IngredientsA diglyceride, or diacylglycerol (DAG), is a glyceride consisting of two fatty acid chains covalently bonded to a glycerol molecule through ester linkages. More precisely, diglycerides are esters of the trihydric alcohol glycerol in which two of the hydroxyl groups are esterified with long-chain fatty acids. The formal IUPAC-accepted chemical name is diacylglycerol, though the older term diglyceride remains widely used in food science, nutrition labeling, and regulatory contexts.
Two possible forms exist: 1,2-diacylglycerols and 1,3-diacylglycerols. When the stereochemistry is unknown or when the mixture is racemic, sn-1,2- and 2,3-diacylglycerols are sometimes termed α,β-diacylglycerols, while sn-1,3-diacylglycerols may be designated α,α′-diacylglycerols. These two positional isomers differ meaningfully in their metabolic behavior and biological effects, which is central to understanding the health literature on DAG-enriched oils.
Since diacylglycerol is synthesized via phosphatidic acid, it will usually contain a saturated fatty acid at the C-1 position on the glycerol moiety and an unsaturated fatty acid at the C-2 position. Diacylglycerol can have many different combinations of fatty acids attached at the C-1 and C-2 positions.
Diglycerides are natural components of food fats, though minor in comparison to triglycerides. Diacylglycerol (DAG) is a natural component (2–10%) of edible fats and oils from various sources that have been consumed for many years. DAG naturally occurs in smaller amounts within dietary oils and fats and can also be commercially synthesized by enzyme-catalyzed esterification of glycerol with fatty acids from oils such as canola, soybean, corn, olive, and cottonseed.
Diacylglycerols are formed in animal and plant tissues as intermediates in the biosynthesis of triacylglycerols and other glycerolipids, and during the hydrolysis of these by lipases. They are seldom found in natural fats except as the products of partial hydrolysis of triglycerides, but are easily prepared synthetically and have important applications mainly because of their ability to function as emulsifiers.
The commercial source of mono- and diacylglycerols may be either animal (cow- or hog-derived) or vegetable, derived primarily from soybean and canola oil, or they may also be synthetically produced. Commercial production of DAG oil results from the enzymatic esterification of fatty acids from natural edible plant oils. Commercially produced vegetable-derived DAG oil contains more than 80% DAG, less than 20% TAG, less than 5% monoacylglycerols, and small amounts of emulsifiers and antioxidants to maintain quality.
Many researchers have focused on the enzymatic production of DAG by esterification, glycerolysis, and partial hydrolysis of oils and fats because of the beneficial advantages of employing enzymes, including mild reaction conditions, high regioselectivity, and high catalysis efficiency. Enzymatic synthesis of DAG is widely employed for its environmentally friendly processes, higher yield, and mild conditions; DAG can be produced through esterification, glycerolysis, partial hydrolysis, and related approaches.
As a food additive, diglycerides — in combination with monoglycerides — are designated E 471 in the European Union. Mono- and diacylglycerols are common food additives used to blend together certain ingredients, such as oil and water, which would not otherwise blend well. They are often found in bakery products, beverages, ice cream, chewing gum, shortening, whipped toppings, margarine, and confections.
DAG has not historically been isolated and used as a standalone traditional remedy in any documented ethnopharmacological tradition. Its role in the historical human diet is as an endogenous minor lipid component naturally present in all plant and animal fats. Diacylglycerol is a natural component (2–10%) of edible fats and oils from various sources that have been consumed for many years.
The targeted use of DAG as a functional dietary ingredient is entirely modern in origin. DAG oil was developed in Japan and launched in February 1999 by Kao Corporation as Healthy Econa cooking oil, and is now widely used for cooking and salad oil in Japan. Kao Corporation subsequently introduced DAG in other products, such as mayonnaise, margarine, and canned tuna. In 1998, the Japanese Ministry of Health, Labour and Welfare (MHLW) approved the use of DAG as a "food for specified health use" (FOSHU), and in 2000 the US Food and Drug Administration (FDA) classified DAG as a food ingredient that is generally recognized as safe (GRAS).
In 2000, the Food and Drug Administration (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 for use in home cooking and vegetable oil spreads.
DAG operates on two distinct levels: as a dietary lipid with metabolic consequences, and as an endogenous intracellular second messenger in cell signaling.
In biochemical signaling, diacylglycerol functions as a second messenger signaling lipid and is a product of the hydrolysis of the phospholipid phosphatidylinositol 4,5-bisphosphate (PIP2) by the enzyme phospholipase C (PLC), a membrane-bound enzyme that, through the same reaction, produces inositol trisphosphate (IP3). Although inositol trisphosphate diffuses into the cytosol, diacylglycerol remains within the plasma membrane, due to its hydrophobic properties.
There is now much evidence to suggest that protein kinase C (PKC) acts as a transducer element in cell-signaling processes following stimulation of membrane receptors linked to phospholipase(s)-C (PLC). Occupancy of such receptors by specific agonists — hormones, neurotransmitters, and growth factors — promotes hydrolysis by PLC of the membrane phospholipid phosphatidylinositol 4,5-bisphosphate to yield the second messengers inositol 1,4,5-trisphosphate (IP3) and 1,2-sn-diacylglycerol (DAG).
Being lipid-soluble, DAG remains in the plasma membrane where it is available to activate PKC, which translocates from the cytoplasm to the cell membrane following cell stimulation. The conformational change to specific intracellular proteins brought about through phosphorylation by PKC is an early event in a cascade of biochemical reactions that either propagate or abrogate the initial signal, leading to a variety of cellular responses.
PKC enzymes are activated by signals such as increases in the concentration of diacylglycerol (DAG) or calcium ions (Ca²⁺), and hence play important roles in several signal transduction cascades; the PKC family consists of fifteen isozymes in humans. Protein kinase Cs (PKCs) define a central DAG-sensing node in intracellular phosphoinositide signaling pathways that regulate cell growth, differentiation, apoptosis, and motility.
IP3 stimulates the release of calcium ions from the smooth endoplasmic reticulum, whereas DAG is still membrane-associated and activates protein kinase C (PKC); however, for DAG to activate PKC, there needs to be a cytosolic increase in calcium ions, which is accomplished by IP3.
Diacylglycerol kinases (DGKs) metabolize DAG by phosphorylating it to generate phosphatidic acid (PA). DAG kinase terminates DAG signaling by converting it to phosphatidic acid.
The metabolic significance of dietary DAG — particularly the 1,3-isomer produced in commercial DAG oil — rests on how it is processed differently from triacylglycerol (TAG).
Dietary fat is mainly composed of triglycerides. Because triglycerides cannot be absorbed by the digestive system, triglycerides must first be enzymatically digested into monoacylglycerol, diacylglycerol, or free fatty acids. Diacylglycerol is a precursor to triacylglycerol (triglyceride), which is formed by the addition of a third fatty acid to the diacylglycerol under the catalysis of diglyceride acyltransferase.
DAG, especially 1,3-DAG, is hydrolyzed to 1(3)-MAG (monoacylglycerol) after digestion, which is not efficiently hydrolyzed again and reassembled as TAG; hence, the consumption of DAG oil is less likely to result in fat storage in adipose tissue and the body.
DAG oil consumption leads to increased β-oxidation and decreased fatty acid synthesis, resulting in reduced postprandial TAG levels in the bloodstream. The physiological effect of DAG is believed to be attributed to its metabolic pathway, which is different from triacylglycerol (TAG) metabolism.
In humans, dietary DAG is more susceptible to oxidation; in animals, 1,3-DAG, a major component of DAG oil, is rapidly oxidized. Short-term human studies with indirect calorimetry demonstrate greater fat oxidation with DAG oil consumption compared with triacylglycerol (TAG) oil consumption.
Phosphatidic acid (PA) is dephosphorylated by lipin 1 to form diacylglycerol (DAG), which is then esterified with another acyl-CoA molecule to form triglyceride (TG) by acyl-CoA:diacylglycerol acyltransferase (DGAT). This makes DAG the immediate biosynthetic precursor to triglycerides in both liver and adipose tissue, placing it at a critical metabolic branch point: DAG can proceed toward triglyceride storage or toward β-oxidation, depending on enzymatic context.
Studies in animals and humans indicate that diets containing diacylglycerol (DAG) oil (containing more than 80% DAG) decrease body weight gain and body fat accumulation, especially visceral fat.
Animal data are more consistently positive than human data. Murase et al. showed that body weight decreased by 70% on a 30% high DAG oil diet (63% 1,3-DAG) compared with a high TAG oil diet in mice after 5 months, with this lower weight corresponding to a reduction in visceral fat weight of 73% in the epididymal depot.
In humans, a 2022 meta-analysis of randomized controlled trials (RCTs) provided a quantitative synthesis. In the overall analysis, intake of DAG oil can significantly reduce body weight (BW), body mass index (BMI), and waist circumference (WC) in healthy people, and serum triacylglycerol (TAG) in people with diseases related to glucose and lipid metabolism, but has no significant effect on blood glucose (BG). Meta-regression analysis based on duration of intervention was significant for BW, BMI, and WC: the longer the intake of DAG oil, the better the weight loss effect.
Individual trials, however, show inconsistent results. One crossover trial in 26 overweight women consuming 40 g/d of either DAG or control oil for 28 days in a randomized crossover design found that relative to control oil, DAG oil did not alter endpoint postprandial energy expenditure, fat oxidation, serum lipid profiles, or hepatic lipogenesis; however, DAG oil consumption reduced accumulation of body fat within trunk, android, and gynoid regions at the endpoint compared with control oil.
A 2025 randomized, double-blind, placebo-controlled trial found that over 100 healthy volunteers were recruited, most of whom (85.8%) were overweight or obese, and were provided DAG or triacylglycerol (TAG) oil as part of specific dietary interventions for 8 weeks. Significant decreases in waist circumference, hip circumference, serum triacylglycerol, total cholesterol, and small dense LDL cholesterol levels were observed in the DAG intervention group, and total body fat and visceral fat area (VFA), especially liver fat, also significantly improved.
A 12-week clinical study 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 LDL cholesterol were more pronounced in the DAG group than in the TAG control group.
Evidence strength: Moderate. Several RCTs and at least one meta-analysis support modest but statistically significant reductions in body weight, BMI, waist circumference, and visceral fat with prolonged DAG oil consumption. Clinical studies show inconsistent results regarding DAG oil's impact on serum TAG levels and body weight. Many trials were conducted or sponsored by the commercial developer of DAG oil (Kao Corporation), which represents a notable limitation in the evidence base. Effect sizes appear modest and dependent on duration.
The most consistently demonstrated clinical effect of DAG oil is a reduction in postprandial (after-meal) elevations of serum triglycerides and remnant lipoprotein cholesterol.
A landmark double-blind, randomized, crossover trial in 43 healthy Japanese men and women tested the acute effect of a single meal. In a double-blind, randomized, crossover design, 43 healthy Japanese men and women ingested test meals containing 10 g of DAG oil or TAG oil. Blood samples were collected in a fasting state and at 2, 3, 4, and 6 h after ingestion. Postprandial TAG, remnant-like particle cholesterol (RLP-C), and chylomicron TAG concentrations were significantly lower after the DAG meal compared with the TAG meal.
In subjects with impaired glucose tolerance (IGT), serum concentrations of TG, RLP-TG, and RLP-cholesterol increased throughout a 4-hour study period following an oral fat tolerance test; however, the responses above baseline after the DAG load were significantly smaller than those after the TAG load (p<0.05).
A study in 41 individuals with high fasting triglyceride concentrations using a randomized, double-blind, crossover design found that postprandial TAG concentrations were significantly lower after the DAG meal compared with the TAG meal.
In postprandial studies, serum triglycerides and remnant-like particle cholesterol concentrations have shown to be lower following ingestion of DAG-enriched oil compared to conventional dietary oil, and DAG oil appears to be effective for preventing postprandial hyperlipidemia, which is a risk factor for arteriosclerosis.
In a mouse model of diabetes, diets containing 1,3-DAG-rich oil or TAG oil were administered to diabetic apoE-deficient mice for 20 weeks. In diabetic apoE-deficient mice, 1,3-DAG reduced the extent of atherosclerotic lesions in the aortic arch and thoracic aorta by 37% and 44%, respectively, compared to TAG, and plasma total cholesterol and triglyceride levels were significantly lower in the 1,3-DAG-fed group. This remains animal-only evidence for the atherosclerosis endpoint.
Evidence strength: Moderate to good for the acute postprandial triglyceride-lowering effect in humans; this is one of the most replicated findings in the DAG literature. Long-term cardiovascular endpoint data in humans are absent.
The effects of DAG on glycemic endpoints are less clear and more contested than its lipid effects.
In comparison to TAG oil, DAG oil resulted in considerably lower postprandial concentrations of insulin and glucose-dependent insulinotropic polypeptide. However, some studies showed that DAG oil was unable to enhance glucose metabolism in diabetes or overweight diabetics.
One small study of lean Japanese subjects found that substitution of DAG for TAG decreased VLDL-cholesterol by 45.6% at 2 hours, and decreased serum insulin by 41.3% at 4 hours after ingestion; the incremental area under the curve for VLDL-C was positively correlated with the incremental area under the curve for insulin; and DAG elevated plasma serotonin levels by 47.3% at 2 hours, while TAG did not influence serotonin.
A five-week diet enriched in 1,3-DAG in subjects with insulin resistance found that there had been no previously published studies of the potential effects of DAG on postprandial glucose or insulin, and that 5 weeks of a diet enriched in 1,3-DAG had no effects on fasting or postprandial measures of lipid or glucose metabolism in a group of subjects with insulin resistance.
A meta-analysis conducted in 2008 by Xu et al. revealed that DAG oil reduced body weight in both diabetic and healthy individuals, and that the effect was dose-correlated. A subsequent meta-analysis found that DAG intake decreased insulin and fasting blood glucose levels, and that the length of the intervention had a substantial impact on blood glucose levels.
Evidence strength: Weak to preliminary for glucose metabolism endpoints. Findings across trials are heterogeneous, with some showing benefit and others showing no effect. The serotonin-raising effect noted in one study requires replication.
In a high-fat diet-induced obese mouse model, DAG significantly lowered serum total cholesterol, LDL levels, and visceral fat weight, attenuated hepatic steatosis, and altered hepatic lipid distribution. Lipidomic profiling revealed that DAG markedly downregulated hepatic triglycerides, ceramides, and monoacylglycerols, while normalizing sterol lipid levels.
A 2025 human trial found that total body fat and visceral fat area, especially liver fat, significantly improved in the DAG intervention group; serum lipidomics suggested that the DAG intervention improved fat accumulation in visceral tissues, especially in the liver, by regulating adipocyte lipolysis and thermogenesis.
Evidence strength: Preliminary in humans; better supported in animal models. The hepatic steatosis data from the human trial cited above requires confirmation in larger studies specifically designed with hepatic endpoints as primary outcomes.
DAG oil consumption for 14 days has been reported to stimulate energy expenditure. Based on these reports, enhanced fat oxidation and energy expenditure by daily DAG oil intake could contribute to long-term reductions in body weight and fat accumulation. The literature provides support for the notion that dietary DAG is more rapidly oxidized than dietary TAG, and that DAG oil consumption increases whole-body fat oxidation, compared with TAG oil. The effects of DAG oil consumption on energy expenditure, however, remain inconclusive.
Diacylglycerol is a natural component of edible oils with metabolic characteristics distinct from those of triacylglycerol (TAG). Consumption of DAG oil (containing more than 80% DAG) induces greater fat oxidation than consumption of TAG oil, and the enhanced fat metabolism in overweight subjects who consumed DAG oil partly explains the greater loss of body weight and body fat related to DAG oil consumption in weight-loss studies.
One study also demonstrates that DAG ingestion increases plasma serotonin, proposing a possible mechanism for a postprandial increase in energy expenditure by DAG.
Evidence strength: Moderate for acute increases in fat oxidation; energy expenditure effects remain inconclusive. No large, long-term human study has definitively established sustained thermogenic benefits.
The primary dosage form studied in clinical research is DAG-enriched cooking oil, typically containing more than 80% diacylglycerol and used as a direct substitute for conventional triglyceride-based oils.
No standardized pharmacopeial monograph dosage or official dietary supplement recommended daily intake has been established by a regulatory authority for DAG as an isolated supplement. All clinical dosages in the literature reflect use as a dietary oil substitute rather than as a concentrated supplement.
The EFSA Panel on Food Additives and Nutrient Sources added to Food (ANS) evaluated the safety of mono- and di-glycerides of fatty acids (E 471). The Panel considered that it is very likely that hydrolysis of mono- and di-glycerides of fatty acids by lipases in the gastrointestinal tract would occur, resulting in the release of glycerol and fatty acids. Glycerol and fatty acids were re-evaluated and the Panel concluded that there was no safety concern regarding their use as food additives.
Toxicological studies with mono- and di-glycerides rich in unsaturated fatty acids were considered for the re-evaluation of E 471. No evidence for adverse effects was reported in short-term, subchronic studies, chronic, reproductive and developmental toxicity studies. Neither carcinogenic potential nor a promotion effect in initiation/promotion was reported.
Overall, a 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 as part of the diet. 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.
In rats, only traces of cottonseed oil monoglycerides were found in faeces, indicating that after hydrolysis, the components were well absorbed (97.8 ± 0.4%). In another study, the absorption of hydrolysis products from diglycerides of fatty acids was calculated to be 58.8 ± 14.3%.
A significant and documented safety concern arose with commercial DAG oil regarding the presence of glycidyl fatty acid esters as processing contaminants.
According to the EFSA Panel on Contaminants in the Food Chain (CONTAM), refined vegetable oil — which can be used for manufacturing of mono- and di-glycerides of fatty acids (E 471) — is the only identified source of glycidyl esters of fatty acids. Glycidyl esters of fatty acids are hydrolyzed in the gastrointestinal tract to produce free glycidol, which is classified as probably carcinogenic to humans (Group 2A) by IARC and as a carcinogenic and genotoxic compound by the EFSA CONTAM Panel. The Panel noted that there is no limit for glycidyl esters in the specifications for mono- and di-glycerides of fatty acids (E 471), and considered that their possible presence would need further assessment as their presence could raise a safety concern.
In September 2009, Kao Corporation, the producer of Econa Cooking Oil, voluntarily suspended sales of all their DAG oil products in Japan as well as shipment of their products following concerns raised by European researchers about the glycidyl ester content. In its press release announcing the temporary suspension of Econa products, Kao cited questions raised by European researchers on the uncertain health effects of fatty acid glycidyl esters, noting that these are introduced as a by-product of the deodorization process; Kao maintained that the main ingredient DAG is proven safe and planned to resume sales after reducing the amount of fatty acid glycidyl esters in its production method.
The German Federal Institute for Risk Assessment (BfR) concluded that current levels of exposure of infants and some adults could present a hazard to human health from glycidyl esters, and recommended that the levels of glycidyl esters in vegetable oils should be reduced as far as possible.
The UK assessment group recognized the safe history of use of E 471 within the EU and US. EFSA did not consider it appropriate to set a numerical acceptable daily intake (ADI) for the additive E 471, and the use of mono- and di-glycerides of fatty acids was considered to be of low toxicological concern.
The proper regulation of diacylglycerol in cells is critical for proper biological function. Abnormally high or low levels of diacylglycerol are predicted to alter lipid biosynthesis and the activity of enzymes that depend on diacylglycerol, like PKC. PKC enzyme dysfunction has been linked to many human disease pathologies, including cancer, diabetes, and heart disease. These observations pertain to endogenous DAG signaling and are not directly applicable to dietary DAG oil consumption, but they underscore the importance of understanding DAG's systemic roles.
One study referenced in the DAG oil literature assessed fat-soluble vitamin status and found it was not affected by diacylglycerol consumption, though this finding has not been the subject of a dedicated large trial.
One preclinical study examined reproductive and developmental toxicity of DAG oil in rats. DAG oil containing 80% or greater DAG (at a 1,3-:1,2-DAG ratio of 7:3) was approved by regulatory authorities in Japan as a "Food for Specified Health Use" in 1999; similarly, the United States FDA did not object to the GRAS determination and notification on DAG oil. However, formal human data on DAG use during pregnancy are not available in the peer-reviewed literature.
Health conditions that Diglyceride may help support.
Body systems that Diglyceride may help support.
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