CRP level is associated with visceral adipose tissue and is significantly associated with the components of insulin resistance syndrome in healthy Japanese subjects. These data support a possible role of visceral adipose tissue in inflammation component of atherosclerosis, and further studies are needed to study the mechanism of CRP elevation caused by visceral adipose tissue.

Summary This review assesses the feasibility of using glycemic index (GI) as a predictor of appetite, hunger and satiety by surveying published human intervention studies. We also discuss the relationship between GI and two appetite/satiety control hormones, leptin and ghrelin. Ingestion of high-GI food increased hunger and lowered satiety in short-term human intervention studies. This effect may be attributed to the rapid decline in blood glucose level following a hyperinsulinemic response caused by a sharp and transient increase in blood glucose level that occurs after the ingestion of high-GI food, which is defined as the glucostatic theory. However, appetite, hunger and satiety after the ingestion of foods with varying GI were inconsistent among long-term human intervention studies. From the few relevant long-term studies available, we selected two recent well-designed examples for analysis, but they failed to elicit clear differences in glycemic and insulinemic responses between high-and low-GI meals (consisting of a combination of different foods or key carbohydrate-rich foods incorporated into habitual diets). One of the reasons that these studies could not predict glycemic response to mixed meals is presumably that the GI of each particular food was not reflected in that of the mixed meals as a whole. Thus, it is difficult to conclude that the GI values of foods or mixed meals are a valid long-term predictor for appetite, hunger and satiety. Both insulin and insulin-mediated glucose uptake and metabolism in adipose tissue affect blood leptin concentration and its diurnal pattern. Circulating ghrelin level is suppressed by carbohydrate-rich meals, presumably via glycemia and insulinemia. Accordingly, low-GI foods may not necessarily increase satiety or suppress appetite and/or hunger because of the lack of insulin-mediated leptin stimulation and ghrelin suppression. However, insulin-mediated leptin stimulation and ghrelin suppression per se is not consistent among studies; thus we were not able to identify a clear relationship among GI, satietogenic leptin, and appetitic ghrelin.

We evaluated the absorption and metabolism of palatinose in rats by the carbohydrate load test and the 13 C-and H 2 -breath tests. We compared the results of these tests with those of sucrose, since sucrose is an isomer of palatinose and generally known to be degraded and absorbed from the small intestine. In the carbohydrate load test, blood glucose and plasma insulin levels after oral administration of palatinose rose more gradually and reached a maximum that was lower than that after sucrose administration. C fru ] showed no difference between palatinose and sucrose. In the H 2 -breath test, the concentration of H 2 in the expired air was measured for 420 min. H 2 was hardly detected with both palatinose and sucrose and no significant difference was observed between the two groups. These results suggest that palatinose is utilised in vivo at a rate equal to that of sucrose.

This study was conducted to investigate the inhibitory effects of palatinose and Palatinit, which are disaccharides (or disaccharide alcohol) connected through an alpha-1,6-glucosyl linkage, on the hydrolysis of other carbohydrates, using an enzyme extract from the rat small intestine and a purified sucrase-isomaltase complex. Palatinose and its hydrogenated product, Palatinit, an equimolar mixture of alpha-O-D-glucopyranosyl-1,6-D-sorbitol (GPS) and alpha-O-D-glucopyranosyl-1,6-D-mannitol (GPM), inhibited the hydrolysis of sucrose and maltose. Palatinose and Palatinit also inhibited the hydrolysis of dextrin and soluble starch. Kinetic analysis of the enzymatic inhibition by GPS and GPM on sucrose hydrolysis revealed that both GPS and GPM competitively inhibit sucrase catalytic activity. These results suggest that disaccharides with an alpha-1,6-glucosyl linkage competitively inhibit intestinal alpha-glucosidases and may reduce the rate of hydrolysis of sucrose and other alpha-glucosylsaccharides.

SummaryWe previously reported that the increase in blood glucose was more suppressed when palatinose was taken with sucrose or glucose than when either of these sugars was taken alone. In the present study, we examined whether or not palatinose suppresses glucose absorption using everted intestinal sacs from rats. Glucose absorption in the everted rat intestinal sac was measured with 0, 1, 2.5 or 5 m M of palatinose added to 20 m M glucose. The measurement was repeated five times for each palatinose level to calculate a mean value. The result showed glucose absorption to be reduced as the palatinose level increased. It was significantly reduced when 5 m M palatinose was added as compared with no palatinose addition ( p Ͻ 0.05). These results suggest that palatinose suppresses glucose absorption. Key Words glucose absorption, enzyme inhibition, blood glucosewhich is also called isomaltulose, has been used in various food products as a non-cariogenic natural sugar which has a good taste comparable to that of sugar ( 1 , 2 ). Palatinose is characterized by excellent digestibility. Palatinose is catalyzed by an isomaltase, and the digestibility of palatinose is estimated to be about one-fifth that of sucrose ( 3 ). Thus, palatinose causes a gradual increase in blood glucose ( 4 , 5 ). Furthermore, it is a safe sugar that does not cause diarrhea even when taken in large quantities because a sufficient amount of isomaltase is available in the small intestine.Recent studies have identified several functions associated with the property of gradually increasing blood glucose ( 6 , 7 ). We recently found that palatinose inhibited the blood glucose increases which occur in response to sucrose or glucose ( 8 ). One of the potential mechanisms of this suppressive effect is the inhibition of enzymes that degrade carbohydrates such as sucrose, maltose and starch ( 9 ). However, since this inhibitory effect alone cannot explain the suppressive effect of palatinose on the increase in blood glucose with the ingestion of glucose, which is a simple sugar, palatinose may suppress glucose absorption per se. The present study was therefore designed to investigate whether palatinose has any suppressive effects on glucose absorption using everted rat intestine. Materials and Methods1. Animals. Male Wistar rats weighing about 250 g (supplied by Charles River Laboratories Japan, Inc.) were used. The animals were anesthetized with pentobarbital, subjected to abdominal section, and exsanguinated by transection of the descending aorta. A 10-cm section of the jejunum was removed 15 cm below Treitz's ligament of the small intestine. Table 1.3. Preparation of isolated everted intestinal segments. Each intestinal segment isolated was thoroughly washed with physiological saline and then with the standard buffer. The segment was then everted, and the upper portion was fixed to a polyethylene tube with a piece of thread and the bottom portion was tied with another piece of thread. The intestinal segment was filled with 2 mL of the standard buffer....