Abstract

We examined whether a modification of a starch into an alpha-amylase resistant form can lead to a reduction of postprandial glucose and insulin responses, and consequently to a change of lipid metabolism in liver and adipose tissue. For this purpose, a processed starch was prepared using a cornstarch (70% amylose and 30% amylopectin) and monoacylglycerol (monostearate; MS), forming monostearate-starch complex (MS-treated cornstarch). When we determined in vitro hydrolysis of MS-treated cornstarch using alpha-amylase and intestinal microvillar alpha-glucosidases, the glucose production rate of the MS-treated cornstarch was slower than the non-treated cornstarch. Measurement of a transmural potential difference (delta PD) evoked by the MS-treated cornstarch in everted rat jejunum showed that the absorption rate of glucose released from the MS-treated cornstarch was also remarkably slower than that from the non-treated cornstarch. The postprandial plasma insulin response to the MS-treated cornstarch was reduced, although plasma glucose response was unchanged. In a feeding study, two groups of five or six male Wistar-strain rats were fed defined diets containing 61.1% MS-treated cornstarch or 58.2% non-treated cornstarch ad libitum for 14 days. Food intakes during the period were similar between the two groups. Feeding the MS-treated cornstarch resulted in a significantly lower maltase activity in upper jejunum than did the non-treated cornstarch feeding. The activities of lipogenic enzymes--fatty acid synthetase (FAS), malic enzyme (ME), and glucose-6-phosphate dehydrogenase (G-6-PDH)--significantly decreased in epididymal adipose tissue of rats fed the MS-treated cornstarch. In the liver, FAS activity was lower in the MS-treated cornstarch group. The results indicated that MS-treated cornstarch was digested less rapidly, and lowered blood insulin response, consequently leading to a declined lipogenesis of adipose tissue and liver. This study suggests that the rate of intestinal hydrolysis of starch is an important determinant of metabolic responses such as glycemic and lipogenic responses to diets.

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