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Journal of the American College of Nutrition, Vol. 19, No. 6, 789-796 (2000)
Published by the American College of Nutrition

Original Research

Double-Blind Controlled Study on the Effects of Dietary Diacylglycerol on Postprandial Serum and Chylomicron Triacylglycerol Responses in Healthy Humans

Hiroyuki Taguchi, MS, Hiroyuki Watanabe, PhD, Kouji Onizawa, Tomonori Nagao, MS, Naohiro Gotoh, PhD, Takuji Yasukawa, MS, Rikio Tsushima, PhD, Hiroyuki Shimasaki, PhD and Hiroshige Itakura, MD

Biological Science Laboratories, Kao Corporation (H.T., H.W., K.O., T.N., N.G., T.Y., R.T.), JAPAN
Department of Biochemistry, Teikyo University School of Medicine (H.S.), JAPAN
Division of Clinical Nutrition, The National Institute of Health and Nutrition (H.I.), JAPAN

Address reprint requests to: Hiroyuki Taguchi, MS, Biological Science Laboratories, Kao Corporation, 2606, Akabane, Ichikai, Haga, Tochigi, 321-3497, JAPAN. E-mail: 304468{at}kastanet.kao.co.jp


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Objective: The effects of dietary diacylglycerol (DG) on postprandial lipemia in healthy humans were investigated.

Methods: Forty normolipidemic male volunteers ingested fat emulsions containing either DG oil or triacylglycerol (TG) oil, at different doses: 10 g (n = 13), 20 g (n = 10) and 44 g (n = 17). Two test emulsions were given at seven-days intervals in random order. Fatty acid compositions of the test oils had been adjusted to be equal. Fasting and postprandial serum lipid concentrations in each group and plasma lipoprotein lipids in the 20 g-fat ingestion group were measured during the postprandial intervals.

Results: When DG emulsion was ingested, serum TG concentrations were significantly lower (p < 0.05) in the late postprandial phase, i.e., 4 hours, 6 hours as compared to the TG emulsion. The magnitude of postprandial lipemia (the area bounded by the curve above the fasting concentration) after ingestion of 44 g-DG emulsion was significantly less than that of 44 g-TG emulsion (6.54 ± 5.12 and 8.45 ± 7.54 mmol · h/L, mean ± SD, respectively). Chylomicron TG, cholesterol, and phospholipid concentrations at 4 hours after ingestion of DG emulsion were significantly lower (p < 0.05) than those after the ingestion of TG emulsion at the same time point. No marked differences were observed for VLDL, LDL and HDL lipids between the test emulsions.

Conclusion: In the usual range of fat intake (10–44 g), postprandial response after ingestion of DG emulsion was significantly less than that after ingestion of TG emulsion in healthy human subjects.

Key words: diacylglycerol, triacylglycerol, oral fat-loading test, postprandial lipemia, chylomicron, dietary fat


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Serum triacylglycerol (TG) concentration increases after the ingestion of a meal containing fats. In healthy humans, almost all fats ingested are absorbed [1] and then enter the blood circulation essentially in the form of chylomicrons. Chylomicron TG is cleared from the circulation by enzymatic hydrolysis [2] and receptor-mediated uptake [3]. Because of the slow clearance of chylomicron TG (~10 hours), humans usually spend most of the time in a postprandial hypertriglyceridemic state. Since chylomicrons and their cholesterol-rich remnants are implicated in atherogenesis [4–8], there is a possibility that we can reduce the risk of coronary artery disease and atherosclerosis by avoiding excess TG accumulation during the postprandial phase.

Numerous studies on factors that influence the magnitude of postprandial lipemia have been performed in healthy subjects [9–12] and patients with various diseases [13–15]. Dietary fiber [16,17], glucose [18], soybean protein [19] and exercise [20,21] have been shown to reduce the magnitude of postprandial lipemia. Several recent studies have also demonstrated the acute effects of dietary fatty acids on postprandial lipemia [22–25].

Diacylglycerol (DG) is found naturally as a minor component in various vegetable oils and fats [26]. Although human adults ingest 1 to 5 g of DG every day, little attention has been paid to its nutritional characteristics because DG has been recognized only as an intermediate in the process of TG digestion [1]. Dietary TG is hydrolyzed by gastric or pancreatic 1,3-specific lipases to form 1,2- or 2,3-DG. DG is further hydrolyzed to 2-monoacylglycerol (MG). Most of the 2-MG is absorbed without undergoing further lipolysis. Since DG that occurs during the digestive processes of TG is in 1,2- or 2,3-configuration, ingestion of 1,3-DG compared to TG may exert a different effect on lipid metabolism. Recently, our group has shown that intragastric infusion of DG comprising mainly 1,3-species induces a slower extrusion of the lymphatic chylomicron TG and cholesterol in rats as compared to TG [27]. Although the mechanisms underlying these effects of DG are still unclear, it is expected that dietary DG may have similar nutritional effects in humans.

The present study was therefore performed to compare the acute effects of dietary DG and TG in the usual range of fat intake (10 to 44 g) on postprandial lipemia in healthy human subjects.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Subjects
Forty healthy men volunteered to participate in this study. The characteristics of the subjects are presented in Table 1. None of the subjects had a history of diabetes or dyslipidemia. None were taking any drugs that could interfere with lipid metabolism. The subjects consumed their usual diet and maintained their eating and exercise habits for the period of this study. The nature and purpose of the study were explained to each subject before he gave his consent to participate. All procedures were approved by the Ethics Committee of Kao Corporation and carried out in accordance with the Helsinki Declaration of 1975 as revised in 1983.


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  		Table 1. Characteristics of the Subjects

 
DG and TG Preparations
DG oil was synthesized by esterifying glycerol with fatty acids from rapeseed oil using the reverse reaction of immobilized lipase as previously described [27]. TG oil was prepared by blending rapeseed, soybean and safflower oil so that the fatty acid composition of the TG oil was similar to that of the DG oil. All of the material oils were purchased from Nisshin Oil Mills Ltd. (Tokyo, Japan). As shown in Table 2, the DG oil was composed of 1,3-DG (56.4%, wt/wt), 1 (or 3), 2-DG (26.6%, wt/wt) and TG (17.0%, wt/wt). The TG oil was composed of TG (98.8%, wt/wt) and DG (1.2%, wt/wt). According to the calculation from the molecular formula and acylglycerol compositions shown in Table 2, the fatty acid content of the DG oil (862 mg/g) was slightly lower than that of the TG oil (899 mg/g). Energy values of the DG and TG oils determined by bomb calorie meter were 37.7 kJ/g (9.0 kcal/g) and 38.1 kJ/g (9.1 kcal/g), respectively. The calorie measurements were performed by Japan Food Research Laboratories (Tokyo, Japan).


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  		Table 2. Acylglycerol and Fatty Acid Compositions of Diacylglycerol and Triacylglycerol Oils

 
Test Emulsions
Subjects consumed two test emulsions differing only in the fat with an interval of seven days. Each emulsion (100 g) contained 10 g of fat (either DG or TG oil), 47.5 g of water and 1.3 g of emulsifying agent (polyglycerolesters; SY-Glyster-MS-500, Sakamoto Yakuhin Kogyo, Osaka, Japan). To the mixture of fat and water was added 12.5 g of UCCade lemon (UCC Ueshima Coffee, Kobe, Japan), 12.5 g of TORYS CONC orange (Suntory, Osaka, Japan), 12.88 g of reduced starch hydrolysate (GOH-30, Mitsubishi Chemical Foods, Tokyo, Japan) and 3.32 g of erythritol (Mitsubishi Chemical Foods) to stabilize the mixture and for flavoring. The mixture was emulsified using a high pressure emulsifier (Nanomizer, Tokyo, Japan). The mean diameter of emulsified particles, determined using a laser diffraction particle size analyzer (SALD-100, Shimadzu, Kyoto, Japan), was the same for the two test emulsions (0.25 µm).

The energy values (combustion energy) of whole test emulsions were determined by Japan Food Research Laboratories (Tokyo, Japan). DG- and TG-based emulsions provided 7.74 kJ/g (1.85 kcal/g) and 7.79 kJ/g (1.86 kcal/g), respectively. Fat and carbohydrate contents of the emulsion were 52% (wt/wt) and 48% (wt/wt), respectively. Protein, phospholipid and cholesterol were not present in these test emulsions.

Experimental Protocol
This was a cross-over study performed in a double-blind controlled manner. Two test emulsions were given randomized so that half of the subjects received the DG emulsion first and the other half received the TG emulsion. On the day before the test, the subjects ingested between 6:00pm and 8:00pm standardized food prepared by the investigator and thereafter during the night were allowed no food or drink except sugar-free beverages, coffee, tea and water. In the next morning, no food or drink (except for water) was allowed before the commencement of the study. The subjects were admitted to the laboratory at 8:00am, and fasting blood samples were drawn from the forearm antecubital vein. The subjects ingested one of the two test emulsions at 9:00am over a period of 10 minutes. The test emulsions contained one of the test oils at different doses: 10 g (n = 13), 20 g (n = 10) or 44 g (n = 17) per 60 kg body weight. After ingestion, the subjects stayed seated under constant temperature and humidity. Blood samples were drawn every two hours for six hours (10 g-fat group), every two hours for eight hours (44 g-fat group) or at four and six hours after ingestion (20 g-fat group).

Lipid Analyses
Blood samples were collected into tubes containing either EDTA or no anticoagulant. Serum and plasma were separated by centrifugation at 1500 x g for 15 minutes at 4°C. Serum TG [28], total and free cholesterol [29], phospholipid [30] and non-esterified fatty acid (NEFA) [31] concentrations were measured by an automatic analyzer using standard enzymatic techniques. Plasma glucose concentrations were determined by a glucose oxidase method [32]. Serum insulin was assayed by an immunoenzymatic method [33].

Lipoprotein fractions were obtained from plasma samples of subjects following ingestion of the 20 g-fat emulsion by sequential ultracentrifugation [34] using a Hitachi RP65T rotor in a Hitachi SCP85H2 ultracentrifuge. Densities were adjusted by addition of potassium bromide. The chylomicron fraction was isolated by ultracentrifugation at 20,000 rpm for 30 minutes at 15°C. The very low density lipoprotein (VLDL, d < 1.006 g/mL) fraction was isolated by a second ultracentrifugation at 40,000 rpm for 6 h at 15°C. Low density lipoprotein (LDL, 1.006 < d < 1.063 g/mL) and high density lipoprotein (HDL, d > 1.063 g/mL) fractions were isolated at 40,000 rpm for 12 hours at 15°C. TG, total cholesterol and phospholipid concentrations of the isolated lipoprotein fractions were determined by enzymatic methods as described above.

Statistical Analysis
Data were presented as means ± SD. Some of the data were plotted as variations in concentration over the fasting value (taking fasting values as zero) to normalize the variations of initial values. The results were also expressed as means ± SD. The magnitude of postprandial lipemia (area under the serum TG concentration curve above the baseline) was calculated for the 44 g-fat group by the trapezoidal rule [5]. The statistical significance (p < 0.05) of the differences observed between the postprandial values and corresponding fasting values and between the DG and TG emulsion was assessed using Student’s t test for paired values. These statistical comparisons were performed with Stat-View Version J.4.11 (Abacus, Berkeley, CA).


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Changes in Serum TG Concentrations
Serum TG concentrations exhibited a significant increase relative to fasting levels for both DG and TG emulsions at all doses (Fig. 1). The postprandial serum TG responses to the emulsions increased in a dose-dependent manner. Ingestion of 44 g fat (Fig. 1 A) increased the postprandial serum TG concentrations from fasting levels until four hours and returned to the baseline by eight hours. At six hours, serum TG concentrations in the DG group were significantly lower than those in the TG group. The postprandial lipemia induce by both oils at 44 g doses was compared by calculating the area bounded by the curve above the fasting levels. The postprandial lipemia induced by the DG emulsion (6.54 ± 5.12 mmol · h/L, mean ± SD) was significantly (p < 0.05) less (23%) than that induced by the TG emulsion (8.45 ± 7.54 mmol · h/L, mean ± SD). Serum TG concentrations at four and six hours after ingestion of 20 g DG oil were significantly lower than those after ingestion of 20 g TG oil (Fig. 1 B). Samples at two hours were not collected in this group because the position and shape of the postprandial TG peak do not differ within the moderate amounts of fat doses [12]. The difference in the postprandial serum TG concentrations between the DG and the TG group was reproduced with as little as 10 g fat at the six-hour point (Fig. 1 C). Since serum TG levels returned to the fasting level by six hours after ingestion of both fats, no measurements were made thereafter.



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  		Fig. 1. Mean (± SD) changes from baseline ({Delta}) in serum triacylglycerol concentrations after ingestion of diacylglycerol emulsion (bull;) or triacylglycerol emulsion ({square}). (A) 44g fat ingestion (n = 17); (B) 20g fat ingestion (n = 10); (C) 10g fat ingestion (n = 13); a: Significantly different from fasting levels, p < 0.05 (Student’s t test for paired values); b: Significantly different from the corresponding values for the triacylglycerol emulsion, p < 0.05 (Student’s t test for paired values).

 
Changes in Serum Cholesterol, Phospholipid, Insulin, and Plasma Glucose Concentrations
Fasting and postprandial concentrations in serum cholesterol, phospholipid, insulin and plasma glucose concentrations after ingestion of the different fat emulsions are presented in Table 3.


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  		Table 3. Fasting and Postprandial Concentrations of Serum Lipids, Insulin and Plasma Glucose Concentrations after Ingestion of Fat Emulsions

 
Serum free cholesterol concentrations increased significantly after the ingestion of both fats at all doses. The postprandial responses to the fat increased in a dose-dependent manner. No significant differences were observed for serum free cholesterol concentrations between the DG and TG emulsion.

Serum esterified cholesterol concentrations did not change significantly after ingestion of 44 g or 20 g of fat. Significant increases in serum esterified cholesterol concentrations were found only after ingestion of the 10 g-DG emulsion. Significant differences between the DG and TG emulsion were observed at two hours after ingestion of 10 g of fat.

Serum phospholipid concentrations were significantly increased after the fat ingestion at all doses. Serum phospholipid levels in the DG group were significantly lower than those in the TG group at four and six hours after ingestion of 44 g of fat and at two hours after ingestion of 10 g of fat.

Serum NEFA levels decreased markedly at two hours after fat ingestion (44 g and 10 g). The concentrations returned to the baseline levels or above baseline at eight hours (44 g) or four hours (10 g) postprandially. No significant difference was observed in serum NEFA concentrations between the DG and TG emulsion at all doses. Since the test emulsions contained glucose (11.5 g/100 g emulsion), the subjects ingested 50 g of glucose in 44 g-fat group. Plasma glucose concentrations therefore tended to increase after ingestion of 44 g of fat. However, significant decreases in plasma glucose concentrations were observed after ingestion of 20 g and 10 g of fat. Postprandial changes in plasma glucose concentrations did not differ between the groups.

Serum insulin concentrations markedly increased and subsequently decreased to the fasting levels eight hours after ingestion of 44 g of either fat. For smaller doses (10 g and 20 g), the insulin levels tended to increase temporarily and then decrease below the baseline levels except at the six-hour point of the 10 g-fat group, where the levels returned above the baseline. Serum insulin concentrations did not differ between the groups at any dose examined.

Changes in Plasma Lipoprotein Levels
For detailed analysis of the effects of DG on postprandial lipemia in humans, plasma lipoprotein fractions were separated and analyzed following ingestion of 20 g of fat. Changes of plasma chylomicron lipid concentrations after ingestion of 20 g of fat are shown in Fig. 2. Chylomicron TG (Fig. 2A), cholesterol (Fig. 2B) and phospholipid (Fig. 2C) concentrations increased at four hours after ingestion of either emulsion and returned to fasting levels by six hours. The increment of the postprandial concentrations of chylomicron TG, cholesterol and phospholipid after DG fat ingestion was smaller than that after TG fat ingestion. The difference in the concentrations of chylomicron TG at four hours was statistically significant (Fig. 2A).



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  		Fig. 2. Mean (± SD) changes from baseline ({Delta}) in plasma chylomicron lipid concentrations after ingestion of diacylglycerol emulsion (bull;) or triacylglycerol emulsion ({square}) at a dose of 20g fat (n = 10). (A) Chylomicron triacylglycerol concentrations; (B) Chylomicron cholesterol concentrations; (C) Chylomicron phospholipid concentrations; a: Significantly different from fasting levels, p < 0.05 (Student’s t test for paired values), b: Significantly different from the corresponding values for the triacylglycerol emulsion; p < 0.05 (Student’s t test for paired values).

 
Fasting and postprandial lipid concentrations of plasma VLDL, LDL, and HDL after ingestion of the fat emulsions are shown in Table 4. Plasma VLDL TG, cholesterol, and phospholipid concentrations increased significantly four hours postprandially and returned to the baseline levels by six hours. Plasma VLDL TG levels at four and six hours in the DG group were significantly less than those in the TG group. The changes in LDL and HDL lipid levels after the ingestion of fat emulsion were either small or none. There were no marked changes in HDL lipid concentrations after the fat ingestion, but there was a tendency that HDL TG levels in the DG group were slightly higher than those in the TG group.


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  		Table 4. Fasting and Postprandial (4 and 6 h) Concentrations of Plasma Lipoprotein Lipid after Ingestion of 20g Fat Emulsions

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
The results of this double-blind, randomized, controlled study indicated that the ingestion of DG, as compared to TG, causes smaller increases in serum TG concentrations, particularly in the late postprandial phase in healthy human subjects. Serum TG concentrations after ingestion of 44 g of DG oil were significantly low (p < 0.05) at six hours postprandially as compared to those after ingestion of 44 g of TG oil. The magnitude of postprandial lipemia for the DG emulsion was significantly lower (23%) than that for the TG emulsion (p < 0.05). Moreover, we showed that the difference was reproducible even with low fat doses (10 and 20 g). Since we did not collect blood samples at two hours (20 g-fat group) and quitted collection after six hours (10 g- and 20 g-fat groups), we could not accurately compare the magnitude of postprandial lipemia in these cases. However, we anticipated that the magnitude of postprandial lipemia caused by DG oil even at low doses is less than that caused by TG oil from the pattern of the postprandial TG concentration curves for both fats.

Since the calculated fatty acid content of the DG oil (862 mg/g) is lower than that of the TG oil (899 mg/g), the theoretical amounts of fatty acid ingested differed between the emulsions. However, the differences in serum and chylomicron TG concentrations observed in this study were far greater than those expected from the small difference in the amounts of fatty acid ingested. Hara et al. [35] and Murata et al. [36] observed a reduction of serum TG concentrations in rats fed DG diet as compared to these fed TG diet. Murata et al. [27] also showed that the lymphatic transport of chylomicron TG caused by the DG oil was slower than that induced by TG oil using rats intragastrically infused with the emulsions. We speculate that a common mechanism is underlying these observations including the results of the present study because fatty acid contents had been adjusted to be equal in these animal studies.

In the lipoprotein analysis, we observed marked differences only in the postprandial chylomicron TG and little or no difference in VLDL, LDL or HDL TG concentrations between two fats (20 g). Among several mechanisms that may be involved in the decreased response of chylomicron TG to the dietary DG, it is unlikely that the impaired absorption of the dietary fat from the small intestine reduced postprandial chylomicron TG responses. Dietary DG had the same digestibility coefficient as TG with similar fatty acid composition (manuscript in preparation). It seems also unlikely that dietary DG increased the rate of chylomicron TG clearance. In this study, no marked inter-group differences were observed in the postprandial serum insulin concentrations that can influence the rate of chylomicron TG clearance [13].

As previously reported by Murata et al. [27], the decreased response of chylomicron TG to the dietary DG in healthy humans may be due to the reduction of re-esterification and chylomicron assembly in the small intestine or to the reduction of subsequent secretion of chylomicron into the circulation. Dietary DG used in the present study was composed mainly of 1,3-species. Based on the nature of gastric and pancreatic lipases, we suppose that the final digestive products of 1,3-DG are predominantly free glycerol and free fatty acids. The final digestion products of TG, in contrast, are 2-MG and free fatty acids. Free glycerol is readily absorbed and transported into the blood circulation or may be phosphorylated to sn-glycerol-3-phosphate and utilized for the synthesis of TG. Yang and Kuksis, however, reported that a large portion of TG formed through the sn-glycerol-3-phosphate pathway was stored in the cytoplasm of intestinal mucosal cells rather than being directly used for the chylomicron assembly [37, 38]. Thus, the differences in the metabolic fates of the digestion products of these acylglycerols in the intestinal mucosal cells could be responsible for the differences in plasma chylomicron TG concentrations. Detailed quantitative analyses of the metabolic fates of digestion products of DG in the intestinal lumen and mucosal cells are required to confirm this hypothesis.

Ingestion of medium-chain TG (MCT) [39–41] and structured TGs with medium- or short-chain fatty acids [39,42,43] as compared to ordinary TG have been shown to reduce the rate of chylomicron formation and to prevent the rapid increase of serum TG concentrations. The results obtained in the present study indicate that one can reduce the magnitude of postprandial lipemia by replacing the TG oil with the DG oil. As DG is found in natural vegetable oils and fats [26], DG is thought to be natural structured fat based on its glycerol-backbone structure. MCT are used in enteral and parenteral feeding emulsions, but they are far less useful than long-chain TG in the normal human diet. Utilization of structured TGs in the usual diet is also markedly restricted due to their physicochemical nature such as smoke points. On the other hand, DG oil is suitable in the usual diet by replacing TG oil because the physicochemical nature of DG is comparative to that of TG.

In conclusion, this double blind controlled study using healthy men has shown that one can reduce the magnitude of postprandial lipemia by consuming DG oil in place of TG oil. Based on the correlation of coronary artery disease and postprandial lipemia, it can be speculated that dietary DG might be less atherogenic than TG. Further studies are required to clarify the chronic effects of dietary DG on lipid metabolism in humans.


   ACKNOWLEDGMENTS
 
We thank Dr. Yukihisa Miyazawa, the vice-president of Teikyo University School of Medicine Hospital, for his help in performing this clinical study. We also thank Ms. Ritsuko Ikeda and Ms. Miwa Kosuda for technical assistance.

Received September 30, 1999. Accepted September 22, 2000.


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TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

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