30+
Years of Research
7
Peer-Reviewed Sources
3
Key Enzymes Identified
106
ATP Per Fat Molecule
Peer-Reviewed Sources Evidence-Based 7 Citations

The Science Behind Allulose

How Rare Sugar Activates Your Fat-Burning Enzymes: CPT1, CPT2, and Beta-Oxidation Pathways

Published January 2, 2025
12 min read
Jaca Rare Sugar Research Division
  • 1 Allulose activates CPT1, CPT2, and beta-oxidase—the three critical enzymes in mitochondrial fat burning
  • 2 Unlike artificial sweeteners, allulose is metabolically active—it promotes fat oxidation rather than just passing through
  • 3 Allulose increases UCP1 and GLP-1—enhancing thermogenesis and satiety through proven hormonal pathways
  • 4 Dual mechanism: allulose simultaneously blocks fat-creating enzymes while activating fat-burning enzymes
Official FDA Statement
U.S. Food & Drug Administration

"The latest data suggests that Allulose is different from other sugars in that it is not metabolized by the human body in the same way as table sugar. Allulose has fewer calories, produces only negligible increases in blood glucose or insulin levels, and does not promote dental decay. As such, we've issued guidance today stating that we intend to exercise enforcement discretion to allow Allulose to be excluded from the total and added sugars declarations on the Nutrition Facts and Supplement Facts labels when Allulose is used as an ingredient."

Susan Mayne, Ph.D.
Director, FDA Center for Food Safety and Applied Nutrition
FDA Full Guidance
Section I

What Makes Allulose Different from Other Sweeteners

D-Allulose (also known as D-psicose) is a rare monosaccharide that occurs naturally in small quantities in foods like figs, raisins, and wheat. While it provides approximately 70% of the sweetness of regular sugar, allulose delivers less than 0.4 calories per gram because of its unique molecular structure.

Unlike artificial sweeteners that simply pass through your system or sugar alcohols that can cause digestive distress, allulose actively participates in metabolic processes that promote fat oxidation.

Molecular Distinction

The molecular formula of allulose (C₆H₁₂O₆) is identical to fructose, but the spatial arrangement of atoms differs at the C-3 carbon position. This seemingly minor structural difference creates profound metabolic consequences. While fructose promotes fat storage, allulose has been shown in clinical research to enhance fat breakdown through multiple enzymatic pathways.

Jaca Sugar provides 100% pure allulose without any additives, preservatives, or fillers—ensuring you receive the full metabolic benefits that research has demonstrated.

106
ATP molecules produced per fat molecule via beta-oxidation
(compared to just 36 ATP from glucose)
Section II

The Mitochondrial Fat-Burning Pathway

To understand how allulose promotes fat burning, we must first understand the fundamental process of mitochondrial fatty acid oxidation. Your mitochondria—the powerhouses of your cells—are where body fat is converted into usable energy through a carefully orchestrated biochemical process.

Enzyme 01
CPT1 — Carnitine Palmitoyltransferase 1

The Gatekeeper of Fat Burning. CPT1 is located on the outer mitochondrial membrane and serves as the rate-limiting enzyme in fatty acid oxidation. This means CPT1 controls how fast your body can burn fat for energy.

CPT1 catalyzes the first step of the carnitine shuttle: converting long-chain fatty acyl-CoA into acylcarnitine. This conversion is essential because long-chain fatty acids cannot cross the inner mitochondrial membrane without first being attached to carnitine.

→ Allulose enhances CPT1 activity, "opening the gate" for more fat to be burned.

Enzyme 02
CPT2 — Carnitine Palmitoyltransferase 2

Completing the Carnitine Shuttle. CPT2 resides on the inner face of the inner mitochondrial membrane and performs the reverse reaction of CPT1. Once acylcarnitine crosses into the mitochondrial matrix, CPT2 converts it back to acyl-CoA.

The coordinated action of CPT1 and CPT2, along with the carnitine/acylcarnitine translocase (CACT), forms the "carnitine shuttle system"—the essential transport mechanism for getting fatty acids where they need to go for burning.

→ Allulose enhances both CPT1 and CPT2 simultaneously, making the entire transport system more efficient.

Enzyme 03
Beta-Oxidase Enzymes — The Fat-Burning Spiral

Where Fat Actually Burns. Once fatty acids arrive in the mitochondrial matrix as acyl-CoA, they undergo beta-oxidation—a repetitive cycle that cleaves two carbons at a time from the fatty acid chain.

Each cycle produces one molecule of acetyl-CoA (which enters the citric acid cycle for energy production), one NADH, and one FADH₂ (which feed the electron transport chain to generate ATP).

→ Allulose enhances beta-oxidase enzyme activity, increasing the rate at which each cycle of fat breakdown occurs.

Reference: Schreurs M, et al. "Regulatory enzymes of mitochondrial β-oxidation as targets for treatment of the metabolic syndrome." Obesity Reviews. 2010;11(5):380-388. PubMed
Section III

Additional Metabolic Benefits

The fat-burning benefits of allulose extend beyond the carnitine shuttle and beta-oxidation. Research has identified two additional mechanisms that contribute to reduced body fat:

UCP1 & Thermogenesis

Uncoupling Protein 1 (UCP1) is expressed in brown adipose tissue and plays a crucial role in thermogenesis—the generation of heat from energy. Allulose increases UCP1 expression, causing more calories to be burned as heat rather than stored.

Lipogenesis Inhibition

While allulose activates fat-burning enzymes, it simultaneously inhibits fat-creating (lipogenic) enzymes including Fatty Acid Synthase (FAS) and Acetyl-CoA Carboxylase 1 (ACC1).

Reference: "The Metabolic and Endocrine Effects of a 12-Week Allulose-Rich Diet." Nutrients. June 2024. PMC
Section IV

The GLP-1 Connection

One of the most exciting discoveries about allulose is its ability to stimulate the release of GLP-1 (Glucagon-Like Peptide-1)—the same hormone targeted by popular weight management medications.

GLP-1 Effects
  • Enhances insulin secretion in response to glucose
  • Inhibits glucagon release
  • Slows gastric emptying, promoting satiety
  • Acts on brain receptors to reduce appetite

A landmark study published in Nature Communications demonstrated that oral administration of allulose induces GLP-1 release and activates vagal afferent signaling, reducing food intake and promoting glucose tolerance.

Reference: Iwasaki Y, et al. "GLP-1 release and vagal afferent activation mediate the beneficial metabolic and chronotherapeutic effects of D-allulose." Nature Communications. 2018. Nature

Experience the Science with Jaca Sugar

Jaca is 100% pure allulose—the rare sugar born from fruit. No additives, no preservatives, no fillers. Just the pure metabolic benefits that science has revealed.

Shop Jaca Rare Sugar
Section V

Why Jaca is the Premium Choice

Not all allulose products are created equal. Some brands include additives that can diminish the metabolic benefits or cause off-putting tastes and textures. Jaca Sugar stands apart:

  • 100% Pure Allulose – No fillers, no additives, no preservatives
  • Born from Fruit – Derived from natural sources, not synthetic processes
  • Superior Taste – Unlike competitors with stinging or waxy characteristics, Jaca delivers clean sweetness
  • FDA GRAS Status – Generally Recognized As Safe
Conclusion

The Bottom Line

The science is clear: allulose is far more than a simple sugar substitute. Through its activation of CPT1, CPT2, and beta-oxidation enzymes, combined with UCP1 upregulation, lipogenesis inhibition, and GLP-1 stimulation, allulose represents a breakthrough in metabolic nutrition.

For those seeking a sweetener that tastes like sugar, cooks like sugar, and actively supports fat metabolism, Jaca Sugar offers the purest and most effective allulose available. The rare sugar revolution is here—and the science is on your side.

Frequently Asked Questions

What enzymes does allulose activate for fat burning?

Allulose increases the activity of three key fat-burning enzymes: CPT1 (Carnitine palmitoyltransferase 1), CPT2 (Carnitine palmitoyltransferase 2), and beta-oxidase. These enzymes work together in the mitochondria to break down stored body fat into energy.

How does allulose promote fat burning at the cellular level?

Allulose promotes fat burning by enhancing the carnitine shuttle system in mitochondria. It upregulates CPT1 and CPT2 enzymes that transport fatty acids into mitochondria, increases beta-oxidation enzyme activity, boosts UCP1 (uncoupling protein 1) expression, and inhibits lipogenic enzymes like fatty acid synthase.

What is the carnitine shuttle system and how does allulose affect it?

The carnitine shuttle is the mechanism that transports long-chain fatty acids into mitochondria for oxidation. CPT1 on the outer mitochondrial membrane converts fatty acyl-CoA to acylcarnitine, which is then transported inside where CPT2 converts it back for beta-oxidation. Allulose enhances this entire process.

Does allulose block fat storage?

Yes, research shows allulose inhibits key lipogenic (fat-creating) enzymes including fatty acid synthase and acetyl-CoA carboxylase 1 (ACC1). By blocking these enzymes, allulose helps prevent the formation of new fat molecules while simultaneously promoting the burning of existing body fat.

What is UCP1 and how does allulose increase it?

UCP1 (Uncoupling Protein 1) is found in brown adipose tissue and promotes thermogenesis—the process of burning calories as heat. Allulose has been shown to increase UCP1 expression, which enhances energy expenditure and contributes to reduced body fat accumulation.

Why is Jaca the best allulose product for fat metabolism?

Jaca is 100% pure allulose without additives, preservatives, or pollutants that could impact the metabolic benefits. Unlike some competitors that have off-tastes or waxy textures, Jaca delivers pure rare sugar born from fruit, ensuring you get the full fat-burning enzyme activation without compromise.

Scientific References

1. Schreurs M, et al. "Regulatory enzymes of mitochondrial β-oxidation as targets for treatment of the metabolic syndrome." Obesity Reviews. 2010;11(5):380-388. PMID: 19694967
2. Wanders RJ, et al. "The enzymology of mitochondrial fatty acid beta-oxidation and its application to follow-up analysis of positive neonatal screening results." J Inherit Metab Dis. PMC2946543
3. Chen L, et al. "Carnitine palmitoyltransferase 1 facilitates fatty acid oxidation in a non-cell-autonomous manner." Cell Reports. December 2024. PMC11726389
4. "The Metabolic and Endocrine Effects of a 12-Week Allulose-Rich Diet." Nutrients. June 2024. PMC11207032
5. Iwasaki Y, et al. "GLP-1 release and vagal afferent activation mediate the beneficial metabolic and chronotherapeutic effects of D-allulose." Nature Communications. 2018;9(1):113
6. Han Y, et al. "A Preliminary Study for Evaluating the Dose-Dependent Effect of d-Allulose for Fat Mass Reduction in Adult Humans." Nutrients. 2018;10(2):160. PMC5852736
7. Frontiers in Pharmacology. "Mitochondrial CPT1A: Insights into structure, function, and basis for drug development." March 2023.