NJ026-0401

Odd-chain fatty acids in health and disease: metabolic functions, therapeutic potential, and emerging applications

Ji Soo Kim1, Dae Kyeong Kim1, and Somi Kim Cho1,2*

1Interdisciplinary Graduate Program in Advanced Convergence Technology and Science, Jeju National University, Jeju 63243, Republic of Korea. 2Faculty of Biotechnology, College of Applied Life Sciences, SARI, Jeju National University, Jeju 63243, Republic of Korea

Correspondence to: Somi Kim Cho, somikim@jejunu.ac.kr

Received: April 3, 2026; Revised: July 9, 2026; Accepted: July 21, 2026; Published: July 22, 2026

NATPRO J. 2026, 3, 27-35 

https://doi.org/10.23177/NJ026.0401 

Copyright ©  The Asian Society of Natural Products

Abstract

Odd-chain fatty acids (OCFAs), primarily pentadecanoic acid and heptadecanoic acid, have traditionally been regarded as biomarkers of dairy fat intake. However, emerging evidence suggests that OCFAs are influenced not only by dietary sources but also by endogenous metabolism and gut microbiota-derived precursors. Interest in OCFAs has therefore expanded beyond their conventional role as nutritional biomarkers, following accumulating biological, epidemiological, and nutritional observations. Epidemiological studies have consistently reported inverse associations between higher circulating levels of OCFAs and the risk of metabolic diseases, including type 2 diabetes, cardiovascular disease, and non-alcoholic fatty liver disease, although causal relationships remain to be fully established. At the metabolic level, OCFAs exhibit unique features, notably their ability to generate propionyl-CoA and provide anaplerotic input into the tricarboxylic acid cycle, which may support metabolic flexibility. In addition, OCFAs may modulate inflammation, lipid remodeling, mitochondrial function, and potentially regulate epigenetic processes through acyl-CoA-mediated chromatin modifications. Advances in lipidomics, microbiome research, and biotechnology have further expanded interest in OCFAs as bioactive lipids with translational relevance. Moreover, recent developments in precision fermentation and microalgal production systems have enabled scalable OCFA production, facilitating their application in nutraceutical and pharmaceutical contexts. In this review, we summarize current knowledge on OCFA sources and metabolism, their associations with human health and disease, emerging metabolic and mechanistic insights, and recent advances in technological development, patent activity, and market trends.

Keywords

odd-chain fatty acid, pentadecanoic acid, heptadecanoic acid, metabolic functions, therapeutic potential

1. Introduction

Fatty acids are commonly classified according to chain length, degree of saturation, and the number of carbon atoms within the acyl chain [1]. Odd-chain fatty acids (OCFAs) are fatty acids with an odd number of carbon atoms and are present at relatively low concentrations in human tissues and plasma compared with major even-chain fatty acids [2]. Among OCFAs, pentadecanoic acid (C15:0) and heptadecanoic acid (C17:0) are the most widely studied species in human nutrition, metabolism, and disease research [2, 3]. These fatty acids have long been used as biomarkers of dairy fat intake, but their biological significance has historically received less attention beyond this nutritional biomarker role [4].

In recent years, accumulating evidence from epidemiological, lipidomic, and experimental studies has suggested that OCFAs may have biological relevance beyond their conventional role as dietary biomarkers. Interest in OCFAs has further increased as inverse associations have been reported between higher circulating OCFA levels and several metabolic diseases, including type 2 diabetes (T2D), cardiovascular disease (CVD), and non-alcoholic fatty liver disease (NAFLD) [5-7]. Advances in metabolomics and systems biology further support the role of lipid-derived metabolites in cellular regulation [8]. In this context, OCFAs represent a distinct class of fatty acids with unique metabolic properties and potential functional relevance. Emerging evidence also indicates that microbiome-derived metabolites, particularly propionate, contribute to endogenous OCFA metabolism [9]. Collectively, these findings suggest that OCFAs should be considered not only as dietary biomarkers but also as lipid species with potential biological and translational relevance.

In this review, we summarize current knowledge on the sources, metabolism, biological functions, and disease associations of OCFAs, with emphasis on C15:0 and C17:0. We also discuss emerging mechanistic insights and translational developments related to OCFA production and application. By integrating nutritional, metabolic, mechanistic, and translational perspectives, this review aims to provide a balanced overview of OCFAs as both informative biomarkers and potential bioactive lipid mediators.

2. Literature selection strategy

This narrative review was prepared based on literature identified through PubMed and Google Scholar searches. The search included peer-reviewed articles published up to July 2026, with emphasis on studies addressing the metabolism, dietary and endogenous sources, biological functions, disease associations, mechanistic implications, and translational applications of odd-chain fatty acids. The main search terms included “odd-chain fatty acids,” “pentadecanoic acid,” “C15:0,” “heptadecanoic acid,” “C17:0,” “propionyl-CoA,” “anaplerosis,” “gut microbiota,” “type 2 diabetes,” “cardiovascular disease,” “NAFLD,” “inflammation,” “lipidomics,” “epigenetics,” “histone propionylation,” “cancer,” “precision fermentation,” and “microalgae.” Additional relevant articles were identified from the reference lists of selected publications. Because this article is a narrative review rather than a systematic review or meta-analysis, formal risk-of-bias assessment and quantitative evidence synthesis were not performed.

3. Metabolism of odd-chain fatty acids

3.1. Sources of OCFAs

OCFAs originate from dietary, endogenous, and microbial sources. Dairy products and ruminant fats remain the most established dietary contributors, largely because the rumen provides a specialized microbial ecosystem for the formation of odd- and branched-chain fatty acids [3]. During rumen fermentation, dietary carbohydrates are converted into volatile fatty acids, including acetate, propionate, and butyrate [10]. Among these, propionate-derived carbon can contribute to the formation of straight-chain OCFAs such as C15:0 and C17:0 [11]. These microbial fatty acids are incorporated into rumen microbial lipids and subsequently transferred into ruminant milk and meat lipids, explaining why circulating C15:0 and C17:0 have traditionally been used as biomarkers of dairy and ruminant fat intake [3, 12]. Fish and selected plant-derived foods may contain trace amounts of OCFAs, but their contribution to habitual human OCFA exposure is generally smaller than that of dairy and ruminant-derived foods [10]. Gut microbiota ferment dietary fiber and other indigestible carbohydrates to short-chain fatty acids, particularly propionate, which can serve as a precursor for host OCFA synthesis [13]. In addition, host metabolic pathways, including propionyl-CoA–initiated fatty acid synthesis, peroxisomal alpha-oxidation of even-chain fatty acids, elongation, and tissue lipid remodeling, may contribute to circulating and tissue OCFA profiles [14]. Previous studies suggest that C17:0 may be more strongly influenced by endogenous or microbiome-linked pathways than C15:0, whereas C15:0 more consistently reflects dairy and ruminant fat exposure [2]. These observations suggest that circulating OCFAs extend beyond simple dietary markers and should be interpreted as a composite indicator reflecting the interplay among diet, gut microbial metabolism, host fatty acid synthesis, peroxisomal processing, and tissue lipid turnover. 

Beyond natural dietary and endogenous sources, microbial and microalgal biotechnology is emerging as a scalable platform for OCFA production. Recent reviews highlight that OCFAs can be produced from renewable carbon sources through microbial fermentation using mixed cultures or single-strain systems, including bacteria, oleaginous yeasts, and microalgae [15, 16]. In engineered yeasts such as Yarrowia lipolytica, OCFA biosynthesis can be enhanced by increasing propionyl-CoA availability, optimizing the balance between acetyl-CoA and propionyl-CoA, modifying competing metabolic pathways, and controlling fermentation substrates [17]. Microalgal and thraustochytrid systems, such as Schizochytrium limacinum, also serve as promising alternative sources because they can convert volatile fatty acid-rich substrates into lipid products containing both polyunsaturated fatty acids and OCFAs [18]. Ultimately, these microorganisms represent a highly sustainable and controllable source of OCFAs, offering distinct advantages over traditional sources. Together, these sources indicate that OCFAs are not derived from a single dietary origin but arise from interconnected nutritional, microbial, host metabolic, and technological pathways. 

3.2 Unique metabolic characteristics

A defining feature of OCFAs is their distinct metabolic fate. While even-chain fatty acids are fully degraded to acetyl-CoA, β-oxidation of OCFAs generates acetyl-CoA together with a single molecule of propionyl-CoA in the final cycle, owing to their odd-numbered acyl chain (Figure 1) [19]. This terminal propionyl-CoA is the biochemical hallmark that distinguishes OCFA catabolism from that of even-chain fatty acids. Propionyl-CoA is subsequently converted to methylmalonyl-CoA and then to succinyl-CoA, which enters the tricarboxylic acid (TCA) cycle [20]. This conversion is a metabolically important step because propionyl-CoA cannot enter the cycle directly like acetyl-CoA, providing a biochemical basis for the potential contribution of OCFAs to metabolic flexibility [19]. This metabolic routing provides an anaplerotic input into the TCA cycle. Through OCFA-driven anaplerosis, OCFA-derived propionyl-CoA may contribute to replenishment of TCA cycle intermediates under selected metabolic conditions. However, the quantitative contribution of OCFA-derived propionyl-CoA to total TCA cycle flux in humans remains incompletely defined and is likely to vary according to tissue type, nutritional state, microbiome activity, and circulating OCFA availability. Therefore, OCFA-driven anaplerosis should be interpreted as a plausible and biologically relevant metabolic route rather than as a universally established dominant energy pathway. OCFAs can also arise through biosynthetic pathways. In contrast to the conventional fatty acid synthesis pathway, which typically begins with acetyl-CoA and proceeds through two-carbon elongation by malonyl-CoA, OCFA synthesis can be initiated when propionyl-CoA serves as a three-carbon primer [21]. Subsequent elongation by malonyl-CoA units can generate straight-chain OCFAs such as C15:0 and C17:0 [21]. This pathway links gut microbiota-derived propionate, host propionyl-CoA pools, and endogenous OCFA synthesis. Accordingly, circulating OCFA profiles reflect not only dietary intake but also the availability of propionate and propionyl-CoA, the activity of fatty acid synthetic enzymes, and the balance between synthesis, oxidation, and incorporation into complex lipids.

Peroxisomal metabolism provides another route contributing to OCFA formation and remodeling. Peroxisomal α-oxidation can shorten certain even-chain fatty acids by one carbon, thereby generating odd-chain fatty acids; this pathway has been proposed as one mechanism contributing to C17:0 formation from C18:0-derived substrates [22, 23]. In addition, peroxisomes participate in the shortening and remodeling of very-long-chain fatty acids, linking OCFA metabolism to broader lipid homeostatic pathways [24]. These peroxisomal routes are particularly relevant because they provide an endogenous source of OCFAs that is independent of direct dietary intake.

Such products could be positioned as next-generation cosmeceuticals or prescription therapeutics, particularly for patients with antibiotic-resistant acne. Additionally, endolysins may be combined with existing treatments to enhance efficacy while reducing antibiotic dosage [10].

However, several challenges must be addressed for successful product development. These include protein stability under formulation conditions, efficient delivery into the pilosebaceous unit, and maintenance of enzymatic activity on the skin surface [7]. Advances in formulation science, such as encapsulation and nanocarrier systems, may help overcome these limitations [11].

4. OCFAs in health and metabolic regulation

4.1 Type 2 diabetes and insulin resistance (T2D)

Higher circulating levels of OCFAs are consistently associated with a lower risk of T2D across multiple large prospective cohort studies [5, 6]. These findings have contributed to the view that circulating C15:0 and C17:0 may serve as metabolic biomarkers linked to favorable glucose-related outcomes. Lipidomic analyses further demonstrate that OCFA-containing lipid species are inversely associated with diabetes risk, with particularly strong associations observed for C17:0-containing phospholipids and evidence of sex-specific differences [25]. These findings support an inverse association between OCFAs and glucose metabolic health, although the strength and specificity of these associations may vary depending on lipid class and biological context.

Several biological pathways have been proposed to explain how OCFAs might relate to glucose metabolic regulation. First, OCFAs may reflect a lipid profile associated with lower ectopic lipid accumulation and improved lipid partitioning, thereby indirectly relating to insulin sensitivity [19]. Second, OCFA-derived propionyl-CoA can be converted to succinyl-CoA and enter the tricarboxylic acid cycle, providing a potential anaplerotic route that may support mitochondrial substrate flexibility under specific metabolic conditions [19]. Third, experimental studies, particularly those focused on C15:0, suggest possible effects on inflammatory signaling, lipid handling, and cellular stress responses, which are processes closely linked to insulin resistance [25]. Despite these emerging insights, the precise molecular pathways linking OCFAs to glucose homeostasis remain incompletely understood and warrant further mechanistic investigation.

4.2 Cardiovascular disease (CVD)

OCFAs have also been linked to cardiovascular health. Epidemiological studies have reported inverse associations between circulating OCFA levels and the risk of coronary heart disease and cardiovascular mortality [22, 24]. In line with these findings, a prospective dietary study found that higher intake of OCFAs was associated with a significantly reduced risk of cardiometabolic mortality, whereas even-chain saturated fatty acids exhibited opposite patterns [23]. These associations may be mediated by multiple mechanisms, including improvements in lipid profiles, reduction of systemic inflammation, and modulation of endothelial function. Circulating C15:0 and C17:0 have been associated with more favorable lipid-related metabolic profiles in observational cohorts, including lower triglyceride-related and hepatic metabolic markers [26]. In addition, C15:0 has been reported to attenuate dyslipidemia-related phenotypes and to influence pathways involved in lipid metabolism [27], suggesting that OCFAs may indirectly affect cardiovascular risk through these pathways. OCFAs may be linked to cardiovascular risk through modulation of inflammatory pathways [19]. Chronic low-grade inflammation contributes to endothelial dysfunction, atherosclerotic plaque development, and adverse cardiovascular remodeling [28]. Previous studies of C15:0 have reported reductions in inflammatory and fibrotic responses in cell-based and animal models, including changes in cytokine-related and tissue-remodeling phenotypes [19, 27]. These findings suggest that C15:0 may influence inflammatory signaling networks relevant to cardiometabolic disease, although whether similar effects occur at clinically meaningful levels in humans remains to be established.  Collectively, current findings across multiple endpoints suggest a favorable association between OCFAs and cardioprotection; however, direct causality has yet to be established.

4.3 Liver disease and metabolic dysfunction

The role of OCFAs in liver health has gained increasing attention. Studies have shown that higher levels of C15:0 are associated with lower liver fat accumulation and improved hepatic metabolic markers [7]. In addition, lipidomic analyses have revealed that reductions in OCFA-containing phospholipids are associated with mitochondrial dysfunction and non-alcoholic fatty liver disease (NAFLD) progression [8]. In patients with NAFLD, lower circulating levels of C15:0 and C17:0 have been associated with higher NAFLD activity scores and other markers of metabolic dysfunction, suggesting that reduced OCFA levels may accompany more severe hepatic metabolic disturbance [9]. Circulating fatty acid profiles, including OCFAs, have also been linked to liver fibrosis and disease severity [29]. These findings suggest that circulating OCFAs may reflect hepatic metabolic status and disease severity, rather than proving direct protection against liver disease. Preclinical models have suggested that C15:0 supplementation can ameliorate features of liver injury and fibrosis and improve lipid-related abnormalities, although direct causal evidence in humans remains limited [6]. Taken together, these observations suggest that OCFAs may contribute to hepatic metabolic homeostasis across the spectrum from steatosis to fibrosis, and raise the possibility that individual OCFAs, particularly C15:0, may represent both biomarkers of liver disease severity and candidates for therapeutic intervention. To consolidate the reported associations between circulating OCFAs and metabolic disease-related outcomes, the major findings, proposed implications, and key limitations are summarized in Table 1.

5. Functional properties of OCFAs

5.1 Anti-inflammatory and metabolic effects 

Experimental studies have begun to elucidate the functional roles of OCFAs. C15:0, in particular, has been proposed to exert anti-inflammatory and metabolic regulatory effects [6, 27]. C15:0 acts as a PPAR agonist in reporter-based Chinese hamster ovary cell assays, and anti-inflammatory phenotypic profiling in primary human cell systems shows decreased MCP-1, PAI-1, IL-6, and TNF-α [6]. The in vivo component of the same study further suggested that orally administered C15:0 may attenuate several disease-related phenotypes in nonalcoholic steatohepatitis models [6]. Furthermore, functional testing in the methionine- and choline-deficient diet (MCD) mouse model showed that supplementation with C15:0 reduced serum aspartate aminotransferase levels and hepatic infiltration of ceroid-laden macrophages compared with the MCD diet alone [9]. C17:0 suppresses inflammatory JAK/STAT3 signaling in primary hepatocytes, and these findings suggest that attenuation of hepatic inflammatory signaling may be a shared property of both C15:0 and C17:0 under at least some experimental conditions [25]. However, the broader metabolic profiles of C15:0 and C17:0 appear to diverge substantially. In a large cross-sectional analysis of 15,919 participants from the EPIC-InterAct study, higher plasma phospholipid C15:0 concentrations were inversely associated with circulating triglycerides, total cholesterol, and hepatic injury markers including alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyl transferase (GGT), providing epidemiological support for a link between C15:0 and systemic lipid and hepatic metabolic regulation in humans [30]. In contrast to the relatively consistent evidence supporting beneficial metabolic effects of C15:0, experimental data on C17:0 remain limited. Taken together, these findings suggest that while C15:0 and C17:0 may share certain anti-inflammatory signaling properties at the cellular level, their broader metabolic effects diverge substantially, with functional evidence for C17:0 remaining comparatively limited.

5.2 Lipid remodeling and redox regulation

OCFAs may also influence lipid remodeling and cellular redox balance through their incorporation into complex membrane lipids and their effects on mitochondrial metabolism [3, 4, 27]. Lipidomic studies have shown that hepatic odd-chain phosphatidylcholine species are inversely associated with NAFLD severity. These species reflect the incorporation of OCFAs into membrane phospholipids and are linked to mitochondrial dysfunction-related alterations in hepatic lipid metabolism [8]. These findings suggest that OCFAs contribute to membrane lipid composition and hepatic lipid remodeling during metabolic disease progression, with OCFA-containing membrane lipids potentially linking these processes to mitochondrial function and cellular redox regulation. Current evidence is strongest for C15:0, which has been shown to restore mitochondrial membrane potential and reduce excessive mitochondrial ROS production in HepG2 cells, a human cellular model exposed to metabolic stress [6]. In vivo, oral C15:0 supplementation reduced total cholesterol, body weight gain, triglyceride levels, hepatic fibrosis severity, and liver iron-related pathology. Consistent with these findings, C15:0 treatment across multiple cells mimicking vascular inflammation, fibrosis, and metabolic stress demonstrated broad anti-inflammatory and cytoprotective activities [31], suggesting that C15:0 may suppress redox-driven inflammatory and cell stress signaling through mitochondrial stabilization. By contrast, evidence for C17:0 in redox regulation remains limited, and its specific mechanistic contribution to membrane lipid remodeling or mitochondrial redox control has not been clearly established [25]. Taken together, these findings suggest that OCFAs may participate in both lipid remodeling and redox regulation, but current mechanistic support is substantially stronger for C15:0 than for C17:0, highlighting the need for further studies to clarify the distinct roles of individual OCFAs in lipid remodeling and redox biology.    

5.3 Potential implications in cancer 

Although evidence regarding the role of OCFAs in cancer remains limited and is derived primarily from in vitro studies, accumulating data suggest that individual OCFAs may influence cancer cell behavior, including proliferation, apoptosis, stemness, and treatment responsiveness [32-34]. In breast cancer stem-like cells, C15:0 suppressed stemness, migration, and invasion while inducing caspase-dependent apoptosis through inhibition of IL-6-induced JAK2/STAT3 signaling, suggesting that C15:0 may modulate signaling pathways associated with cancer cell survival and stem-like phenotypes [32]. Evidence for C17:0 has also begun to emerge. In pancreatic cancer cells, C17:0 reduced colony formation, induced apoptosis, and enhanced gemcitabine chemosensitivity, suggesting potential effects on both intrinsic survival pathways and responsiveness to chemotherapy in specific tumor contexts [33]. Beyond these tumor-specific observations, OCFAs have also been proposed to influence cancer cell biology through protein acetylation-dependent mechanisms. Among several OCFAs evaluated as potential HDAC6 inhibitors, C15:0 exhibited the strongest inhibitory activity and promoted α-tubulin acetylation in MCF-7 breast and A549 lung cancer cells in a dose-dependent manner [34]. These findings raise the possibility that OCFAs may influence cancer cell behavior through mechanisms involving protein acetylation and cellular signaling. Taken together, the available evidence suggests that OCFAs may have preliminary functional relevance in cancer cell models. Based on their reported effects on lipid metabolism and redox homeostasis, it is conceivable that OCFAs may also influence redox-dependent cell death pathways, including ferroptosis, although direct experimental evidence remains lacking. Clarifying these potential mechanisms will require further validation in animal models and clinical studies.

6. Emerging mechanisms: metabolism–epigenetics crosstalk

Recent advances in the field of metabolic epigenetics have revealed that metabolites can directly influence gene expression through chromatin modifications. Acyl-CoA molecules, including acetyl-CoA, succinyl-CoA, and propionyl-CoA, serve as substrates for histone acylation [35]. Given that OCFAs generate propionyl-CoA as a terminal three-carbon product during β-oxidation, it is plausible that OCFA metabolism may contribute to histone propionylation. As noted above, complete β-oxidation of C15:0 yields six acetyl-CoA and one propionyl-CoA, and C17:0 yields seven acetyl-CoA and one propionyl-CoA, providing a quantifiable route to the intracellular propionyl-CoA pool. This modification has been associated with active transcriptional states and may link metabolic flux to gene regulation. Recent studies have demonstrated that metabolic pathways involving propionyl-CoA can regulate histone modifications and influence disease-related gene expression [36]. Previous studies have shown that perturbations in propionyl-CoA metabolism can reshape chromatin acylation patterns and transcriptional programs in disease-relevant contexts [37]. As with anaplerotic flux, the quantitative contribution of OCFA-derived propionyl-CoA to chromatin acylation in humans remains poorly defined and is likely to vary with tissue type, metabolic state, and disease context. Therefore, although direct evidence connecting OCFAs to specific epigenetic changes in human disease is still limited, these findings suggest that OCFAs may represent an important link between metabolism and gene regulation.

7. Therapeutic potential and future perspectives

7.1. Therapeutic potential in metabolic and chronic diseases

The emerging recognition of OCFAs as bioactive lipids has important implications for therapeutic development. Accumulating epidemiological and experimental evidence suggests that OCFAs may not only serve as biomarkers of dietary intake but also represent functionally active molecules capable of modulating metabolic homeostasis [3, 4]. Therefore, OCFAs may serve as dietary interventions or pharmacological targets for metabolic diseases. 

Future research should focus on elucidating the molecular mechanisms underlying OCFA actions at the cellular and systemic levels, in relation to mitochondrial metabolism, anaplerosis, and lipid signaling pathways [19, 38]. In parallel, distinguishing the relative contributions of dietary intake versus endogenous synthesis will be critical for interpreting circulating OCFA levels and for rational therapeutic targeting. Growing evidence also highlights the importance of microbiome–OCFA interactions, as microbial metabolism influences both OCFA production and downstream host responses [15]. Beyond metabolic disorders, emerging data suggest that OCFAs may play roles in cancer biology and other chronic diseases, potentially through effects on cellular energetics, inflammation, and epigenetic regulation. In this context, investigation of epigenetic mechanisms, including OCFA-derived acyl-CoA–mediated histone modifications, represents an important area for future study. Advances in metabolomics, lipidomics, and epigenomics, together with systems biology approaches, will be instrumental in deepening our understanding of OCFA biology and in translating these insights into clinically relevant interventions. 

7.2 Translational opportunities: from metabolism to technology and products

Recent technological advances, particularly in precision fermentation and microalgal biotechnology, have enabled the scalable production, precise quantification, and functional evaluation of OCFAs, including C15:0 and C17:0 [15]. Together, these advances support the development of sustainable sources of OCFAs, enabling their broader application beyond traditional dairy-derived origins. In parallel, enzymatic synthesis and catalytic elongation using propionyl-CoA or propionate-derived substrates are being explored to generate OCFAs with high purity and batch-to-batch consistency, which is critical for pharmaceutical and nutraceutical applications [17, 39]. Together, these technological developments are transforming OCFAs from observational biomarkers into actionable molecular entities.

OCFAs have begun to transition into commercial products across pharmaceutical, medical nutrition, and dietary supplement sectors [40]. The most established example is triheptanoin, an odd-chain triglyceride that delivers heptanoate-derived propionyl-CoA and acetyl-CoA [41]. Triheptanoin has received regulatory approval for the treatment of rare metabolic disorders, including long-chain fatty acid oxidation disorders and GLUT1 deficiency syndrome, highlighting the clinical relevance of odd-chain carbon metabolism. Beyond pharmaceuticals, C15:0 has entered the nutraceutical and functional nutrition space, supported by observational and early interventional studies suggesting biological activity consistent with a functional saturated fatty acid. Within this context, OCFAs represent a differentiated lipid category with well-substantiated scientific rationale, making them attractive for evidence-based applications. These trends suggest that OCFAs have the potential to evolve from niche biomarkers into strategic ingredients with sustained commercial relevance.

7.3 Patent trends and market landscape of odd-chain fatty acids

Recent years have witnessed a growing number of patent filings related to OCFAs, reflecting increasing interest in their functional and therapeutic applications. Patent activity is concentrated in pharmaceutical applications, nutraceutical formulations, and biotechnological production systems [42-44]. Triheptanoin represents a successful case of clinical translation, demonstrating the feasibility of targeting odd-chain carbon metabolism. In parallel, C15:0 has emerged as a functional lipid ingredient in dietary supplements, with patents emphasizing anti-inflammatory and metabolic regulatory properties. Notably, recent patent filings increasingly emphasize OCFA-based formulations targeting metabolic syndrome, inflammation, and aging-related conditions, reflecting a shift toward functional lipid therapeutics. Technological innovations, particularly microbial fermentation using engineered organisms such as Yarrowia lipolytica, have enabled scalable production [45]. From a market perspective, OCFAs are transitioning from niche biomarkers to commercially relevant bioactive compounds. OCFAs currently occupy a niche within the broader global fatty acid market and are projected to continue robust growth through 2030 [46, 47]. Within this expanding landscape, specialty fatty acids including structured lipids, medical nutrition fats, and evidence‑backed nutraceutical ingredients represent the fastest‑growing and highest‑value segments. Industry analyses increasingly identify odd‑chain and designer fatty acids as differentiated lipid categories, driven by sustainability considerations, non‑ruminant sourcing, reproducible purity, and mechanistically grounded health rationales. Taken together, these developments indicate that OCFAs are evolving from niche observational biomarkers into strategic commercial ingredients whose value proposition spans clinical efficacy, manufacturing scalability, and market differentiation.

8. Conclusion

OCFAs, particularly C15:0 and C17:0, are increasingly recognized as lipid species with biological relevance beyond their traditional use as biomarkers of dairy and ruminant fat intake. Current evidence indicates that circulating OCFA levels reflect multiple inputs, including dietary exposure, gut microbiota-derived precursors, endogenous fatty acid synthesis, peroxisomal processing, and tissue lipid remodeling. This complexity makes OCFAs useful indicators of nutritional and metabolic status, but also limits their interpretation as simple dietary biomarkers or direct markers of disease protection.

Epidemiological and lipidomic studies have reported inverse associations between circulating OCFAs and metabolic diseases such as T2D, CVD, and NAFLD (Figure 2). However, most human evidence remains observational, and causal relationships have not been fully established. Previous studies suggest that C15:0 may influence lipid metabolism, inflammatory signaling, mitochondrial stress responses, redox balance, and tissue remodeling, whereas mechanistic evidence for C17:0 remains more limited and context-dependent. Therefore, C15:0 and C17:0 should be considered related but biologically non-identical fatty acids rather than interchangeable members of a single functional class.

Overall, OCFAs represent a promising but still incompletely defined class of biologically relevant lipids. Future studies should clarify whether OCFAs are merely disease-associated biomarkers or active contributors to metabolic regulation through controlled intervention studies and mechanistic validation in clinically relevant models. A balanced interpretation of the current evidence suggests that their therapeutic and translational potential is encouraging, but still requires rigorous experimental and clinical confirmation.

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Cite this article;

Kim J. S.; Kim D. K.; Cho S. K. Odd-chain fatty acids in health and disease: metabolic functions, therapeutic potential, and emerging applications. NATPRO J. 2026, 3, 27-35