppressed fatty acid synthesis in the liver, whereas dietary monounsaturated fatty acids or saturated fatty acids (MUFA and SFA) were quickly metabolized after intake and the tissue MUFA and SFA are mostly endogenous. Thus, in the present experiment, the effects of various amounts of dietary PUFA, MUFA or SFA on the fatty acid concentrations of tissues were examined in rats fed an equal amount of energy-containing diet/body weight for 1 or 2 weeks. (1) When rats were fed diets containing 0-20% of olive, corn or fish oil, the MUFA concentrations in total lipids of plasma and liver was not significantly increased inspite of a large intake, whereas the PUFA concentrations were increased with increasing dietary intake. Plasma cholesterol ester fatty acid compositions of these rats were similarly changed. The liver lipogenic enzyme activities, and the plasma and liver triacylglycerol concentrations were decreased with increasing dietary PUFA. (2) When rats were fed diets with increasing amount of MUFA or SFA but with a fixed amount of PUFA, the fatty acid concentrations in the tissues were not significantly changed. Therefore, the tissue PUFA concentrations reflected dietary PUFA, whereas the tissue concentrations of MUFA and SFA did not, but were controlled by PUFA.

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