IngredientsDiacylglycerol — abbreviated DAG, also written as diglyceride or diacylglyceride — is a class of glycerolipid defined by a glycerol backbone esterified with two fatty acid chains. DAGs possess two fatty acids attached to a glycerol backbone, represented in two principal conformations: 1,2-diacylglycerol and 1,3-diacylglycerol. A third stereoisomeric form, sn-2,3-DAG, also exists. DAG exists in three stereoisomers: sn-1,2-DAG, sn-1,3-DAG, and sn-2,3-DAG.
DAG is a natural component of fats and oils. All cooking oils naturally contain small quantities of diacylglycerol (1,2(or 2,3) and 1,3), ranging from 0.8% in rapeseed oil to 9.5% in cottonseed oil. Corn oil and olive oil are reported to contain about 2.8% and 5.5% diacylglycerol oil, respectively. Soybean oil contains approximately 1% DAG, and safflower oil contains approximately 2.1%. As a dietary molecule, DAG is also produced endogenously during normal digestion: following the ingestion of triacylglycerol, diacylglycerol is produced in the gastrointestinal tract as a metabolic intermediate, either as sn-1,2-diacylglycerol or as sn-2,3-diacylglycerol.
Monoacylglycerol (MAG) and diacylglycerol (DAG) are structured lipids that have been widely used in various pharmaceutical, cosmetic, and food industries.
DAG oil is described as a world-leading antiobesity functional cooking oil synthesized via structural modification of conventional fats and oils; it is made from the esterification of fatty acids originating from natural edible plant oils, such as soybean and rapeseed oils. DAG oil is a cooking oil in which the ratio of triglycerides (triacylglycerols, TAGs) to diacylglycerols (DAGs) is shifted to contain mostly DAG, unlike conventional cooking oils which are rich in TAGs. Vegetable DAG oil, for example, contains approximately 80% DAG and is used as a 1:1 replacement for liquid vegetable oils in all applications.
Commercially produced vegetable-derived DAG oil contains greater than 80% DAG, less than 20% TAG, less than 5% monoacylglycerols, and small amounts of emulsifiers and antioxidants to maintain quality.
The main industrial production methods include: direct esterification, selective hydrolysis, and glycerolysis. More specifically, through an enzymatic process, the DAG content of a combination of soy and canola oils is significantly increased. In recent years, the use of lipase in the preparation of diacylglycerol oil has gained popularity; enzymatic esterification, enzymatic glycerolysis, and enzymatic hydrolysis are some of the main methods used. Enzymatic preparation of diacylglycerol has several advantages, including mild reaction conditions and low content of harmful substances.
DAG oil was developed in Japan and launched in February 1999 by Kao Corporation as "Healthy Econa" cooking oil. In 2000, the FDA granted Kao and its partner, Archer Daniels Midland Company, "generally recognized as safe" (GRAS) status for their DAG oil product. In the United States, DAG oil was commercially available as Enova oil and could be used in home cooking and vegetable oil spreads.
In contrast to many plant-derived dietary supplements, DAG as an isolated, concentrated ingredient is a modern innovation rather than the subject of well-documented traditional pharmacopeial use. The natural presence of diacylglycerols at low concentrations in all edible plant oils means that human exposure to the compound is ancient, but deliberate exploitation of its biological properties is comparatively recent.
Diacylglycerol has a long-standing history in the field of nutrition, albeit often under the broader umbrella of natural fats and oils. While isolated DAG is a more recent innovation, its presence in natural edible oils has contributed to health practices for centuries.
On the regulatory and commercial level, the formal history of concentrated DAG oil begins in Japan. DAG oil, containing 80% or greater (w/w) of DAG consisting of 1,3- and 1,2(2,3)-DAG at a ratio of 7:3, was approved by the regulatory authorities in Japan as a "Food for Specified Health Use" in 1999. Since 1999, DAG oil has been marketed in Japan as a "Food for Specified Health Use" and was accepted as "Generally Recognized As Safe (GRAS)" by the US FDA in 2000.
The defining structural feature of DAG is the presence of exactly two, rather than three, fatty acid chains on a glycerol backbone. Research has shown that oil containing 70% of the unusual 1,3-species has metabolic characteristics distinct from those of triacylglycerol of similar fatty acid composition. The predominance of the 1,3-isomer, rather than the 1,2-isomer, is central to DAG's functional properties. The ratio of 1,3-DAG to 1,2-DAG in DAG oil is approximately 7:3.
The fatty acids esterified to the glycerol backbone in commercial DAG oils reflect those of the source vegetable oils (principally soybean and canola/rapeseed). The constituents of diacylglycerol oil are commonly found in diets as components of conventional dietary oils, as approved food additives (i.e., mono- and diacylglycerols), and as metabolites of normal lipid metabolism following the consumption of dietary fat.
The distinct biological effects of DAG, particularly 1,3-DAG, arise primarily from differences in digestive handling relative to triacylglycerol (TAG). Because the energy value and absorptive and digestive properties are similar, the different effects of diacylglycerol compared with triacylglycerol are due to their structural differences.
When TAG is digested, the primary hydrolysis product released at the sn-2 position is 2-monoacylglycerol (2-MAG). This 2-MAG directly enters the "monoacylglycerol pathway" for re-esterification into TAG within enterocytes (intestinal epithelial cells), enabling efficient packaging of dietary fat into chylomicrons. In contrast, 1,3-DAG yields 1-monoacylglycerol (1-MAG) upon digestion. Reacylation to triacylglycerol in small intestinal cells was found to be slower with diacylglycerol feeding than triacylglycerol feeding. This slower re-esterification means less newly absorbed fat is packaged directly into chylomicrons.
Unlike TAG, the predominant isomer of DAG, 1,3-DAG, undergoes digestion and yields significantly lower levels of re-esterified TAG in intestinal epithelial cells, thereby reducing postprandial TAG levels.
Expression of mRNA of beta-oxidative and uncoupling proteins 2 was increased in liver and/or intestinal cells on feeding diacylglycerol compared with triacylglycerol. Upregulated mRNA expressions associated with fatty acid (FA) transport (FA translocase and FA binding protein), β-oxidation (acyl-CoA oxidase and medium-chain acyl-CoA dehydrogenase), and thermogenesis (uncoupling protein-2) in the small intestine by DAG may explain in part the mechanisms for increased postprandial energy expenditure.
The hepatic exposure to fatty acids following DAG intake may lead to greater β-oxidation by the liver than that after TAG intake. Enhanced β-oxidation may lead to increased satiety.
A proposed novel molecular mechanism involves serotonin signaling. A substitution of DAG oil for TAG oil in diet has been reported to reduce body fat and body weight, possibly by increasing postprandial energy expenditure. Research has found that DAG ingestion elevates plasma serotonin levels by about 50% compared with TAG ingestion. Research demonstrated that 1-monoacylglycerol, a digestive product of DAG, increases serotonin release from human intestinal cells (Caco-2), and enhances expression of genes associated with β-oxidation, FA metabolism, and thermogenesis, and that serotonin increases expression of these genes, proposing a novel molecular mechanism for DAG-mediated promotion of negative caloric balance.
Compared with the TAG-containing meal, the DAG-containing meal tended to induce higher postprandial energy expenditure and significantly lower postprandial respiratory quotient, suggesting that the DAG-containing meal has high postprandial lipid oxidation activity and a potential effect on high diet-induced thermogenesis.
Diacylglycerol acyltransferase-1 (DGAT-1) is an enzyme involved in the formation of dietary fat into circulating triglycerides within the body. Once dietary fat is digested and absorbed, the resulting fatty acids are re-esterified into triglycerides. Inhibition of DGAT-1 results in delayed and decreased re-esterification of dietary fats into circulating triglycerides. It is hypothesized that this effect may lead to decreased deposition of excess dietary fat as adipose tissue, possibly due to increased fatty acid oxidation in the enterocytes.
It is important to distinguish the dietary/nutritional role of exogenous DAG from the intracellular signaling role of endogenously generated DAG. Bioactive lipids like diacylglycerols, ceramides, eicosanoids, and endocannabinoids serve as second messengers linking nutrient state to insulin signaling, inflammation, and stress response; pathologic accumulation of these species enhances insulin resistance and lipotoxicity. This endogenous, intracellular signaling function of DAG (principally 1,2-DAG acting as an activator of protein kinase C) is a separate biochemical context from the dietary supplementation of 1,3-DAG–rich oil.
The most extensively studied application of DAG oil is as an adjunct to weight management. Clinical trials have focused on the use of DAG oil as adjunctive therapy for weight loss and body fat reduction, especially in metabolic syndrome. However, few quality, independent clinical trials have been conducted.
An early double-blind controlled study by Nagao et al. (2000), published in the Journal of Nutrition, examined the effects of long-term ingestion of dietary diacylglycerols in a double-blind controlled study of human lipid metabolism in healthy men (n = 38; aged 27 to 49 years, BMI 21.8 to 27.4 kg/m²). The test oils (10 g/day) were included in bread, mayonnaise, or shortbread and served for breakfast.
A larger randomized, double-blind, parallel intervention trial by Maki et al. (2002) published in the American Journal of Clinical Nutrition assessed the efficacy of an oil containing mainly 1,3-diacylglycerol in reducing body weight and fat mass when incorporated into a reduced-energy diet; the study enrolled 131 overweight or obese men and women. Food products containing DAG or TAG oil and having the same fatty acid composition were incorporated into a reduced-energy diet (2100–3350-kJ/day deficit) for 24 weeks. In an intention-to-treat analysis, body weight and fat mass decreased significantly more in the diacylglycerol group than in the triacylglycerol group (P = 0.025 and 0.037, respectively). By the end of the trial, mean body weight had decreased 3.6% and 2.5% in the diacylglycerol and triacylglycerol groups, respectively. Fat mass decreased 8.3% and 5.6% in the respective groups. The trial was funded by the Kao Corporation.
A 1-year trial with 312 Japanese subjects (double-blind, placebo-controlled parallel design) investigated long-term effects. The trial enrolled Japanese men (n=174) and women (n=138), aged 22 to 73 years, with BMI ≥25 and/or fasting serum triglyceride ≥150 mg/dL. Participants substituted their usual home cooking oil with the assigned test oils. In the intention-to-treat analysis, body weight decreased significantly in the diacylglycerol group compared to the triacylglycerol group (P=0.013).
A separate study by Yuan et al. (2010) in overweight, hypertriglyceridemic women found that diacylglycerol oil reduces body fat but does not alter energy or lipid metabolism.
Evidence strength: 1,3-DAG oil is believed to have the ability to increase β-oxidation, to enhance body weight loss, to suppress body fat accumulation, and to lower serum triacylglycerol levels postprandially. However, certain animal and human studies indicate positive physiological effects while others report no effect. A significant limitation across multiple positive trials is that most were funded by the Kao Corporation, the primary commercial developer of DAG oil. Overall evidence in this area is considered preliminary to moderately supportive, with a need for more independent replication.
Intake of diacylglycerol has been shown to affect lipid and glucose metabolism. Effects include lowering of plasma triacylglycerol, decreasing postprandial hyperlipidemia and hemoglobin A1c, increasing energy expenditure, and reducing diet-induced obesity compared with triacylglycerol of similar fatty acid composition.
A double-blind controlled study by Taguchi et al. (2000), published in the Journal of the American College of Nutrition, examined effects on postprandial serum and chylomicron triacylglycerol responses in healthy humans. A 12-week clinical trial in obese individuals found that fasting serum triglyceride levels were significantly reduced in the DAG group compared to baseline, and within-group reductions in triglycerides and low-density lipoprotein (LDL) cholesterol were more pronounced in the DAG group than in the triacylglycerol (TAG) control group (p < 0.05).
In summary, DAG ameliorates fasting and postprandial TG-rich lipoproteins and glucose metabolism, which may be favorable for metabolic disorders observed in the metabolic syndrome.
One study indicated that the substitution of DAG for TAG suppresses the postprandial increase in serum VLDL-C and insulin.
Evidence strength: Multiple short-term human trials (including randomized, double-blind designs) consistently demonstrate reductions in postprandial triglyceridemia compared to isocaloric TAG oil. This is one of the more robustly supported effects, though long-term independent trials are limited.
Several studies have explored DAG oil in populations with type 2 diabetes or dysglycemia. A study published in Diabetes Care (Yamamoto et al., 2006) found that diet therapy with diacylglycerol oil delays the progression of renal failure in type 2 diabetic patients with nephropathy (Diabetes Care, 2006;29(2):417-419). A separate long-term study (Yamamoto et al., 2001), published in the Journal of Nutrition, found that long-term ingestion of dietary diacylglycerol lowers serum triacylglycerol in type II diabetic patients with hypertriglyceridemia.
A single-arm trial in China examined DAG oil in overweight or obese patients with diabetes or prediabetes. Participants used diacylglycerol oil to cook food every day for two months. The investigators concluded that diacylglycerol oil may help to improve glucose and lipid metabolism in overweight and obese patients with abnormally elevated blood glucose levels. However, this was a small-sample clinical trial with no control group, which restricts how broadly the findings may be applied. Further high-quality studies are needed to demonstrate the effects of diacylglycerol oil in humans.
An ongoing multicenter, prospective, double-blind, randomized controlled trial registered as of 2025 is investigating DAG oil in patients with metabolic syndrome and asymptomatic hyperuricemia. A multicenter, double-blind, randomized controlled trial involving 176 patients was designed; all patients with chronic metabolic syndrome complicated by asymptomatic hyperuricemia who meet inclusion criteria will be randomized to either DAG-rich oil (≥80%) or conventional cooking oil (TAG-rich oil) for 12 weeks. Fasting blood glucose, 2-hour postprandial blood glucose, fasting insulin, glycated hemoglobin, lipid profile, and average carotid intima-media thickness will be evaluated as secondary outcomes.
Evidence strength: Human evidence in diabetic populations is limited and frequently small in scale or lacking independent controls. The renal nephropathy finding (Diabetes Care, 2006) is notable but requires independent replication.
Excess adiposity plays a crucial role in the development of metabolic syndrome. The elevated fasting and postprandial triglyceride-rich lipoprotein levels are the central lipid abnormality observed in the metabolic syndrome. Recent studies have indicated that DAG is effective for fasting and postprandial hyperlipidemia and preventing excess adiposity by increasing postprandial energy expenditure.
A Cambridge-published 12-week double-blind randomized controlled parallel-design study enrolled healthy overweight subjects (n=23; BMI 27–35 kg/m², aged 37–67 years) to examine the influence of food items in which part of the TAG oil was replaced with DAG oil combined with high alpha-linolenic acid (ALA) content on metabolic markers. The two groups received 20 g margarine, 11 g mayonnaise, and 12 g oil per day, containing either high ALA and sn-1,3-DAG or high ALA and TAG.
1,3-DAG has a positive effect on cardiometabolic risk; it can reduce body weight, reduce blood lipids, and improve glucose metabolism.
Clinical studies have shown that DAG oil reduces the postprandial increase in serum and chylomicron triacylglycerol levels and prevents accumulation of body fat, especially visceral fat. There is strong evidence on serum lipid profile improvements including increasing high-density lipoprotein (HDL), associated with a decrease in body mass index (BMI).
Evidence strength: Studies demonstrating improvements in cardiometabolic markers are generally supportive, but many are of modest sample size, short duration, and principally funded by the commercial developer. Independent large-scale trials are lacking.
Several human studies have measured energy expenditure after DAG versus TAG meals. DAG-rich oil has been suggested to suppress postprandial hyperlipidemia and promote negative caloric balance by increasing energy expenditure, due to small intestine physiochemical dynamics that differ from TAG. A randomized crossover clinical trial by Yanai et al. (2008) studied the effect of DAG on postprandial glucose/insulin metabolism by loading carbohydrate with oil. To reveal the mechanism for increased energy expenditure by DAG, plasma serotonin was measured; the study used a randomized crossover design with a 2-week wash-out interval, in which seven male lean Japanese students ingested DAG or TAG oil with 40 g of carbohydrate, and measurements were performed before and at 2, 4, and 6 hours after fat ingestion.
Evidence strength: Changes in postprandial energy expenditure and respiratory quotient are supported by multiple short-term human studies; however, effect sizes are modest and longer-term thermogenic effects have not been well established.
A relatively recent area of investigation involves the effect of DAG oil on uric acid levels. The aim of an ongoing study is to evaluate the efficacy and safety of DAG edible oil intervention in patients with chronic metabolic syndrome complicated by asymptomatic hyperuricemia. A 2024 lipidomics and metabolomics investigation also examined the effect of DAG dietary intervention on hyperuricemia in athletes (published in the Journal of Lipid Research).
Evidence strength: Very preliminary; clinical data in this indication are largely limited to a single ongoing trial and early-stage metabolomics research as of 2025.
DAG oil has been used in clinical trials as a replacement for usual consumption of cooking oil, as well as at a variety of fixed daily dosages. Fixed daily dosages in clinical trials have ranged from 10 g per 60 kg body weight to 0.5 g/kg body weight.
In the Nagao et al. (2000) study, test oils of 10 g/day were included in bread, mayonnaise, or shortbread. In the high-dose safety trial by Yasunaga et al. (2004), moderately lean men (n=42) and women (n=39) consumed either DAG or TAG at a dose of approximately 0.5 g/kg body weight/day as part of their diet for 12 weeks.
Sources reporting clinical dosage summaries note that DAG has most often been used by adults in doses of 10–20 grams by mouth daily for up to 1 year. A broader dosage range reported specifically for weight loss and body fat reduction is: 10 to 45 grams of diacylglycerol per day in foods in place of other fats; generally, each serving contains 8 to 9 grams of diacylglycerol oil, used in place of other dietary fats, in 2 to 5 servings per day.
Dosage forms encountered in clinical research include:
A comprehensive 2008 review of the published safety literature found that feeding rats with unheated or heated diacylglycerol oil at levels up to 5.5% in the diet for 90 days did not cause any toxic effects. In chronic studies, dietary administration of diacylglycerol oil (up to 5.3%) to rats for 2 years or at 9.5% to Beagle dogs for 1 year had no adverse effects. Genotoxicity studies of unheated and heated diacylglycerol oil did not reveal any genotoxic effects. Carcinogenicity studies in rodents demonstrated that diacylglycerol oil is non-carcinogenic. In a two-generation reproductive and developmental toxicity study, gavage administration of diacylglycerol oil at dose levels of 5.0 mL/kg body weight/day did not reveal any adverse effects.
In several human clinical investigations, administration of diacylglycerol oil at levels up to 0.5 g/kg body weight/day for up to 1 year did not cause adverse effects. All subjects completing the high-dose safety study tolerated the test oils well and showed no overt effects. Total caloric and fat intake remained constant and showed no significant differences between groups. There was no significant difference in the occurrence of clinical signs and physical complaints related to test oil consumption. Although some statistically significant effects were reported in hematological and serum chemistry parameters in both DAG and TAG groups, none of these reported changes were considered biologically significant. Overall, the 12-week clinical study revealed no significant or treatment-related adverse effects of DAG oil consumed at a dose of 0.5 g/kg of body weight/day.
Diacylglycerol oil is "generally recognized as safe" (GRAS) as a food ingredient in the United States (FDA, 2000; 2003) and has been approved by the Japanese Ministry of Health, Labor and Welfare (MHLW) as a "food for specified health use" (MHLW, 1998). During the 1970s, the Joint FAO/WHO Expert Committee on Food Additives (JECFA, 1974) and Federation of American Societies for Experimental Biology (FASEB, 1975) reviewed the safety data of partial mono- and diacylglycerol and concluded that these ingredients present no safety concerns at the intended use levels.
The most significant safety issue to emerge with commercially produced DAG oil relates to process contaminants formed during manufacture. It was later discovered that DAG cooking oil contained glycidyl fatty acid esters. Glycidyl fatty acid esters are process contaminants. They are produced from a deodorization process performed under high-temperature conditions during the production of edible oils. DAG oil was found to contain considerably higher glycidyl fatty acid esters levels compared with other commercial edible oils and was discontinued. Glycidyl fatty acid esters are potential mutagens or carcinogens.
Glycidyl fatty acid esters are broken down in the body and glycidol is released. This substance is considered carcinogenic and mutagenic (EFSA, 2016; JECFA, 2017). Intake via food should therefore be minimised.
According to EFSA, glycidyl fatty acid esters are formed from diacylglycerol (DAG) when vegetable oils are heated to temperatures above 200°C. Palm oil contains high levels of DAG (4–12%), therefore more glycidyl fatty acid esters are formed.
Glycidyl esters of fatty acids are hydrolysed in the gastrointestinal tract to produce free glycidol, which is classified as probably carcinogenic to humans (Group 2A) by the IARC (2000) and as a carcinogenic and genotoxic compound by the EFSA CONTAM Panel (EFSA CONTAM Panel, 2016).
According to the 2016 EFSA Scientific Opinion, which conducted an exposure assessment of these process contaminants, there is cause for potential health concern for infants, toddlers, and children: these younger age groups ingest the greatest amount of these substances on average, relative to their body weight.
Partial glycerol products such as monoglycerides and diacylglycerol in hydrolyzed products can form harmful substances, such as glycidyl esters and chloropropanol esters, when subjected to high temperature treatment. As a result, diacylglycerol oils prepared through high-temperature hydrolysis methods often have a high content of harmful substances. Enzymatic preparation of diacylglycerol has several advantages, including mild reaction conditions and low content of harmful substances.
Contraindications have not yet been identified. Information regarding safety and efficacy in pregnancy and lactation is lacking. Experiments in rats have shown no adverse fetal/embryonic effects. In rats, the effects of dietary alpha-linolenic acid-enriched diacylglycerol oil on embryofetal development at 5 mL/kg (4,715 mg/kg/day) — the highest dose tested — had a no-observed-adverse-effect level (NOAEL) for both maternal and developmental toxicity.
No drug interactions are well documented. Clinical trials have reported few or no adverse effects.
Fat-soluble vitamin absorption has been examined; one study (Watanabe et al., 2001) specifically assessed whether DAG consumption altered fat-soluble vitamin status and found that fat-soluble vitamin status was not affected by diacylglycerol consumption.
The safety of DAG cooking oil is inconclusive. While early preclinical and clinical data were reassuring, the discovery of elevated glycidyl fatty acid esters in commercially produced DAG oil — principally arising from the high-temperature deodorization step used in manufacturing — led to the withdrawal of the primary commercial product. The use of lipase in the preparation of diacylglycerol oil has gained popularity as an alternative approach precisely because enzymatic production avoids the high-temperature steps that generate these contaminants. Newer generation DAG oils produced via lower-temperature enzymatic routes may present a different safety profile, but rigorous long-term human data on these newer preparations remain sparse.
Health conditions that Diacylglycerol may help support.
Body systems that Diacylglycerol may help support.
Go back