INTRODUCTION:

Obesity is emerging as a significant global health issue, linked to numerous serious diseases. It is characterized by excessive fat accumulation that adversely affects health, increasing the risk of various conditions. High-risk obesity necessitates intervention to prevent further health complications. As a multifactorial disease, obesity is on the rise, influenced by factors such as physical inactivity, poor diet, environmental conditions, medications, certain medical procedures, underlying health issues, and genetics. The development of obesity primarily hinges on the balance between energy intake and energy expenditure. A 2022 study highlighted the prevalence of obesity, revealing that 1 in 8 individuals worldwide is affected, with over 2.5 billion people categorized as overweight. Notably, the highest incidence of obesity is found among young adults aged 18 and older, underscoring the potential health risks facing future generations.¹ Obesity is commonly assessed using the Body Mass Index (BMI), a tool that evaluates body fat based on an individual's weight and height. A BMI of 24 is classified as normal;

· Values above this threshold indicate overweight or obesity underweight (BMI less than 18.5),

· Normal weight (BMI 18.5 to 24.9),

· Overweight (BMI 25 to 29.9),

· Obese (BMI 30 and above).²

To mitigate the risk of obesity-related diseases, individuals are encouraged to maintain physical activity and a supportive environment. Currently, pharmacological options exist for the treatment of Class III obesity, although these medications often present significant side effects and limited efficacy. Orlistat is the only FDA-approved drug specifically for obesity treatment, but it is associated with side effects such as gastric irritation and oily stools. There is a pressing need for more effective treatments that minimize side effects and enhance patient outcomes.³

Possible Treatment:

There are two main types of agents used for the treatment of obesity: peripheral nervous system (PNS) active agents and central nervous system (CNS) active agents. CNS active agents tend to have more side effects and require higher doses, whereas PNS active agents demonstrate greater efficacy. Thermogenic agents, while often utilized, require high doses and generally exhibit low efficacy. Among the options available for treating obesity, pancreatic lipase inhibitors stand out due to their effectiveness, impacting 70-80% of the metabolic process. The mechanism of fat accumulation in the body primarily involves the breakdown of triglycerides. During metabolism, triglycerides are converted to free fatty acids by the pancreatic lipase enzyme. This process increases fat levels in the body, leading to excessive fat accumulation. The lipase enzyme binds to fat molecules, forming oily globules that are then absorbed by the intestinal mucosa, contributing to fat storage. Pancreatic lipase inhibitors effectively prevent this excess absorption by inhibiting the action of pancreatic lipase.⁴ They bind to the lipase enzyme, preventing it from interacting with fat molecules, thereby inhibiting the breakdown of triglycerides. As a result, fat remains unbroken and is not absorbed into the duodenal mucosa, instead passing through the colon unabsorbed.

The development of obesity is closely linked to body fat metabolism. Approximately 90% of the typical diet consists of mixed triglycerides. Exogenous fats cannot be used directly by the human body and must be hydrolyzed for absorption. The digestive system contains several lipases, including tongue lipase, gastric lipase, and pancreatic lipase. Gastric lipase is significant for regulating the secretion of pancreatic lipase and aids in lipolysis.⁵ However, pancreatic lipase (PL) is the most crucial, as it directly influences the absorption of fatty acids in the intestine. Pancreatic lipase is the primary enzyme secreted by the pancreas, responsible for hydrolyzing dietary lipids. It converts triacylglycerol substrates from ingested fats into monoglycerides and free fatty acids. In the intestine, these monoglycerides and free fatty acids are absorbed by enterocytes, the cells lining the intestinal wall. After fat-containing food is consumed, triglyceride-based lipids are initially hydrolyzed by lipases into monoglycerides, glyceryl esters, and free fatty acids, with higher concentrations of 1,2-glycolide and fatty acids in the resulting products. While the degradation of fat by lingual lipase is minimal, it can account for 50% to 70% of fat digestion in infants and young children. Subsequently, gastric lipase hydrolyzes about 10% to 30% of the fat, and pancreatic lipase accounts for 50% to 70% of fat breakdown in the gastrointestinal tract and small intestine. This process leads to the formation of cholesterol and lipoproteins in the body. Lipid particles mixed with bile acids are absorbed by the small intestine, where they are re-synthesized into triacylglycerols, storing energy as adipose tissue.⁶

Lipase inhibitors work by binding to the active site of lipases in the stomach and small intestine, altering their conformation and inhibiting their catalytic activity. This process reduces the breakdown of lipids, such as triglycerides, thereby decreasing lipid digestion and absorption, which helps control and treat obesity. After acting, lipase inhibitors are typically excreted along with the lipases they bind to, meaning they do not cause long-term effects in the body. Currently, commonly used weight loss medications include peripheral lipase inhibitors and central appetite suppressants, categorized into two main types: (1) medications that inhibit fat absorption, such as orlistat, and (2) central nervous system appetite suppressants, primarily fenfluramine and sibutramine.⁷ However, clinical studies have shown that these appetite suppressants can lead to adverse reactions, including headaches, dizziness, dry mouth, bitterness, constipation, and insomnia. More severe reactions may involve mental health or cardiovascular issues, which limits their clinical use and has led to some medications being withdrawn from the market. Given that the safety of central appetite suppressants is not fully established, the advantages of peripheral lipase inhibitors lie in their inability to enter the bloodstream or affect the nervous system. They do not disrupt the body's mineral balance or bone circulation, making them relatively safe options for obesity treatment.⁸

Orlistat, also known as tetrahydrolipstatin, is an anti-obesity drug approved by the U.S. FDA. It is a saturated derivative of lipstatin, a natural compound produced by Streptomyces toxytricini. Orlistat works to control obesity by reversibly inhibiting gastric and pancreatic lipases in the digestive system. These enzymes are essential for breaking down triglycerides into free fatty acids and monoglycerides, which can then be absorbed. By binding covalently to the serine residues in the active sites of these lipases, orlistat deactivates them. This inhibition prevents triglyceride breakdown, reducing the absorption of free fatty acids. However, orlistat is associated with several side effects, including altered bowel movements, oily stools, and gastric irritation. Additionally, it requires a high dose to achieve a limited effect. Naturally occurring molecules that act as pancreatic lipase inhibitors present a preferable alternative for obesity treatment.

The pancreatic lipase inhibitory effects of natural products have been widely studied to assess their potential as anti-obesity agents. Given the significant success of natural products in obesity management, research efforts have increasingly focused on identifying new pancreatic lipase inhibitors that cause fewer undesirable side effects. To date, numerous natural products, including plant extracts and isolated compounds, have been reported for their ability to inhibit pancreatic lipase. Naturally derived pancreatic lipase inhibitors from herbs offer a promising approach for the treatment of obesity. Compared to synthetic drugs, which often have lower efficacy and more side effects, herbal alternatives present a safer and more effective option for obesity management.⁹

Table 1. Natural molecules as pancreatic lipase:

Name of plant	Molecule name	IC₅₀	Summary
Cassia auriculata¹⁰	Kaempferol 3-O-rutinoside	2.9µM	Kaempferol 3-O-rutinoside from the methanolic extract of the leaves of Eremochloa ophiuroides (centipede grass), has reported to inhibit the pancreatic lipase
Eremochloa ophiuroides¹⁰	Luteolin-6-C-β-D-boivinopyranoside	50.5±3.9µM	Luteolin-6-C-β-D-boivinopyranoside from the methanolic extract of the leaves of Eremochloa ophiuroides (centipede grass), has reported to inhibit the pancreatic lipase
	Orientin	31.6±2.7µM	Orientin from the methanolic extract of the leaves of Eremochloa ophiuroides (centipede grass), has reported to inhibit the pancreatic lipase
	Isoorientin	44.6±1.3µM	Isoorientin from the methanolic extract of the leaves of Eremochloa ophiuroides (centipede grass), has reported to inhibit the pancreatic lipase
	Derhamnosylmaysin	25.9±3.7µM	Derhamnosylmaysin from the methanolic extract of the leaves of Eremochloa ophiuroides (centipede grass), has reported to inhibit the pancreatic lipase
	Isoorientin-2-O-α-L- rhamnoside	18.5±2.6µM	Isoorientin-2-O-α-L-rhamnoside from the methanolic extract of the leaves of Eremochloa ophiuroides (centipede grass), has reported to inhibit the pancreatic lipase
Glycyrrhiza glabra¹¹	Licuroside	14.9μM	Licuroside from Glycyrrhiza glabra roots showed strong inhibition against pancreatic lipase
	Isoliquiritoside	37.6μM	Isoliquiritoside from Glycyrrhiza glabra roots showed strong inhibition against pancreatic lipase
Alpinia galanga¹²	Galangin	48.20mg/mL	Galangin isolated from Alpinia galanga rhizomes was found to inhibit pancreatic lipase
Citrus Unshiu¹³	Hesperidin	32µg/mL	Hesperidin isolated from the peels of Citrus unshiu, depicted reduction in the activity of the porcine pancreatic lipase
	Neohesperidin	46µg/mL	Neohesperidin isolated from the peels of Citrus unshiu, depicted reduction in the activity of the porcine pancreatic lipase
Filipendula kamtschatica¹⁴	3-O-caffeoyl-4-O-galloyl-L-threonic acid	26µM.	3-O-caffeoyl-4-O-galloyl-L-threonic acid, isolated from Filipendula kamtschatica possessing pancreatic lipase’s substrate like structure was found to inhibit the enzyme
Eremochloa ophiuroides¹⁵	Methyl chlorogenate	33.6±2.0µM.	Methyl chlorogenate from the methanolic extract of the leaves of Eremochloa ophiuroides (centipede grass), has reported to inhibit pancreatic lipase
Cassia Mimosoides ¹⁶	3′,4′,7-trihydroxyflavan-(4α→8)-catechin	5.5µM	3′,4′,7-trihydroxyflavan-(4α→8)-catechin from hydromethanolic extract of the fruits Cassia mimosoides L. var. nomame Makino (Nomame Herba) showed pancreatic lipase
Glycyrrhiza glabra ¹⁷	Isoliquiritigenin	7.3μM	Isoliquiritigenin from Glycyrrhiza glabra roots demonstrated strong inhibition against pancreatic lipase
	3,3′,4,4′- tetrahydroxy-2-methoxychalcone	35.5μM	3,3′,4,4′tetrahydroxy-2-methoxychalcone from Glycyrrhiza glabra roots demonstrated strong inhibition against pancreatic lipase
Cassia Siamea ¹⁸	Cassiamin A	41.8µM	Cassiamin A a bianthraquinone from extract of Cassia Siamea, as most active compound for pancreatic lipase inhibition
Oolong Tea plant ^19-21	Epigallocatechin- 3-O-gallate (EGCG)	0.349µM	From Oolong Tea plant, (-)-epigallocatechin-3-O-gallate (EGCG)have been reported to show pancreatic lipase inhibition
	Epigallocatechin-3,5-digallate	0.098µM	From Oolong Tea plant epigallocatechin-3,5-digallate have been reported to show pancreatic lipase inhibition
	Oolonghomobisflavan A	0.048µM	Oolonghomobisflavan A have been reported to show pancreatic lipase inhibition
	Oolonghomobisflavan B	0.108µM	Oolonghomobisflavan B have been reported to show pancreatic lipase inhibition
	Oolongtheanin 3′-O-gallate	0.068µM	Oolongtheanin 3′-O-gallate have been reported to show pancreatic lipase inhibition
	Prodelphinidin B-2,3,3′-di-O-gallate	0.107µM,	Prodelphinidin B-2,3,3′-di-O-gallate have been reported to show pancreatic lipase inhibition
	Assamicain A	0.120µM,	Assamicain A have been reported to show pancreatic lipase inhibition
	Theasinensin D	0.098µM,	Theasinensin D have been reported to show pancreatic lipase inhibition
	Oolongtheanin-3′-O-gallate	0.068µM,	Oolongtheanin-3′-O-gallate have been reported to show pancreatic lipase inhibition
	Theaflavin	0.106µM,	Theaflavin have been reported to show pancreatic lipase inhibition
	Theaflavin-3,3′-O-gallate	0.092µM,	Theaflavin-3,3′-O-gallate have been reported to show pancreatic lipase inhibition
Acanthopanax sessiliflorus ²²	Sessiloside	0.36mg/mL	Sessiloside from the fruits of Acanthopanax senticosus, have been reported for inhibition of pancreatic lipase
	Chiisanoside	0.75mg/mL	Chiisanoside from the fruits of Acanthopanax senticosus, have been reported for inhibition of pancreatic lipase
	Silphioside F	0.22mM.	Silphioside F from the fruits of Acanthopanax senticosus, have been reported for inhibition of pancreatic lipase
	Copteroside B	0.25mM.	Copteroside B from the fruits of Acanthopanax senticosus, have been reported for inhibition of pancreatic lipase
	Hederagenin 3-O-β-D-glucuronopyranoside 6′-O-methyl ester	0.26mM.	Hederagenin 3-O-β-D-glucuronopyranoside 6′-O-methyl ester from the fruits of Acanthopanax senticosus, have been reported for inhibition of pancreatic lipase
	Gypsogenin 3-O-β-D- glucuronopyranoside	0.29mM.	Gypsogenin 3-O-β-D-glucuronopyranoside from the fruits of Acanthopanax senticosus, have been reported for inhibition of pancreatic lipase
Platycodin grandiflorum ²³	Platycodin D	0.18±0.03 mM.	Platycodin grandiflorum. Platycodin D has been reported for the inhibition of pancreatic lipase competitively
	Chakasaponins I	0.17mM	Chakasaponins I, isolated from butanol soluble fraction prepared from the flower buds of Chinese tea plant were reported to have an inhibitory effect against porcine pancreatic lipase
	Chakasaponins II	0.18mM	Chakasaponins II, isolated from butanol soluble fraction prepared from the flower buds of Chinese tea plant were reported to have an inhibitory effect against porcine pancreatic lipase
	Chakasaponins III	0.53mM	Chakasaponins III, isolated from butanol soluble fraction prepared from the flower buds of Chinese tea plant were reported to have an inhibitory effect against porcine pancreatic lipase
Dioscorea nipponica Makino ²⁴	Dioscin	20µg/mL	Dioscin from the methanol extract of roots of Dioscorea nipponica Makino possessed the inhibitory potential against pancreatic lipase
	Diosgenin	28µg/mL	Diosgenin from the methanol extract of roots of Dioscorea nipponica Makino possessed the inhibitory potential against pancreatic lipase
	Prosapo- genin A	1.8µg/mL	Prosapogenin A from the methanol extract of roots of Dioscorea nipponica Makino possessed the inhibitory potential against pancreatic lipase
	Prosapogenin C	42.2µg/mL	Prosapogenin C from the methanol extract of roots of Dioscorea nipponica Makino possessed the inhibitory potential against pancreatic lipase
	Gracillin	28.9µg/mL	Gracillin from the methanol extract of roots of Dioscorea nipponica Makino possessed the inhibitory potential against pancreatic lipase
Gardenia jasminoides²⁵	Crocin	2.1mg/mL	Crocin from the fructus of Gardenia jasminoides ELLIS water extract, were found to have potent hypotriglyceridemic and hypo cholesterolemic effects, along with the pancreatic lipase inhibition
	Metabolite crocetin	2.6mg/mL	Metabolite crocetin from the fructus of Gardenia jasminoides ELLIS water extract, were found to have potent hypotriglyceridemic and hypo-cholesterolemic effects, along with the pancreatic lipase inhibition
Actinidia arguta²⁶	3-O-trans-p-coumaroyl actinidic acid	14.95±0.21µM	3-O-trans-p-coumaroyl actinidic acid isolated from an ethyl acetate extract of the roots of Actinidia arguta, have been reported to possess pancreatic lipase
	ursolic acid	15.83±1.10µM	Ursolic acid isolated from an ethyl acetate extract of the roots of Actinidia arguta, have been reported to possess pancreatic lipase
	23-hydroxyursolic acid	41.67±0.66µM	23-hydroxyursolic acid isolated from an ethyl acetate extract of the roots of Actinidia arguta, have been reported to possess pancreatic lipase
	Corosolic acid	20.42±0.95µM	Corosolic acid isolated from an ethyl acetate extract of the roots of Actinidia arguta, have been reported to possess pancreatic lipase
	Asiatic acid	76.45±0.51µM	Asiatic acid isolated from an ethyl acetate extract of the roots of Actinidia arguta, have been reported to possess pancreatic lipase
	Betulinic acid	21.10±0.55µM	Betulinic acid isolated from an ethyl acetate extract of the roots of Actinidia arguta, have been reported to possess pancreatic lipase
Salvia officinalis ²⁷	Carnosic acid	12µg/mL	Carnosic acid from the methanolic extract of Salvia officinalis leaves, were reported to inhibit pancreatic lipase
	Carnosol	4.4µg/mL	Carnosol from the methanolic extract of Salvia officinalis leaves, were reported to inhibit pancreatic lipase
	Roylenoic acid	35µg/mL	Roylenoic acid from the methanolic extract of Salvia officinalis leaves, were reported to inhibit pancreatic lipase
	7-methoxyrosmanol	32µg/mL	7-methoxyrosmanol from the methanolic extract of Salvia officinalis leaves, were reported to inhibit pancreatic lipase
	Oleanolic acid	83µg/mL	Oleanolic acid from the methanolic extract of Salvia officinalis leaves, were reported to inhibit pancreatic lipase
Black tea ²⁸	Caffeine	1.12mg/mL	Caffeine from black tea were reported to inhibit pancreatic lipase
Dried ginger powder ²⁹	Ginger alcohol, ginger phenol	1.29mg/mL	Ginger alcohol, ginger phenol from dried ginger powder were reported to inhibit pancreatic lipase
Adzuki bean ³⁰	Polyphenols	12.5μg/mL	Polyphenols from adzuki bean were reported to inhibit pancreatic lipase
Buckwheat ³¹	Flavonoids, buckwheat alcohol	1.94mg/mL	Flavonoids, buckwheat alcohol from buck wheat are reported to inhibit pancreatic lipase
White birch ³²	Birch acid	21.10mM	Birch acid from white birch were reported to inhibit pancreatic lipase
Mangosteen (Garcinia)³³	α-mangostin	5.0μM	α-mangostin from mamgosteen were reported to inhibit pancreatic lipase
Chamaecrista ³⁴	Luteolin	7.1μM	Effect of luteolin from Chamaecrista nomame and reported that glycosylation mainly affects and modulate PLE activity
Cudrania tricuspidate ³⁵	5,7,4′-Trihydroxy-6,8diprenylisoflavone	65.0μM	isolated a compound 5,7,4′-Trihydroxy-6,8diprenylisoflavone from Cudrania tricuspidata and a showed PLE inhibition
Santalum acuminatum ³⁶	Cyanidin-3 glucoside	0.6mg/mL	Methanolic extract of Santalum acuminatum contain compounds cyanidin-3 glucoside and quercetin
	Quercetin	0.6mg/mL	Methanolic extract of Santalum acuminatum contain compounds cyanidin-3 glucoside and quercetin
Alpinia officinarum ³⁷	Galangin	48.20mg/ml	It was proposed that the compounds galangin and 3-methylgalangin could be responsible for the PLE inhibition.
	3-methylgalangin	3mg/mL	It was proposed that the compounds galangin and 3-methylgalangin could be responsible for the PLE inhibition.
Camellia sinensis ³⁸	Chakasaponins I	0.17mM	Camellia sinensis such as chakasaponins I, reported to have a PLE inhibition
	Chakasaponins II	0.18mM	Camellia sinensis such as chakasaponins II and reported to have a PLE inhibition
	Chakasaponins III	0.53mM	Camellia sinensis such as chakasaponins III and reported to have a PLE inhibition
Panax ginseng ³¹	Ginseng saponin	500μg/mL	The effects of Panax ginseng and isolated ginseng saponin that showed PLE inhibition activity
Sapindus rarak ¹⁸	Rarasaponins I	131μM	Studied the activity of Sapindus rarak and identified rarasaponins I and showed PLE inhibition activity
	Rarasaponins II	172μM	Studied the activity of Sapindus rarak and identified rarasaponins II, showed PLE inhibition activity
	Raraoside A	151μM	Studied the activity of Sapindus rarak and identified raraoside A and showed PLE inhibition activity
	Saponin E1	270μM	Studied the activity of Sapindus rarak and identified saponin E1 and showed PLE inhibition activity
Actinidia arguta ³⁹	3-O-trans-p-coumaroyl actinidic acid,	14.95± 0.21μM	3-O-trans-p-coumaroyl actinidic acid, reported with PLE inhibitory activity
	Ursolic acid	15.83±1.10 μM	Ursolic acid reported with PLE inhibitory activity
	23-hydroxyursolic acid	41.67± 0.66μM	23-hydroxyursolic acid reported with PLE inhibitory activity
	Corosolic acid,	20.42±0.95 μM	Corosolic acid, reported with PLE inhibitory activity
	Asiatic acid	76.45±0.51 μM	Asiatic acid reported with PLE inhibitory activity
	Betulinic acid	21.10±0.55 μM	Betulinic acid reported with PLE inhibitory activity
Ginkgo biloba ³⁶	Ginkgolides A	22.9μg/ml	Ginkgo biloba and isolated trilactone terpenes such as ginkgolides A showed PLE inhibition
	Ginkgolides B	90.0μg/ml	Ginkgo biloba and isolated trilactone terpenes such as ginkgolides B showed PLE inhibition
	Bilobalide	60.1μg/ml	Ginkgo biloba and isolated trilactone terpenes such as bilobalide showed PLE inhibition
Monarda punctata ^40-42	Carvacrol	4.07mM	Isolated carvacrol from Monarda punctata and reported to have PLE inhibitory activity
	10α-hydroxy-1α,4αendoperoxy-guaia-2-en-12,6α-olide	161.0μM	Isolated sesquiterpene lactone such as 10α-hydroxy-1α,4αendoperoxy-guaia-2-en-12,6α-olide from Chrysanthemum morifolium that showed PLE inhibition

CONCLUSION:

Natural products have long served as an inspiration for developing new therapeutic agents. However, despite this potential, orlistat remains the only natural product-based drug in clinical use for obesity. This underscores the urgent need to discover new leads from natural sources that can be developed into anti-obesity treatments. Natural compounds and dietary phytomolecules offer the advantages of being biologically compatible and chemically diverse. Many natural products, particularly phenolics, terpenes, and saponins, have demonstrated significant inhibition of pancreatic lipase. Although research on pancreatic lipase inhibitors from natural sources is ongoing, none have yet advanced to clinical use. Natural product-inspired molecules could provide promising leads or pharmacophores for further development. Nonetheless, more research is required to validate the inhibitory activity of these plants. Additionally, these promising plants are valuable as starting materials for isolating, identifying, and characterizing phytoactive compounds for the development of anti-obesity functional agents. Natural product-derived lipase inhibitors have emerged as significant areas of research. Compared to synthetic lipase inhibitors, those derived from plants are more accessible, cost-effective, relatively safe, and reliable. However, they may vary in inhibition strength, and identifying active components can be challenging. These natural inhibitors are instrumental in the development of weight-loss drugs and health products. While extensive research has shown that some natural products have notable inhibitory effects on lipase, few have advanced to clinical applications. This limited progress is likely due to factors such as the low concentration of active ingredients, complex extraction processes, and low recovery rates, which hinder large-scale production. This also represents a significant bottleneck in the industrial production of lipase inhibitors from medicinal and edible plants. By further exploring the mechanism of action and structure-activity relationship of natural compounds on pancreatic lipase, and continually screening for highly active inhibitors, lead compounds from natural products could be identified. Subsequent chemical modifications and microbial methods could enhance yield, resulting in pancreatic lipase inhibitors with greater potency and production efficiency, which could ultimately be applied in clinical obesity treatments.

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Received on 03.10.2024 Revised on 08.12.2024

Accepted on 16.01.2025 Published on 10.05.2025

Available online from May 14, 2025

Res. J. Pharmacognosy and Phytochem. 2025; 17(2):116-122.

DOI: 10.52711/0975-4385.2025.00020

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