Visual abstract

Introduction

Obesity is a condition where an excessive amount of body fat accumulates in the body. It causes complications due to weight bearing and leads to metabolic diseases such as diabetes, cardiovascular disease, and high blood pressure. Obesity seriously reduces the quality of life, and enormous socioeconomic costs are incurred to treat obesity. In the United States, the rate of obesity in 1999–2000 increased from 30.5% to 41.9% in 2017–2020 [1]. Similarly, in Korea, 2 databases from the Korean National Health Insurance Service (NHIS) Health Checkup database (2013–2022) and Korea National Health and Nutrition Examination Survey IX (2022), recorded obesity as 30.6% which increased to 38.4% in 2022, and specifically male obesity rose by 37.9% to 49.6% in this time period [2].

In the prevention and treatment of obesity in Korea various strategies have been developed, including protein-supplemented very-low-calorie diets, nutritional supplements, dietary self-monitoring methods, and use of natural alternative sweeteners to reduce calorie intake [3–5]. Anti-obesity drugs are also available in Korea, and are classified into 3 categories according to their mechanism of action: (1) inhibiting intestinal fat absorption; (2) suppressing food intake; and (3) increasing energy consumption and thermogenesis. Some common drugs that have been approved for use are orlistat, phentermine, sibutramine, liraglutide, naltrexone-bupropion (Table 1).

Orlistat has been approved for weight management since 1999 by the US Food and Drug Administration and 2000 by the Korea Ministry of Food and Drug Safety [6]. It is a lipase inhibitor which inhibits intestinal fat absorption, reduces blood pressure, low-density lipoprotein cholesterol, and body weight, although common side effects include oily fecal spotting (27%), fecal urgency (22%), and steatorrhea (20%) [6]. Phentermine-topiramate, initially approved in 2012 in the US for long-term weight management, can achieve up to a 10% weight reduction by mimicking the effects of sympathetic nervous system stimulation (phentermine is a sympathomimetic amine), and together with topiramate, increase satiety and reduce appetite. Common adverse effects associated with phentermine-topiramate include paresthesia (14%-20%), dry mouth (14%-19%), and constipation (15%-16%) [7]. Sibutramine, approved in 1997 by the US and in 2001 by the Korea Ministry of Food and Drug Safety for weight management, functions as a serotonin-norepinephrine reuptake inhibitor, leading to increased neurotransmitter levels and weight loss but with side effects such as dry mouth, hypertension, and insomnia [8]. Liraglutide, which is a glucagon-like peptide-1 receptor agonist, was approved for obesity treatment in the US in 2015; it regulates blood sugar, suppresses appetite, slows gastric emptying, and results in a mean body mass index reduction of 5%, however, it primarily causes gastrointestinal issues [9]. The naltrexone-bupropion combination, approved in the US in 2014 for weight management, activates pro-opiomelanocortin neurons to decrease appetite and increase dopamine and norepinephrine levels, significant weight loss is achieved but treatment is associated with nausea, constipation, and headaches [10]. Despite the efficacy of anti-obesity drugs in managing weight, and related conditions, these pharmaceutical options often come with undesirable side effects. Consequently, consumers have become interested in effective anti-obesity treatments made from natural ingredients that are associated with fewer side effects. Natural products generally have fewer side effects than chemically purified drugs but caution is required concerning potential allergic reactions.

The potential of plant-derived nutrients, fibers, and phytochemicals for preventing and treating obesity has been observed. However, the effects a phytochemical may deliver could be counteracted by various biological processes within the human body. The absorption and metabolism of natural ingredients through the digestive tract are complex and can be impacted by multiple factors, and may potentially lead to discrepancies between in vitro, in vivo, and ex vivo laboratory results and actual effects. It may also be difficult for products of natural ingredients to accurately reach the target tissue or cells. The degree or persistence of the effect may also vary depending on how the ingredient is distributed within the body. For these reasons, differences may arise between experimental outcomes of natural product ingredients and their effects in humans. Therefore, comprehensive research and rigorous validation are crucial to fully understand and overcome these limitations to enable the development of effective obesity treatments from natural sources. In this review, the focus was on the mechanisms of action against obesity for Capsaicin (pepper), Citrus (bitter orange), Curcuma (turmeric), epigallocatechin gallate (green tea), and saponin (glycoside) and their limitations (Table 2).

Materials and Methods

The literature was comprehensively retrieved using databases such as PubMed (https://pubmed.ncbi.nlm.nih.gov/), Google Scholar (https://scholar.google.com/), and ScienceDirect (https://www.sciencedirect.com/). The keywords used in these searches were “anti-obesity,” “mechanism,” “phytochemicals,” “adipogenesis,” “synephrine,” “EGCG,” “curcumin,” “capsaicin,” “saponin,” “limitation” and relevant keywords. Articles indexed in PubMed and published up to 20 September 2024 were included. Each piece of literature was ultimately selected for inclusion based on its relevance to the subject, with a focus on clinical trials and epidemiological studies, as well as in vitro and in vivo studies.

Results

1. Synephrine

1.1. Mechanism of action

Citrus aurantium has a long history of use in traditional Chinese medicine and is now a popular dietary supplement for weight management, supporting energy flow, and treating various conditions such as indigestion, diarrhea, dysentery, constipation, and sputum production [11–13]. The main component of C. aurantium extract is p-synephrine, which comprises over 90% of the total protoalkaloid content [14]. Synephrine has 3 isomeric forms: para, meta, and ortho which occur naturally in foods or is added to supplements [15]. It has been shown in a mouse cell line (3T3-L1 cells) that p-synephrine reduces the activity of CCAAT/enhancer-binding protein alpha (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ) in regulating fat metabolism, thereby showing inhibition of adipogenesis [16]. In humans, 3 mg/kg of p-synephrine significantly improved fat oxidation rates during exercise, and impacted obesity-related metabolism [17]. In HepG2 cells, p-synephrine inhibited glucose production by activating the adenosine monophosphate-activated protein kinase-forkhead box protein O1 pathway [18]. In a review of safety, efficacy, and mechanistic studies of C. aurantium extract and p-synephrine, it was reported that p-synephrine regulates fat metabolism, preventing obesity and lipid accumulation by promoting brown fat formation in vitro [19]. p-Synephrine promotes signaling through β3-adrenaline receptors and part of the insulin signaling pathway, thereby modulating adipocyte differentiation and stimulating weight loss in both in vitro and animal studies [20].

1.2. Limitations of synephrine

P-synephrine’s structural similarity to ephedrine raises concerns [21]. Numerous reports link p-synephrine to serious cardiovascular side effects, including heart attacks, strokes, and angina [22,23]. P-synephrine is difficult to assess in human metabolic and physiological activity [24]. In addition, it is reported that p-synephrine is metabolized in the body and interacts with other chemicals to form complexes which affect human metabolism and physiological activity [25]. Due to these potential adverse effects and complex interactions, the overall safety and efficacy of C. aurantium extract and p-synephrine are limited [26].

1.3. Future strategies to optimize dosage and natural food sources

Despite concerns, some researchers have explored ways to mitigate the limitations of p-synephrine. In an animal study by Huang et al [27], C. aurantium extract and p-synephrine were injected into rats, and dose-dependent reductions in blood pressure and heart rate were observed. In another animal study by Huang et al [28], it was determined that hypertension was significantly improved following oral administration of synephrine (1 mg/kg and 10 mg/kg, for 8 days) in mice with induced hypertension. Calapai et al [29] evaluated the active constituents of C. aurantium L., its active constituents, biological effects, and extraction methods in this review and the toxicity test of C. aurantium extract was explored as an anti-obesity herbal medicine. In a study of the influence of food intake on electrocardiograms of healthy male volunteers, where increased food intake and weight gain were confirmed, significant changes were observed in heart rate and electrocardiogram results, and blood pressure [30]. The widespread consumption of orange-derived products containing synephrine, without reported adverse effects, is often cited as a basis for its presumed safety [31,32]. It was reported that the stability of p-synephrine is not a problem and does not cause toxicity at the standard doses found in consumer products [33]. A study by the U.S. Department of Agriculture indicated that common oranges contain around 6 mg of p-synephrine, with citrus juices containing about 5 mg per 8 ounces, and orange juice ranging from 73 to 158 mg/L [34]. Therefore, because it is safe to consume 8 ounces of orange juice, it is safe to ingest 40 mg of p-synephrine which is considered nontoxic when consumed as part of food [35].

2. Epigallocatechin gallate

2.1. Mechanism of action

Epigallocatechin gallate (EGCG) is a type of polyphenol extracted from green tea leaves, which activates adenosine monophosphate-activated protein kinase (AMPK) and increases fatty acid oxidation in the liver and skeletal muscles. Research shows that EGCG enhances lipolysis [36]. Norepinephrine increases cyclic adenosine monophosphate (cAMP) production, leading to cAMP-dependent protein kinase A (PKA) activation and phosphorylation of hormone-sensitive lipase (HSL) [37]. EGCG specifically inhibits phosphodiesterase, an enzyme that breaks down cAMP, thereby sustaining PKA activation and HSL phosphorylation, leading to greater triglyceride hydrolysis [36]. In addition, EGCG reduces fat formation by inhibiting the adipogenic enzymes PPARγ and C/EBPα [38]. It also induces adipocyte apoptosis in a dose-dependent manner, preventing triglyceride accumulation [39]. This suggests that EGCG directly promotes phosphorylation of hormone-sensitive lipase and increases lipolysis via the PKA-dependent pathway in the presence of norepinephrine in 3T3-L1 adipocytes, providing a potential mechanism for reducing body fat [40].

2.2. Limitations of EGCG

The limitations of EGCG can be classified into 2 main categories. Firstly, EGCG’s structure is prone to oxidation, especially under physiological and high pH conditions, leading to degradation and reduced content during storage [41,42]. Secondly, EGCG exhibits poor bioavailability. Catechin reaches a maximum plasma concentration of up to 0.1–2 μmol/L between 1 to 2 hours after ingestion, and then catechin is rapidly removed (the plasma concentration used as a reference level is within 24 hours of the initial ingestion). Most catechin degradation occurs under conditions in the small intestine where the pH rises, active oxygen species are present, and favorable conditions for the oxidation reaction of catechin are present. Transport of catechin in the intestine is limited by its relationship to efflux transport systems including multidrug resistance proteins, and p-glycoprotein [43,44].

2.3. Future strategies to stabilize and enhance EGCG bioavailability

To protect catechin from oxidative degradation in the gastrointestinal tract, it is stabilized with ascorbic acid [45]. A key strategy in this method involves adding ascorbic acid, which chemically stabilizes EGCG by lowering the pH and reducing oxidative degradation, especially at physiological pH levels where EGCG is typically unstable and prone to browning [46,47]. EGCG’s structural instability and low bioavailability hinder its efficacy as an anti-obesity phytochemical in health supplements [48,49]. Combining ascorbic acid with sucrose can significantly improve EGCG’s bioavailability [50]. Ascorbic acid also regulates p-glycoprotein activity, limiting the efflux of absorbed catechins back into the gut lumen. These combined approaches help stabilize EGCG from degradation in the digestive tract and enhance its absorption, ultimately maximizing its therapeutic potential [51]. Continued innovation in delivery systems and formulations is crucial to overcome these inherent phytochemical limitations.

3. Curcumin

3.1. Mechanism of action

Curcumin has been a cornerstone of Ayurvedic medicine for millennia, with extensive research highlighting its antioxidant and therapeutic properties against inflammation, dementia, and cancer [52,53]. Among these various effects, curcumin has shown significant promise in obesity management [54]. Curcumin improves insulin resistance, hyperglycemia, and hyperlipidemia, induced by obesity, by lowering leptin resistance and increasing adiponectin production [55]. In a review of inflammation-induced obesity and metabolic disease, several studies have shown that curcumin plays a potential role in angiogenesis, adipocyte formation, differentiation, and apoptosis of adipocytes [56]. In mice, curcumin increases fatty acid oxidation in adipocytes and activates AMPK, a crucial enzyme for metabolic regulation [57]. Curcumin is being explored for its ability to suppress adipocyte differentiation and growth by controlling Wnt signaling, alongside promoting fatty acid β-oxidation in mice [58].

3.2. Limitations of curcumin

Curcumin exhibits poor bioavailability, meaning it is not well absorbed, distributed, metabolized, or excreted [59]. Because the enol-keto type present in curcumin compounds is chemically unstable, easy to decompose, and very low solubility in water, the biological utilization of curcumin was less than 1% in in vitro and in vivo tests, and the biological activity of the curcumin compounds’ metabolites is also expected to be different [60]. This is largely due to gastrointestinal barriers like the mucus layer and intestinal epithelium, which limit its transport into the body [61,62].

3.3. Future strategies to adopt cyclodextrin encapsula-tion and nanoformulation

To overcome the limitations of substances with high pharmacological effects but poor bioavailability, such as curcumin, various methods have been studied [63]. Firstly, curcumin can be combined with piperine. Piperine boosts curcumin’s absorption by inhibiting liver enzymes (UDP glucuronosyltransferase, CYP3A4, and p-glycoprotein) that typically break down many drugs for excretion, and this allows curcumin to remain in the bloodstream longer [64]. Secondly, as a method using encapsulation, cyclodextrin can be used. Cyclodextrins, derived from starches, can encapsulate curcumin, boosting its stability and improving its capacity to cross biological membranes [65]. Finally, the development of nanoscale delivery systems has been extensively studied to enhance the bioavailability and stability of natural bioactive compounds such as curcumin. These systems protect curcumin from degradation in the gastrointestinal tract and improve its absorption and targeted delivery organs [66]. In an in vitro study using curcumin-loaded nanostructured lipid carriers with mucoadhesive polymers when exposed to simulated gastric fluid and simulated intestinal fluid, it was reported that the stability could be maintained [67].

4. Capsaicin

4.1. Mechanism of action

Capsaicin is an active ingredient in the fruit of Capsicum, a member of the Solanaceae family [68]. Capsaicin suppresses appetite and induces satiety, resulting in weight loss effects [69]. In experiments (in vitro and in vivo), capsaicin enhanced the expression of PPARγ by activating transient receptor potential vanilloid 1 (TRPV1) channels which increased sirtuin-1 expression and intracellular Ca²⁺ levels in mice [70,71]. In a study examining the effects of capsaicin on lipid metabolism in 3T3-L1 cells, capsaicin promoted lipid catabolism by increasing glycerol release and up-regulating key metabolic regulators, including hormone-sensitive lipase (HSL), carnitine palmitoyltransferase Iα, and uncoupling protein 2 [72]. Capsaicin induces apoptosis, inhibits adipogenesis in 3T3-L1 preadipocytes and adipocytes by decreasing the amount of intracellular triacylglycerols and glycerol-3-phosphate dehydrogenase activity, thereby inhibiting the expression of PPARγ, C/EBPα, and leptin, while enhancing adiponectin protein expression [73]. These effects were also observed in rats where capsaicin administration in rats has been shown to increase uncoupling protein 1 expression, downregulate the leptin gene, reduce fat accumulation, and decrease body weight, total cholesterol, triglycerides and low density lipoprotein cholesterol in the blood [74,75]. In a study using adult male Wistar rats, capsaicin treatment induced browning of white adipose tissue with the upregulation of the browning marker PR domain containing 16 (PRDM16) in retroperitoneal white adipose tissue, and up-regulation of uncoupling protein 1 [76]. When capsaicin 2 mg/kg was administered to female C57BL/6J mice for 12 weeks, it suppressed body mass gain, cholesterol, glucose, and insulin levels likely due to increasing the number of beneficial gut microbiota populations [77].

4.2. Limitations of capsaicin

Capsaicin is widely known for its anti-obesity effect, many related studies have been conducted, and it is widely used in the commercial and pharmaceutical fields. However, there are limitations in clinical development. It can be broadly divided into 3 categories: (1) low solubility in water; (2) short biological half-life; and (3) bioavailability [78]. Capsaicin has poor aqueous solubility (< 0.1 mg/mL) and it has also been limited to topical application [79]. Capsaicin has a short half-life of up to 7 minutes when administered intravenously to rats and has poor solubility, making intravenous administration difficult [80]. The half-life of capsaicin in the human body was determined to be 25 minutes [79]. Capsaicin is reported to cause gastrointestinal side effects such as cramps, nausea, and flatulence following consumption [81].

4.3. Future strategies in encapsulation

Methods to overcome the limitations of capsaicin are necessary and previous studies have explored potential solutions. Recently, research have focused on addressing its poor water solubility, short half-life, and side effects. One promising strategy involves formulating capsaicin into lipid nanoparticles, such as liposomes, which can be adapted for targeted drug delivery [82]. Studies have shown that capsaicin can be incorporated into polymer drug carriers to form sustained-release formulations. The capsaicin within a polymer matrix is evenly distributed and released slowly, steadily, and over a long period of time [78]. To improve capsaicin’s hydrophobicity, forming complexes with water-soluble compounds like cyclodextrin can significantly enhance its dissolution [83]. In addition, encapsulation has been shown to mitigate adverse effects, specifically reduce gastric mucosa injury while increasing solubility, and decreasing cytotoxicity to healthy cells [84]. In conclusion, encapsulated capsaicin may reduce side effects, enhance water solubility, and extend its action.

5. Saponin

5.1. Mechanism of action

The term “saponin” is derived from the Latin word “sapo” which means soap, and as its origin suggests, it forms a soapy foam and has surface activity. It has a bitter taste, with hemolytic action, antimicrobial action, and applications in pharmaceutical industries [85,86]. The saponins are mostly triterpene glycosides with triterpenes or steroid in aglycone. These triterpene glycosides are recognized for their potential to reduce body weight and serum lipid levels, making them a focus in anti-obesity research. Saponins are involved in various stages of fat metabolism and exhibit anti-obesity activity. Firstly, they control appetite and inhibits the action of pancreatic lipase, which breaks down 50%-70% of dietary fats. In addition, it suppresses hyperlipidemia, which increases fat content in the blood through the resynthesis of neutral fat after absorption into the human body, it inhibits adipogenesis, and regulates appetite [87,88]. Lipase inhibition is one of the most important strategies in reducing fat absorption, similar to the action of the obesity drug orlistat which was the first approved for obesity treatment by the US Food and Drug Administration [6]. In a study on the lipase inhibitory activity of plant extracts containing saponin, rats were fed a high-fat diet mixed with Platycodon grandiflorum (bellflower root) extract, and lipase activity was inhibited, and adipose tissue weight decreased [89,90]. In addition, saponins are reported to enhance AMPK activity, a vital regulator of fat metabolism [90]. By activating AMPK, saponin promotes β-oxidation, inhibits adipogenic transcription factors such as PPARγ, C/EBPα, and sterol regulatory element-binding protein-1c [91].

5.2. Limitations of Saponin

Saponin is toxic when it is administered intravenously to the human body and has hemolytic activity in the human body depending on the type of non-glycosylated moiety and sugar chain due to the interaction of sterols with the red blood cell membrane, and as membrane permeability increases, it leads to hemolysis [92,93]. It is also known to act as a fish poison, and is toxic to ruminants, causes gastroenteritis, diarrhea, and liver and kidney degeneration [94,95]. Poisoning from saponin has been reported in sheep [96]. White and crystalline material within the gallbladder of the sheep and eosinophilic crystalline material within the bile ducts, canaliculi, and hepatocytes were observed; these findings were associated with cholangitis [96].

5.3. Future strategies for plant-derived saponins

Animal studies have shown that ginseng saponins and Gypsophila oldhamiana gypsosaponins led to weight loss, reduced hypertriglyceridemia, decreased adipose tissue, lowered blood lipids, and increased fecal fat excretion in obese mice by inhibiting pancreatic lipase [97,98]. Clinical studies on humans also support saponins’ efficacy. Consuming fermented oat-based products resulted in reduced body mass index, total cholesterol, and low-density lipoprotein cholesterol, while increasing HDL-C in obese individuals [99–101]. A study conducted between 1999 and 2002 found that people who regularly consumed soy, rich in soyasaponin A, was linked to better body weight, waist circumference, and lower blood pressure [102].

Discussion

Obesity is linked to many diseases, and it was defined as a global chronic disease by the World Health Organization. Because of an imbalance in energy intake and expenditure, it easily leads to Type 2 diabetes mellitus, non-alcoholic fatty liver disease, cardiovascular disease and cancer [103]. Traditional weight loss methods tend not to be effective and current pharmacological treatment options are limited due to their side effects. As a result, effective strategies with fewer side effects such as using plants and phytochemicals are required for obesity treatment.

This narrative review aimed to summarize phytochemical molecular mechanisms against obesity, as well as discuss the limitations and recent strategies to enhance these preventive and therapeutic agents. Phytochemicals could inhibit adipogenesis and control lipid metabolism. Synephrine, EGCG, curcumin, capsaicin and saponin also play important roles in inhibiting lipase activity, regulating lipid metabolism. However, there are some limitations when using them in managing obesity. Until now, most phytochemicals are being developed as functional formulations in order to support health and prevent obesity. Phytochemicals are not used currently as medicines to treat obesity due to their poor stability, bioavailability, and side effects. Human trials present unique challenges related to complex metabolic processes, dosage, and side effects. Curcumin, EGCG, and capsaicin are poorly absorbed in the gastrointestinal tract due to degradation and low solubility. In the small intestine, most catechins are degraded, and the aqueous solubility of curcumin and capsaicin is low, approximately 0.6 μg/mL and less than 0.1 mg/mL, respectively. This poor aqueous solubility of curcumin and capsaicin means that therapeutic concentrations are rarely achieved without enhancers or advanced nano-formulations. In addition, oral consumption of p-synephrine and capsaicin causes health problems related to cardiovascular, gastrointestinal tract symptoms such as ischemic stroke, angina, ischemic colitis, coronary artery spasms and thrombosis, vascular spasms, cramps, nausea, and flatulence [22,23,81]. Saponin is toxic to ruminants, causes gastroenteritis, diarrhea, even liver and kidney degeneration [94,95]. Due to gastrointestinal tolerability and significant cardiovascular adverse events, doses have been limited before effective concentrations can be reached. While saponins show their promise in lipase inhibition, their application is limited by concerns over toxicity, including potential hemolysis, gastroenteritis, and hepatotoxicity at higher doses, making reliance on safer food-grade or fermented forms more realistic. Although in vivo and clinical studies show promise, more extensive research is crucial to establish the long-term safety and optimal application of phytochemicals as anti-obesity agents.

Overcoming the therapeutic limitations of phytochemicals in anti-obesity applications requires enhanced delivery mechanisms and formulation strategies. Intestinal soluble capsules successfully deliver active ingredients to the small intestine, and lymphatic uptake circumvents hepatic first-pass metabolism which improves systemic availability. However, numerous phytochemicals continue to face challenges with limited solubility, structural instability, and inadequate bioavailability. Delivery technologies need to advance, including more sophisticated lipid-based nanocarrier systems. Another promising approach is nanomaterials which protect phytochemicals from degradation in the gastrointestinal tract, improve their absorption, and reduce adverse effects. Recent studies indicate that fermented botanical products rich in phytochemicals may support obesity management without causing unwanted side effects [99,100,102,104]. Notable examples include encapsulated capsaicin products, typically extracted from green tea or pepper sources [103]. Some commercial plant-derived products of saponin have potential in combating obesity via inhibiting pancreatic lipase such as q-naturale, which is made of saponins extracted from the bark of the Quillaja saponaria tree [105].

Phytochemicals from plant leaves, roots, seeds are considered as anti-obesity agents. Further investigations into their limitations, new sources, and new strategies are needed to fully understand their potential and to develop their use in food, cosmetics, and pharmaceutical applications. Continued research and innovation will pave the way for their successful integration into various applications, contributing to improved human health and well-being.

Article information

Author Contributions

The structure, content, and writing of the article have been prepared by all authors. All authors have read and agreed to the published version of the manuscript.

Conflicts of Interest

The authors have no conflicts of interest to declare.

Author Use of AI Tools Statement

ChatGPT (OpenAI) was used for language editing to improve clarity and readability of the manuscript. The authors take full responsibility for the content.

Funding

This research was supported by the Ministry of Food and Drug Safety (Grant no.: 24202MFDS239) and the Korea Institute of Oriental Medicine (Grant no.: 2024M3H9A1045916).

Ethical Statement

This article is a narrative review and therefore ethical approval was waived.

Data Availability

Not applicable.

References

• [1] Public Health [Internet]. Adult obesity facts: CDC: 2024 Available from: https://www.cdc.gov/obesity/adult-obesity-facts/index.html
• [2] Cho S, Jung J-H, Nam GE, Cho IY, Park K-Y, Jeong S-M, et al, Taskforce Team of the Obesity Fact Sheet of the Korean Society for the Study of Obesity. 2024 Obesity fact sheet in Korea: prevalence of obesity, abdominal obesity, obesity defined by body fat percentage, and underweight in adults in Korea from 2013 to 2022. J Obes Metab Syndr 2025;34(4):405−13.ArticlePubMedPMC
• [3] Cho E, Kim S, Kim HJ, Cho B, Park JH, Kwon H, et al. Effectiveness of a protein-supplemented very-low-calorie diet program for weight loss: a randomized controlled trial in South Korea. Front Nutr 2024;11:1370737. ArticlePubMedPMC
• [4] Jin T, Kang G, Song S, Lee H, Chen Y, Kim S-E, et al. The effects of dietary self-monitoring intervention on anthropometric and metabolic changes via a mobile application or paper-based diary: a randomized trial. Nutr Res Pract 2023;17(6):1238−54.ArticlePubMedPMCPDF
• [5] Kim E. Effects of natural alternative sweeteners on metabolic diseases. Clin Nutr Res 2023;12(3):229−43.ArticlePubMedPMCPDF
• [6] Xenical package insert [Internet]: [cited 2024 Apr 14]. Available from: https://xenical.com/pdf/PI_Xenical-brand_FINAL.PDF
• [7] Qsymia package insert [Internet]: [cited 2024 Apr 14]. Available from: https://qsymia.com/patient/include/media/pdf/prescribing-information.pdf
• [8] Porter JA, Raebel MA, Conner DA, Lanty FA, Vogel EA, Gay EC, et al. The long-term outcomes of sibutramine effectiveness on weight (LOSE Weight) study: evaluating the role of drug therapy within a weight management program in a group-model health maintenance organization. Am J Manag Care 2004;10(6):369−76.PubMed
• [9] Kelly AS, Auerbach P, Barrientos-Perez M, Gies I, Hale PM, Marcus C, et al. A randomized, controlled trial of liraglutide for adolescents with obesity. N Engl J Med 2020;382(22):2117−28.ArticlePubMed
• [10] Apovian CM, Aronne L, Rubino D, Still C, Wyatt H, Burns C, et al. A randomized, phase 3 trial of naltrexone SR/bupropion SR on weight and obesity-related risk factors (COR-II). Obesity (Silver Spring) 2013;21(5):935−43.ArticlePubMedPMCPDF
• [11] Abdelkawy KS, Donia AM, Turner RB, Elbarbry F. Effects of lemon and Seville orange juices on the pharmacokinetic properties of sildenafil in healthy subjects. Drugs R D 2016;16(3):271−8.ArticlePubMedPMCPDF
• [12] An G, Mukker JK, Derendorf H, Frye RF. Enzyme- and transporter-mediated beverage-drug interactions: an update on fruit juices and green tea. J Clin Pharmacol 2015;55(12):1313−31.ArticlePubMed
• [13] Arbo MD, Schmitt GC, Limberger MF, Charão MF, Moro AM, Ribeiro GM, et al. Subchronic toxicity of Citrus aurantium L. (Rutaceae) extract and p-synephrine in mice. Regul Toxicol Pharmacol 2009;54(2):114−7.ArticlePubMed
• [14] Bakhiya N, Ziegenhagen R, Hirsch-Ernst KI, Dusemund B, Richter K, Schultrich K, et al. Phytochemical compounds in sport nutrition: synephrine and hydroxycitric acid (HCA) as examples for evaluation of possible health risks. Mol Nutr Food Res 2017;61(6):1601020. ArticlePubMedPDF
• [15] Koncz D, Tóth B, Bahar MA, Roza O, Csupor D. The safety and efficacy of citrus aurantium (bitter orange) extracts and p-synephrine: a systematic review and meta-analysis. Nutrients 2022;14(19):4019. ArticlePubMedPMC
• [16] Ruiz-Moreno C, Coso JD, Giráldez-Costas V, González-García J, Gutiérrez-Hellín J. Effects of p-synephrine during exercise: a brief narrative review. Nutrients 2021;13(1):233. ArticlePubMedPMC
• [17] Huang Y-C, Li J-M, Chen B-Z, Zhang X-M, Wu R-H, Wu P-P, et al. Recent advance in the biological activity of synephrine in Citri Reticulatae Pericarpium. Eur J Med Chem Rep 2022;5:100061. Article
• [18] Guo LX, Zhang Y, Yin Z, Pu Y, Zheng X. p-Synephrine suppresses hepatic glucose production via the AMPK-FoxO1 signaling pathway in HepG2 cells. Food Sci 2019;40(5):156−61. [in Chinese] https://www.spkx.net.cn/EN/10.7506/spkx1002-6630-20171109-105
• [19] Stohs SJ. Safety, efficacy, and mechanistic studies regarding Citrus aurantium (bitter orange) extract and p-synephrine. Phytother Res 2017;31(10):1463−74.ArticlePubMedPMC
• [20] de Lima LP, de Paula Barbosa A. A review of the lipolytic effects and the reduction of abdominal fat from bioactive compounds and moro orange extracts. Heliyon 2021;7(8):e07695. ArticlePubMedPMC
• [21] Sultan S, Spector J, Mitchell RM. Ischemic colitis associated with use of a bitter orange-containing dietary weight-loss supplement. Mayo Clin Proc 2006;81(12):1630−1.ArticlePubMed
• [22] Stohs SJ. Assessment of the adverse event reports associated with Citrus aurantium (bitter orange) from April 2004 to October 2009. J Funct Foods 2010;2(4):235−8.Article
• [23] Ratamess NA, Bush JA, Stohs SJ, Ellis NL, Vought IT, O’Grady EA, et al. Acute cardiovascular effects of bitter orange extract (p-synephrine) consumed alone and in combination with caffeine in human subjects: a placebo-controlled, double-blind study. Phytother Res 2018;32(1):94−102.ArticlePubMedPDF
• [24] Stohs SJ, Ratamess NA. Effects of p-synephrine in combination with caffeine: a review. Nutr Diet Suppl 2017;9:87−96.Article
• [25] Dodonova SA, Zhidkova EM, Kryukov AA, Valiev TT, Kirsanov KI, Kulikov EP, et al. Synephrine and Its derivative compound a: common and specific biological effects. Int J Mol Sci 2023;24(24):17537. ArticlePubMedPMC
• [26] Bent S, Padula A, Neuhaus J. Safety and efficacy of citrus aurantium for weight loss. Am J Cardiol 2004;94(10):1359−61.ArticlePubMed
• [27] Huang YT, Lin HC, Chang YY, Yang YY, Lee SD, Hong CY. Hemodynamic effects of synephrine treatment in portal hypertensive rats. Jpn J Pharmacol 2001;85(2):183−8.ArticlePubMed
• [28] Rossato LG, Costa VM, de Pinho PG, Carvalho F, de Lourdes Bastos M, Remião F. Structural isomerization of synephrine influences its uptake and ensuing glutathione depletion in rat-isolated cardiomyocytes. Arch Toxicol 2011;85(8):929−39.ArticlePubMedPDF
• [29] Maksoud S, Abdel-Massih RM, Rajha HN, Louka N, Chemat F, Barba FJ, et al. L. Citrus aurantium L. active constituents, biological effects and extraction methods. An updated review. Molecules 2021;26(19):5832. ArticlePubMedPMC
• [30] Widerlöv E, Jostell KG, Claesson L, Odlind B, Keisu M, Freyschuss U. Influence of food intake on electrocardiograms of healthy male volunteers. Eur J Clin Pharmacol 1999;55(9):619−24.ArticlePubMedPDF
• [31] Blumenthal M. Bitter orange peel and synephrine: part 1. HerbalGram 2002;66:77−9. https://www.herbalgram.org/resources/herbalgram/issues/66/table-of-contents/article2833/
• [32] Sun Y, Xia X, Yuan G, Zhang T, Deng B, Feng X, et al. Stachydrine, a bioactive equilibrist for synephrine, identified from four citrus Chinese herbs. Molecules 2023;28(9):3813. ArticlePubMedPMC
• [33] Uckoo RM, Jayaprakasha G, Nelson SD, Patil BS. Rapid simultaneous determination of amines and organic acids in citrus using high-performance liquid chromatography. Talanta 2011;83(3):948−54.ArticlePubMed
• [34] Stohs SJ, Preuss HG, Shara M. The safety of Citrus aurantium (bitter orange) and its primary protoalkaloid p-synephrine. Phytother Res 2011;25(10):1421−8.ArticlePubMedPDF
• [35] Arbo MD, Larentis ER, Linck VM, Aboy AL, Pimentel AL, Henriques AT. Concentrations of p-synephrine in fruits and leaves of Citrus species (Rutaceae) and the acute toxicity testing of Citrus aurantium extract and p-synephrine. Food Chem Toxicol 2008;46(8):2770−5.ArticlePubMed
• [36] Kim S-N, Kwon H-J, Akindehin S, Jeong HW, Lee YH. Effects of epigallocatechin-3-gallate on autophagic lipolysis in adipocytes. Nutrients 2017;9(7):680. ArticlePubMedPMC
• [37] Ravnskjaer K, Madiraju A, Montminy M. Role of the cAMP pathway in glucose and lipid metabolism. Handb Exp Pharmacol 2016;233:29−49.ArticlePubMed
• [38] Kim H, Sakamoto K. (−)-Epigallocatechin gallate suppresses adipocyte differentiation through the MEK/ERK and PI3K/Akt pathways. Cell Biol Int 2012;36(2):147−53.ArticlePubMed
• [39] Lin J, Della-Fera MA, Baile CA. Green tea polyphenol epigallocatechin gallate inhibits adipogenesis and induces apoptosis in 3T3-L1 adipocytes. Obes Res 2005;13(6):982−90.ArticlePubMed
• [40] Chen S, Osaki N, Shimotoyodome A. Green tea catechins enhance norepinephrine-induced lipolysis via a protein kinase A-dependent pathway in adipocytes. Biochem Biophys Res Commun 2015;461(1):1−7.ArticlePubMed
• [41] Tan J, de Brujin WJC, van Zadelhoff A, Lin Z, Vincken JP. Browning of epicatechin (EC) and epigallocatechin (EGC) by auto-oxidation. J Agric Food Chem 2020;68(47):13879−87.ArticlePubMedPMCPDF
• [42] Zeng L, Ma M, Li C, Lui L. Stability of tea polyphenols solution with different pH at different temperatures. Int J Food Properties 2017;20:1−18.Article
• [43] Park Y, Won E, Son D. Effect of pH on the stability of green tea catechins. J Food Hygiene Saf 2002;17(3):117−23. [in Korean] https://www.koreascience.kr/article/JAKO200211921407341.page
• [44] Sun C, Zhao C, Guven EC, Paoli P, Simal-Gandara J, Ramkumar KM, et al. Dietary polyphenols as antidiabetic agents: advances and opportunities. Food Front 2020;1(1):18−44.ArticlePDF
• [45] Furniturewalla A, Barve K. Approaches to overcome bioavailability inconsistencies of epigallocatechin gallate, a powerful anti-oxidant in green tea. Food Chem Adv 2022;1:100037. Article
• [46] Ananingsih VK, Sharma A, Zhou W. Green tea catechins during food processing and storage: a review on stability and detection. Food Res Int 2013;50(2):469−79.Article
• [47] Yoshino K, Suzuki M, Sasaki K, Miyase T, Sano M. Formation of antioxidants from (−)-epigallocatechin gallate in mild alkaline fluids, such as authentic intestinal juice and mouse plasma. J Nutr Biochem 1999;10(4):223−9.ArticlePubMed
• [48] Yin X, Chen K, Cheng H, Chen X, Feng S, Song Y, et al. Chemical stability of ascorbic acid integrated into commercial products: a review on bioactivity and delivery technology. Antioxidants (Basel) 2022;11(1):153. ArticlePubMedPMC
• [49] Li J, Duan H, Liu Y, Wang L, Zhou X. Biomaterial-based therapeutic strategies for obesity and its comorbidities. Pharmaceutics 2022;14(7):1445. ArticlePubMedPMC
• [50] Rawat SG, Tiwari RK, Sonker P, Maurya RP, Vishvakarma NK, Kumar A. EGCG as anti-obesity and anticancer agent. Obesity and cancer 2021;209−33.ArticlePubMed
• [51] Peters CM, Green RJ, Janle EM, Ferruzzi MG. Formulation with ascorbic acid and sucrose modulates catechin bioavailability from green tea. Food Res Int 2010;43(1):95−102.ArticlePubMedPMC
• [52] Kasprzak-Drozd K, Oniszczuk T, Gancarz M, Kondracka A, Rusinek R, Oniszczuk A. Curcumin and weight loss: does it work? Int J Mol Sci 2022;23(2):639. ArticlePubMedPMC
• [53] Kotha RR, Luthria DL. Curcumin: biological, pharmaceutical, nutraceutical, and analytical aspects. Molecules 2019;24(16):2930. ArticlePubMedPMC
• [54] Kocaadam B, Şanlier N. Curcumin, an active component of turmeric (Curcuma longa), and its effects on health. Crit Rev Food Sci Nutr 2017;57(13):2889−95.ArticlePubMedPMC
• [55] Ejaz A, Wu D, Kwan P, Meydani M. Curcumin inhibits adipogenesis in 3T3-L1 adipocytes and angiogenesis and obesity in C57/BL mice. J Nutr 2009;139(5):919−25.ArticlePubMed
• [56] Aggarwal BB. Targeting inflammation-induced obesity and metabolic diseases by curcumin and other nutraceuticals. Annu Rev Nutr 2010;30:173−99.ArticlePubMedPMC
• [57] Shehzad A, Ha T, Subhan F, Lee YS. New mechanisms and the anti-inflammatory role of curcumin in obesity and obesity-related metabolic diseases. Eur J Nutr 2011;50(3):151−61.ArticlePubMedPDF
• [58] Shao W, Yu Z, Chiang Y, Yang Y, Chai T, Foltz W, et al. Curcumin prevents high fat diet induced insulin resistance and obesity via attenuating lipogenesis in liver and inflammatory pathway in adipocytes. PloS One 2012;7(1):e28784. ArticlePubMedPMC
• [59] Nelson KM, Dahlin JL, Bisson J, Graham J, Pauli GF, Walters MA. The essential medicinal chemistry of curcumin: miniperspective. J Med Chem 2017;60(5):1620−37.ArticlePubMedPMCPDF
• [60] Akubu J, Pandey AV. Innovative delivery systems for curcumin: exploring nanosized and conventional formulations. Pharmaceutics 2024;16(5):637. ArticlePubMedPMC
• [61] Stohs SJ, Chen O, Ray SD, Ji J, Bucci LR, Preuss HG. Highly bioavailable forms of curcumin and promising avenues for curcumin-based research and application: a review. Molecules 2020;25(6):1397. ArticlePubMedPMC
• [62] Bertoncini-Silva C, Vlad A, Ricciarelli R, Fassini PG, Suen VMM, et al. Enhancing the bioavailability and bioactivity of curcumin for disease prevention and treatment. Antioxidants (Basel) 2024;13(3):331. ArticlePubMedPMC
• [63] Tabanelli R, Brogi S, Calderone V. Improving curcumin bioavailability: current strategies and future perspectives. Pharmaceutics 2021;13(10):1715. ArticlePubMedPMC
• [64] Bhardwaj RK, Glaeser H, Becquemont L, Klotz U, Gupta SK, Fromm MF. Piperine, a major constituent of black pepper, inhibits human P-glycoprotein and CYP3A4. J Pharmacol Exp Ther 2002;302(2):645−50.ArticlePubMed
• [65] Brewster ME, Loftsson T. Cyclodextrins as pharmaceutical solubilizers. Adv Drug Deliv Rev 2007;59(7):645−66.ArticlePubMed
• [66] Choi SJ. Efficacy and toxicity of nanomaterials in foods. Food Sci Ind 2014;47(1):38−45. [in Korean] https://koreascience.kr/article/JAKO201413241735184.page
• [67] Chanburee S, Tiyaboonchai W. Mucoadhesive nanostructured lipid carriers (NLCs) as potential carriers for improving oral delivery of curcumin. Drug Dev Ind Pharm 2017;43(3):432−40.ArticlePubMed
• [68] Arul B, Kothai R. Anticancer effect of capsaicin and its analogues. Capsicum. London (UK), IntechOpen, 2020.Article
• [69] Li R, Lan Y, Chen C, Cao Y, Huang Q, Ho C-T, et al. Anti-obesity effects of capsaicin and the underlying mechanisms: a review. Food Funct 2020;11(9):7356−70.ArticlePubMed
• [70] Baboota RK, Singh DP, Sarma SM, Kaur J, Sandhir R, Boparai RK, et al. Capsaicin induces “brite” phenotype in differentiating 3T3-L1 preadipocytes. PLoS One 2014;9(7):e103093. ArticlePubMedPMC
• [71] Baskaran P, Krishnan V, Ren J, Thyagarajan B. Capsaicin induces browning of white adipose tissue and counters obesity by activating TRPV1 channel-dependent mechanisms. Br J Pharmacol 2016;173(15):2369−89.ArticlePubMedPMC
• [72] Lee MS, Kim C-T, Kim I-H, Kim Y. Effects of capsaicin on lipid catabolism in 3T3-L1 adipocytes. Phytother Res 2011;25(6):935−9.ArticlePubMedPDF
• [73] Hsu C-L, Yen GC. Effects of capsaicin on induction of apoptosis and inhibition of adipogenesis in 3T3-L1 cells. J Agric Food Chem 2007;55(5):1730−6.ArticlePubMed
• [74] Joo JI, Kim DH, Choi J-W, Yun JW. Proteomic analysis for antiobesity potential of capsaicin on white adipose tissue in rats fed with a high fat diet. J Proteome Res 2010;9(6):2977−87.ArticlePubMed
• [75] Lu M, Cao Y, Ho C-T, Huang Q. The enhanced anti-obesity effect and reduced gastric mucosa irritation of capsaicin-loaded nanoemulsions. Food Funct 2017;8(5):1803−9.ArticlePubMed
• [76] Mosqueda-Solís A, Sánchez J, Portillo MP, Palou A, Picó C. Combination of capsaicin and hesperidin reduces the effectiveness of each compound to decrease the adipocyte size and to induce browning features in adipose tissue of western diet fed rats. J Agric Food Chem 2018;66(37):9679−89.ArticlePubMed
• [77] Wang Y, Tang C, Tang Y, Yin H, Liu X. Capsaicin has an anti-obesity effect through alterations in gut microbiota populations and short-chain fatty acid concentrations. Food Nutr Res 2020;64. ArticlePubMedPDF
• [78] Merritt JC, Richbart SD, Moles EG, Cox AJ, Brown KC, Miles SL, et al. Anti-cancer activity of sustained release capsaicin formulations. Pharmacol Ther 2022;238:108177. ArticlePubMedPMC
• [79] Rollyson WD, Stover CA, Brown KC, Perry HE, Stevenson CS, McNees CA, et al. Bioavailability of capsaicin and its implications for drug delivery. J Control Release 2014;196:96−105.ArticlePubMedPMC
• [80] Hall OM, Broussard A, Range T, Turpin MAC, Ellis S, Lim VM, et al. Novel agents in neuropathic pain, the role of capsaicin: pharmacology, efficacy, side effects, different preparations. Curr Pain Headache Rep 2020;24(9):53. ArticlePubMedPDF
• [81] Arnold JT, Stewart S, Sammut L. Oral capsaicin ingestion: a brief update dose, tolerance and side effects. Res Rev J Herb Sci 2017;5(2):1−5. https://www.researchgate.net/profile/Josh-Arnold-4/publication/315718068_Oral_Capsaicin_Ingestion_A_Brief_Update_-_Dose_Tolerance_and_Side-Effects/links/59f33ee40f7e9b553eba60d0/Oral-Capsaicin-Ingestion-A-Brief-Update-Dose-Tolerance-and-Side-Effects.pdf
• [82] Tenchov R, Bird R, Curtze AE, Zhou Q. Lipid nanoparticles-from liposomes to mRNA vaccine delivery, a landscape of research diversity and advancement. ACS Nano 2021;15(11):16982−7015.ArticlePubMedPMCPDF
• [83] Couto VM, de Oliveira-Nascimento L, Cabeça LF, Geraldes DC, Costa JSR, Riske KA, et al. Capsaicin-cyclodextrin complex enhances mepivacaine targeting and improves local anesthesia in inflamed tissues. Int J Mol Sci 2020;21(16):5741. ArticlePubMedPMC
• [84] Zhou J, Zhang R, Lv P, Zhang S, Zhang Y, Yang J, et al. Acyclic cucurbit[n]urils-based supramolecular encapsulation for enhancing the protective effect of capsaicin on gastric mucosa and reducing irritation. Int J Pharm 2022;626:122190. ArticlePubMed
• [85] Francis G, Kerem Z, Makkar HPS, Becker KL. The biological action of saponins in animal systems: a review. Br J Nutr 2002;88(6):587−605.ArticlePubMed
• [86] Barbosa ADP. An overview on the biological and pharmacological activities of saponins. Int J Pharm Pharm Sci 2014;6(8):47−50. https://journals.innovareacademics.in/index.php/ijpps/article/view/1677/10298
• [87] Marrelli M, Conforti F, Araniti F, Statti GA. Effects of saponins on lipid metabolism: A review of potential health benefits in the treatment of obesity. Molecules 2016;21(10):1404. ArticlePubMedPMC
• [88] Hwang YP, Choi JH, Kim HG, Lee H-S, Chung YC, Jeong HG. Saponins from Platycodon grandiflorum inhibit hepatic lipogenesis through induction of SIRT1 and activation of AMP-activated protein kinase in high-glucose-induced HepG2 cells. Food Chem 2013;140(1–2):115−23.ArticlePubMed
• [89] Han LK, Xu BJ, Kimura Y, Zheng YN, Okuda H. Platycodi radix affects lipid metabolism in mice with high fat diet-induced obesity. J Nutr 2000;130(11):2760−4.ArticlePubMed
• [90] Luo Z, Xu W, Zhang Y, Di L, Shan J. A review of saponin intervention in metabolic syndrome suggests further study on intestinal microbiota. Pharmacol Res 2020;160:105088. ArticlePubMed
• [91] Yao Y, Zhu Y, Gao Y, Shi Z, Hu Y, Ren G. Suppressive effects of saponin-enriched extracts from quinoa on 3T3-L1 adipocyte differentiation. Food Funct 2015;6(10):3282−90.ArticlePubMed
• [92] Milgate J, Roberts D. The nutritional & biological significance of saponins. Nutr Res 1995;15(8):1223−49.Article
• [93] Baumann E, Stoya G, Völkner A, Richter W, Lemke C, Linss W. Hemolysis of human erythrocytes with saponin affects the membrane structure. Acta Histochemica 2000;102(1):21−35.ArticlePubMed
• [94] Cannon JG, Burton RA, Wood SG, Owen NL. Naturally occurring fish poisons from plants. J Chem Educ 2004;81(10):1457. Article
• [95] Wina E, Muetzel S, Becker K. The impact of saponins or saponin-containing plant materials on ruminant production--a review. J Agric Food Chem 2005;53(21):8093−105.ArticlePubMed
• [96] Clayton MJ, Davis TZ, Knoppel EL, Stegelmeier BL. Hepatotoxic plants that poison livestock. Vet Clin North Am Food Anim Pract 2020;36(3):715−23.ArticlePubMed
• [97] Karu N, Reifen R, Kerem Z. Weight gain reduction in mice fed Panax ginseng saponin, a pancreatic lipase inhibitor. J Agric Food Chem 2007;55(8):2824−8.ArticlePubMed
• [98] Zheng Q, Li W, Han L, Koike K. Pancreatic lipase-inhibiting triterpenoid saponins from Gypsophila oldhamiana. Chem Pharm Bull (Tokyo) 2007;55(4):646−50.ArticlePubMed
• [99] Yang J, Wang P, Wu W, Zhao Y, Idehen E, Sang S. Steroidal saponins in oat bran. J Agric Food Chem 2016;64(7):1549−56.ArticlePubMed
• [100] Mårtensson O, Biörklund M, Lambo AM, Dueñas-Chasco M, Irastorza A, Holst O, et al. Fermented, ropy, oat-based products reduce cholesterol levels and stimulate the bifidobacteria flora in humans. Nutr Res 2005;25(5):429−42.Article
• [101] Karmally W, Montez MG, Palmas W, Martinez W, Branstetter A, Ramakrishnan R, et al. Cholesterol-lowering benefits of oat-containing cereal in Hispanic Americans. J Am Diet Assoc 2005;105(6):967−70.ArticlePubMed
• [102] Nie Q, Chen H, Hu J, Tan H, Nie S, Xie M. Effects of nondigestible oligosaccharides on obesity. Annu Rev Food Sci Technol 2020;11:205−33.ArticlePubMed
• [103] Kumar N, Shah P, Agarwal S. Unraveling the potential of natural anti-obesity agents: an insight. Thai J Pharmac Sci 2024;48(2):7. Article
• [104] Shiraiwa M, Harada K, Okubo K. Composition and content of saponins in soybean seed according to variety, cultivation year and maturity. Agric Biol Chem 1991;55(2):323−31.Article
• [105] Timilsena YP, Phosanam A, Stockmann R. Perspectives on saponins: food functionality and applications. Int J Mol Sci 2023;24(17):13538. ArticlePubMedPMC

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