Applied nutritional investigationd-Allulose enhances postprandial fat oxidation in healthy humans
Introduction
Obesity is one of the factors affecting most of the prevalent lifestyle-related health complications such as coronary heart disease, diabetes, and certain types of cancer [1]. Obesity results from an imbalance between energy intake and energy expenditure [1]. However, it is difficult to decrease energy intake from foods because advanced food technology has introduced energy-packed or energy-hidden foods to the market. Therefore, an increase in energy expenditure has emerged as an attractive strategy for treating or preventing obesity. To this end, food ingredients to burn energy have been explored.
d-Allulose (previously referred to as d-psicose), a C-3 epimer of d-fructose, has 70% sweetness of sucrose, is rarely found in nature, and therefore is referred to as a rare sugar [2]. d-Allulose is also formed from d-fructose during cooking and is present in a very small amount in various foods such as fruit juices and cola drinks [3]. The d-allulose content per 100 g ranges from 0.5 to 130.6 mg; fruit juice contains 21.5 mg and cola drink 38.3 mg. The daily intake of d-allulose is ∼0.2 g [3]. About 70% of d-allulose is absorbed and then is excreted via urine. The remaining is not fermented in the large intestine and is excreted into feces [4]. Furthermore, d-allulose is a noncaloric sweetener [5] and has been approved as a Generally Recognized as Safe ingredient by the Food and Drug Administration in 2014.
Studies showed that d-allulose is a potential antidiabetic and antiobese sweetener; 0.2 g/kg of d-allulose decreases absorption of sugar by inhibiting intestinal α-glucosidase in Wistar rats compared with nontreated animals [6]. Intake of 0.2 g/kg of d-allulose activates the translocation of glucokinase from the nucleus to the cytosol in the liver that facilitates glycogen biosynthesis in Wistar and Goto-Kakizaki (type 2 diabetes mellitus [T2DM] model) rats [7]. In healthy humans, a single ingestion of 5 g of d-allulose improves insulin sensitivity after administering maltodextrin [8]. Feeding the 5% d-allulose solution enhances insulin sensitivity in T2DM model Otsuka Long-Evans Tokushima Fatty rats compared with only water [9]. Furthermore, d-allulose decreases body weight and abdominal adipose tissue weight in animal studies [10], [11], [12], [13]. The proposed underlying mechanism of d-allulose–induced antiobese action is that it suppresses the activity of hepatic lipogenic enzymes such as fatty acid synthase (FAS) and glucose-6-phosphate dehydrogenase [10], [12], augments the hepatic carnitine palmitoyltransferase activity essential for fatty acid oxidation [13], and increases energy expenditure [12], [13].
However, no studies thus far have been done to see if and how d-allulose modifies energy metabolism in humans. Furthermore, to apply d-allulose to a broad range of diet regimens, clinical studies are imperative. We thus investigated the effects of a single ingestion of d-allulose on postprandial energy metabolism in 13 healthy individuals. We measured short-term (4-h) energy metabolism as d-allulose is metabolized and excreted from the body quickly after ingestion [14] and has an immediate effect on lipid metabolism in rats [13]. To our knowledge, the present study showed for the first time that d-allulose increased fat oxidation and decreased carbohydrate oxidation in healthy humans. This result suggests the possibility that d-allulose may help control healthy body weight, partially via enhanced energy metabolism in humans.
Section snippets
Participants
Thirteen healthy volunteers (five men and eight women) were recruited. Participants were excluded if they were diagnosed with diabetes or metabolic disorders such as cardiovascular diseases. Individuals with a mean age of 35.7 ± 2.1 y and body mass index (BMI) of 20.9 ± 0.7 kg/m2 participated in the study. This study was conducted according to the principles of the Declaration of Helsinki and approved by the Ethics Committee of Matsutani Chemical Industry Co., Ltd. (Hyogo, Japan). Written
Energy metabolic parameters
No significant difference in REE between the two groups was demonstrated (Fig. 1A). However, ingesting d-allulose caused a significant increase in FEE at 90 min compared with the control group (Fig. 1C). CEE and RQ were significantly lower in the d-allulose group than in the control group; CEE at 90, 210, and 240 min (Fig. 1B), and RQ at 240 min (Fig. 1D) were lower. The AUC of REE, CEE, and FEE for 4 h after a meal are summarized in Figure 1E. The AUC of FEE was significantly increased
Discussion
In previous animal studies, d-allulose decreased body weight and abdominal adipose tissue weight [10], [11], [12], [13], suggesting that the 3% to 5% d-allulose diets may have antiobese action. The proposed mechanism of d-allulose–induced antiobese action is that d-allulose suppresses hepatic lipogenesis [10], [12] and augments hepatic fatty acid oxidation, resulting in enhanced energy expenditure [13]. In partial agreement with previous animal studies [13], the present study demonstrated that
Conclusion
At a low dose, d-allulose enhanced postprandial fat oxidation and decreased carbohydrate oxidation in healthy humans. This indicates that d-allulose has the potential to be an antiobese sweetener in humans. Further studies in humans are needed to confirm these effects using a large number of individuals with various diseases such as diabetes and obesity and feeding d-allulose over a long-term period.
Acknowledgments
The authors acknowledge the volunteers who participated in this study.
References (26)
- et al.
Rare sugar D-allulose: potential role and therapeutic monitoring in maintaining obesity and type 2 diabetes mellitus
Pharmacol Ther
(2015) - et al.
Failure of D-psicose absorbed in the small intestine to metabolize into energy and its low large intestinal fermentability in humans
Metabolism
(2010) - et al.
The glycemic index: methodology and clinical implications
Am J Clin Nutr
(1991) - et al.
In vivo regulation of lipolysis in humans
J Lipid Res
(1994) - et al.
Role of the liver in the control of carbohydrate and lipid homeostasis
Diabetes Metab
(2004) - et al.
Enhancing hepatic glycolysis reduces obesity: differential effects on lipogenesis depend on site of glycolytic modulation
Cell Metab
(2005) - et al.
Hepatic glucokinase modulates obesity predisposition by regulating BAT thermogenesis via neural signals
Cell Metab
(2012) - et al.
A metabolomics approach to the identification of biomarkers of sugar-sweetened beverage intake
Am J Clin Nutr
(2015) - et al.
Obesity therapy: altering the energy intake-and-expenditure balance sheet
Nat Rev Drug Discov
(2002) - et al.
Psicose contents in various food products and its origin
Food Sci Technol Res
(2006)
D-psicose is a rare sugar that provides no energy to growing rats
J Nutr Sci Vitaminol
D-psicose inhibits intestinal α-glucosidase and suppresses glycemic response after carbohydrate ingestion in rats
Tech Bull Fac Agr Kagawa Univ
Suppression of blood glucose levels by D-psicose in glucose tolerance test in diabetic rats
Jpn Pharmacol Ther
Cited by (38)
An improved gravimetric method with anti-solvent addition to measure the solubility of D-allulose in water
2023, Journal of Food EngineeringEffect of fructose and its epimers on postprandial carbohydrate metabolism: A systematic review and meta-analysis
2020, Clinical NutritionCitation Excerpt :The remaining 37 reports were retrieved in full, of which 23 were excluded. The final analysis consisted of 14 reports [68–81], including a total of 40 trial comparisons in 400 participants. No trials were identified assessing the effect of small doses of sorbose.
This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. The authors have no conflicts of interest to declare and have nothing to disclose.