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Aim: To determine the effects of simultaneously ingesting glucose and fat on postchallenge glycemia and lipidemia in 12 healthy young Japanese women. Methods: Three test trials were administered in a randomized crossover design: glucose (1 g/kg, G trial); fat cream (0.35 g/kg as fat; F trial); glucose + fat cream (GF trial). Blood samples were taken before and at 0.5, 1, 2, 4, and 6 h post-ingestion. Results: The GF trial's serum glucose peak value was lower than the G trial's, and its remnant lipoprotein-cholesterol (RLP-C) increase was less than the F trial's. The GF trial's apolipoprotein (Apo) B48 increase happened faster than the F trial's. The G and GF trials' insulinogenic index (I/G30) values were negatively correlated with the area under the curve (AUC) of glucose for 2 h. Fasting insulin level and HOMA-IR were positively (and QUICKI and I/G30 were negatively) correlated with the AUC of insulin for 2 h. The F and GF trials' fasting TG, RLP-C, ApoB48, and ApoC-III levels were positively correlated with the AUC of TG and RLP-C for 6 h. The fasting ApoB48 level predicted the AUC of ApoB48 for 6 h. Conclusion: The glucose peak was ameliorated by co-ingesting fat. I/G30 predicted an early postchallenge (0-2 h) glucose rise. The fasting insulin level, HOMA-IR, QUICKI, and I/G30 predicted an insulin rise. The RLP-C rise by fat ingestion was ameliorated by co-ingesting glucose. Fasting TG, RLP-C, ApoB48, and ApoC-III levels predicted postchallenge TG and RLP-C rises. The fasting ApoB48 level predicted postchallenge apoB48, i.e., a rise in intestinal lipoprotein.

Aim: Our previous study demonstrated that the ingestion of fructose with fat exacerbated and delayed postprandial lipid metabolism (J Atheroscler Thromb 2013; 20: 591). Herein, we investigated the effect of ingesting a water-soluble dietary fiber, resistant maltodextrin (RMD), which has been reported to be effective for ameliorating postprandial glycemia and lipidemia, on fructose-induced postprandial hyperlipidemia in healthy young women. Methods: Healthy young Japanese women with apolipoprotein E3/3 phenotype were enrolled. They underwent 4 test trials in a randomized crossover design: fat cream (0.35 g/kg of fat; F trial), fat cream with RMD (5 g; FR trial), fat cream with fructose (0.5 g/kg; FFr trial), and fat cream with fructose and RMD (FFrR trial). Blood samples were taken before (0) and at 0.5, 1, 2, 4, and 6 h after ingestion. Results: The serum glucose and insulin concentrations peaked at 0.5 h in the FFr and FFrR trials, and no difference was observed between these trials. There was no increase in glucose concentration in the F or FR trials. The serum triglyceride and apolipoprotein B48 concentrations peaked at 4 h in all trials. In the F and FR trials (but not in the FFr and FFrR trials), the serum triglyceride concentration returned to the fasting level at 6 h. In all trials, the apolipoprotein B48 concentration did not return to baseline at 6 h. Conclusion: Co-ingestion of RMD did not significantly inhibit fructose-induced postprandial hyperlipidemia.

Reactive oxygen species (ROS) and highly reactive oxygen species (hROS) secreted by leukocytes are crucial to innate immunity; however, they pose a risk of oxidative stress. To monitor their balance in daily health check-ups, optical technologies for the simultaneous measurement of ROS (superoxide radicals) and hROS (hypochlorite ions) that utilize only a few microliters of whole blood have been developed. The aim of this study was to clarify whether this system could assess the effects of fat ingestion on postprandial oxidative status. Eight healthy young Japanese women ingested a beverage containing oral fat tolerance test cream. Blood samples were collected before and 0.5, 1, 2, 4, and 6 h after fat ingestion. Blood ROS and hROS levels, oxidative stress markers, and biochemical markers were monitored. Consistent with previous studies, triglyceride levels significantly increased at 4 h ( p <0.01) and returned to near-baseline levels 6 h after ingestion. ROS levels peaked significantly at 2 h ( p <0.05), and hROS levels peaked significantly at 1 ( p <0.05) and 2 h ( p <0.01) after ingestion. This study offers an insight into the acute effects of fat ingestion on leukocyte activity and provides a methodology for monitoring postprandial oxidative status.

Aim: Postprandial hyperlipidemia is a major risk factor for coronary heart disease. Our previous study revealed that ingesting fructose with fat cream delays and exacerbates postprandial lipidemia. A rare sugar, D-allulose, has recently attracted attention as an alternative zero-calorie sweetener to natural sugars. In this study, we investigated the effect of ingesting D-allulose with fat cream on postprandial glycemia and lipidemia in young women. Methods: Eleven young Japanese women with apolipoprotein E3/3 phenotype were enrolled. They underwent 4 test trials: fat cream (0.35 g/kg as fat; F trial), fat cream with D-allulose (0.5 g/kg; FA trial), fat cream with fructose (0.5 g/kg; FFr trial), or fat cream with sucrose (0.5 g/kg; FS trial). Blood samples were taken before (0) and at 0.5, 1, 2, 4, and 6 h after ingestion.Results: In the FA trial, serum glucose and fructose concentrations at 0.5 and1 h were significantly lower than those in the FFr and FS trials. In the FA trial, the serum glucose concentration did not increase during the experiment. Serum triglyceride and remnant-like particle-triglyceride concentrations peaked at 2 h in the F trial, and at 4 h in the FA, FFr, and FS trials. Conclusion:When ingested with fat, D-allulose showed almost no glycemic response in contrast to fructose or sucrose. However, ingesting D-allulose with fat may delay postprandial lipidemia similar to these sugars.