eISSN: 1897-4317
ISSN: 1895-5770
Gastroenterology Review/Przegląd Gastroenterologiczny
Bieżący numer Archiwum Artykuły zaakceptowane O czasopiśmie Rada naukowa Bazy indeksacyjne Prenumerata Kontakt Zasady publikacji prac
Panel Redakcyjny
Zgłaszanie i recenzowanie prac online
Portal dla gastroenterologów!
SCImago Journal & Country Rank
vol. 19
Poleć ten artykuł:
Artykuł oryginalny

Inhibitory effect of stinging nettle (Urtica dioica L.) extract on body weight gain in rats on a high-fat diet

Kenan Kaçak
Turan Yaman
Ahmet Uyar
Ahmet Ufuk Kömüroğlu

Siirt State Hospital, Siirt, Turkey
Department of Pathology, Faculty of Veterinary Medicine, Van Yuzuncu Yil University Van, Turkey
Department of Pathology, Faculty of Veterinary Medicine, Hatay Mustafa Kemal University, Hatay, Turkey
Health Service Vocational School of Higher Education, Van Yuzuncu Yil University, Van, Turkey
Gastroenterology Rev 2024; 19 (1): 23–32
Data publikacji online: 2023/07/31
Plik artykułu:
Pobierz cytowanie
Metryki PlumX:


Overweight and obesity are serious illnesses that result from an imbalance between energy intake and expenditure, leading to the subsequent accumulation of excess fat in the body [1]. The prevalence of overweight and obesity have been increasing worldwide at an alarming rate over the past few years and have become major public health concerns among all global populations and age groups [2]. Obesity is associated with several diseases, including coronary heart disease, type 2 diabetes, metabolic syndrome, stroke, and cancers, and it is therefore also associated with significantly increased morbidity and mortality rates [3].

Lifestyle changes and pharmacotherapy interventions have been investigated as potential obesity treatment methods [4]. However, despite some short-term benefits, drug treatments have been associated with various problems, including weight gain after drug discontinuation, intolerable side effects, and addiction [5]. Due to the complex pathogenesis of obesity, lifestyle modification interventions have also had disappointing results, and there remains a need for simple, acceptable obesity treatments [5].

Herbal supplements [6], natural products, and medicinal plants, including both crude extracts and compounds isolated from plants, are the most common complementary and alternative methods used to induce weight loss and prevent dietary obesity, and they are widely used across the globe. Plants contain several components with different anti-obesity and antioxidant properties that can affect body metabolism and fat oxidation. Furthermore, plant extracts have been widely used in recent years to better manage obesity [7, 8].

The stinging nettle plant, Urtica dioica (UD), is a species of the family Urticaceae, whose roots, leaves, and seeds are used in folk treatments for many diseases [9]. Steroids [10], terpenoids [11], phenylpropanoids, coumarins [12], and polysaccharides [13] have been isolated from their roots, and 7 flavanol glycosides (kaempherol-3-O-glucoside and -3-O-rutinoside; quercetin-3-Olucoside and -3-O-rutinoside; and isorhamnetin-3-O-glucoside, -3-O-rutinoside, and -3-Oneohesperidoside) [10] have been isolated from their flowers. These major flavonoid glycosides have immunostimulatory, anticarcinogenic, anti-inflammatory, antioxidant, and antiallergenic properties [14, 15]. UD has been demonstrated to have anti-inflammatory [16], acute diuretic, natriuretic, and hypotensive effects [17], and it has also been reported to treat stomach pain [18], liver failure [19], rheumatic pain, colds, and coughs [20].


The present study sought to investigate the preventive effects of UD seed extract on high-fat diet-induced (HFD) obesity in rats.

Material and methods


Thirty-two 4–5-week-old male Wistar albino rats were provided by the animal house of the Medical School of Yuzuncu Yil University. Animals were housed at 20 ±2°C in a 24-h light/dark cycle. All animals were kept in stainless cages and fed with a wheat-soybean-meal-based diet. Water and feed were offered ad libitum. The animals received humane care according to the criteria outlined in the ‘Guide for the Care and Use of Laboratory Animals’ prepared by the National Academy of Science and published by the National Institutes of Health. Ethical regulations were followed in accordance with national and institutional guidelines for the protection of animal welfare during experiments. Ethical approval was obtained from the Animal Experiments Local Ethics Committee of Van Yuzuncu Yil University (26.01.2017/01).

Plant material

For extraction, the UD seeds were ground in an electric mill. UD seed extract was obtained with ether [15]. UD extract was given by daily orogastric gavage to 300 mg/kg body weight [21, 22].

High-fat diet

A standard pellet feed obtained from a special commercial feed manufacturer was milled. Subsequently, 300 g/kg of butter was added to the feed to form a high-calorie (approximately 4000 kcal/kg), high-fat (60% of its energy consisted of saturated fat) pellet feed that was fed to all of the rats in the 2 HFD groups [23].

Experiment design

Male Wistar albino rats (n = 32) were randomly divided into 4 groups of 8 rats each.

Control group: During the experiment, the rats received a standard pellet diet and tap water ad libitum.

HFD group: During the experiment, the rats received the high-fat pellet diet ad libitum.

HFD + UD group: During the experiment, the rats received UD extracts (300 mg/kg bw) and the HFD.

UD group: During the experiment, the rats received UD extracts (300 mg/kg bw) and standard pellet diet.

UD extracts were given by daily orogastric gavage. After 75 days, all the rats were weighed, euthanised, and necropsied, and then tissue and blood samples were taken.

Biochemical examination

For biochemical analysis, blood and tissue samples were taken from the rats at the end of the experiment. Alanine transaminase (ALT), aspartic transaminase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), γ-glutamyl transferase (GGT), cholesterol, triglyceride, high-density lipoprotein (HDL) cholesterol, and high-density lipoprotein (LDL) cholesterol activities were examined.

Histopathological examination

Tissue samples taken from sacrificed rats were fixed in 10% neutral formalin and embedded in paraffin by routine methods. Sections 5 µm in thickness were cut for histological examination. The slides were examined and photographed using an E-400 light microscope (Nikon, Japan) equipped with a DS-Ri2 video camera and DSU3 microscope video camera controller (Nikon, Japan). Each section was evaluated for histopathological findings such as hepatic steatosis, necrosis, inflammation, and fibrosis. Ten 200× light microscopic fields were viewed on each section and scored for the severity of hepatic steatosis, according to the following criteria [24] for hepatic steatosis: grade 0, no fat; grade 1, steatosis occupying less than 33% of the hepatic parenchyma; grade 2, 34–66% of the hepatic parenchyma; and grade 3, more than 66% of the hepatic parenchyma.

Oil Red O staining

The GBL (Gül Biology Laboratory) commercial kit was used. Sections were stained according to the procedure specified in the kit.

Statistical analysis

All data were expressed as mean ± standard deviation (SD). The statistical analyses were made using SPSS 20.0 for MS Windows. One-way ANOVA statistical test was used to determine the differences between means of the treatment and the control group, accepting the significance level at p ≤ 0.05.


Body weight

The effects of the HFD and UD on the body weights of the rats are shown in Figure 1.

Figure 1

Effects of the HFD and UD on the body weights of the rats


Histopathological findings

The histopathological examinations showed a normal histological structure in the liver tissues of the rats in the control group (Figure 2 A). However, the rats in the HFD group all had sharply circumscribed vacuoles of different sizes in their hepatocyte cytoplasm, and many also had coagulative necrosis in their liver parenchyma. The nuclei of the necrotic hepatocytes were darkly stained and pyknotic, and their cytoplasms were eosinophilic. Hydropic degeneration was also present, to varying degrees, in hepatocytes of the rats in the HFD group. Some of the rats in the HFD group also had congestion in some of their vena centralis, as well as dilatation in their sinusoids (Figure 2 B). All the rats in the HFD + UD group had similar histopathology findings to the rats in the HFD group, but to a significantly lesser extent. In particular, their fat vacuoles were considerably reduced and were restricted to the hepatocytes in the centrilobular region. Similarly, there was a noteworthy reduction in the amount of necrosis (Figure 2 C). The histopathological examinations showed a normal histological structure in the liver tissues of the rats in the control and UD groups (Figure 2 D).

Figure 2

A – Normal histological structure of the liver in the Control group. B – Sharply circumscribed fat vacuoles of varying sizes (arrows) in the hepatocytes, and coagulative necrosis (arrowheads) and vena centralis congestion in the HFD group. C – Sharply circumscribed fat vacuoles (arrowheads) of varying sizes observed in the hepatocytes of the centrilobular region in the HFD + UD group. D – Normal histological structure of the liver (H&E) in the UD group


Because severe hepatic steatosis was observed in both groups of rats that were fed the HFD, we aimed to clarify whether the fat accumulation was induced in the liver via staining of the liver tissues with Oil Red O. This clearly demonstrated that there were Grade 2 triglyceride deposits in the hepatocytes of the rats in the HFD group and Grade 1 triglyceride deposits in the rats in the HFD + UD group. No deposits were detected in the rats in the control or UD groups (Figures 3 A–D).

Figure 3

Oil Red O staining results in the groups. A – No deposits observed in the Control group. B – Large orange-red oil deposits observed in HFD group (arrows). C – Smaller orange-red oil deposits observed in the HFD + UD group (arrows). D – No deposits observed in the UD group


Biochemical findings

Serum AST, ALT, ALP, and LDH levels are biomarkers of liver damage that can function as biochemical indicators of liver-protective effects. Serum ALT and ALP levels were significantly higher in the HFD group than in the other 3 groups. Although they were substantially lower in the HFD + UD group, they were still higher than in the control group. There were no statistically significant differences between the serum AST and LDH levels between any of the groups. The mean values of the control and intervention groups with the standard errors are shown in Table I.

Table I

Effect of HFD and UD extract on serum AST, ALT, LDH, and ALP levels

ParametersControlHFDHFD + UDUD
AST [U/l]79.40 ±4.12a83.33 ±5.58a90.13 ±5.47a88.71 ±4.49a
ALT [U/l]37.71 ±1.52a53.37 ±2.35b41.55 ±1.51a36.50 ±1.94a
LDH [U/l]571.00 ±80.35a532.78 ±66.42a473.63 ±49.73a595.57 ±94.512a
ALP [U/l]281.86 ±26.82a396.11 ±31.71b322.25 ±15.77c233.14 ±26.19a

[i] AST – aspartate aminotransferase, ALT – alanine aminotransferase, LDH – lactate dehydrogenase, ALP – alkaline phosphatase. Each value represents the mean ± SD. Different letters in each row represent statistical significance (p < 0.05).

The triglyceride, high-density lipoprotein (HDL), low-density lipoprotein (LDL), and cholesterol levels of the rats in all 4 of the groups are shown in Figures 4–7. When compared to the rats in the control group, rats of the HFD group had higher levels of triglyceride, LDL, and cholesterol, while HDL levels were reduced. However, the triglyceride and LDL levels were lower, and the HDL and cholesterol levels were higher, in the rats in the HFD + UD group when compared with those in the HFD group.

Figure 4

Effects of the HFD and UD on the triglyceride levels. Each value represents the mean ± SD. Different superscripts in each column represent statistical significance at p < 0.05

Figure 5

Effects of the HFD and UD on the HDL levels. Each value represents the mean ± SD. Different superscripts in each column represent statistical significance at p < 0.05

Figure 6

Effects of the HFD and UD on the LDL levels. Each value represents the mean ± SD. Different superscripts in each column represent statistical significance at p < 0.05

Figure 7

Effects of the HFD and UD on the cholesterol levels. Each value represents the mean ± SD. Different superscripts in each column represent statistical significance at p < 0.05



Malnutrition due to increased consumption of ‘ready-to-eat’ foods containing high levels of fat and carbohydrates can cause hepatic steatosis and obesity [25], and human studies have shown that an HFD, defined as one in which more than 30% of dietary energy comes from fats, can induce obesity [26]. Several different methods have been investigated to reduce body weight and its associated complications. Disappointing results from both lifestyle modifications and pharmacotherapy treatments have forced researchers and physicians to look for new, safe, and effective treatment alternatives [5]. Many plants have, therefore, been examined for anti-obesity properties, along with potential mechanisms to isolate and extract their pure components. Herbal remedies stand out as a potentially effective option to reduce body weight and body fat [27]. The present study, therefore, sought to investigate the histopathological and biochemical preventive effects of UD extract on HFD-induced obesity in rats.

Plants and their mineral or chemical components and extracts, especially those commonly used in food, are widely used in alternative and complementary medicine to prevent or treat obesity and its related complications [28]. For instance, human studies have reported significant weight loss associated with Nigella sativa [29], extra virgin olive oil [30], and pistachio nut [31] treatments. Studies on rats [3234] and mice [2, 35] have also reported considerable weight loss in association with plants and plant extracts. The anti-obesity mechanisms of plants include reduced lipid absorption and energy intake, increased energy expenditure, decreased pre-adipocyte differentiation and proliferation, decreased lipogenesis, and increased lipolysis [36]. Virgin olive oil [30], capsinoids [37], and Lycium barbarum [38] lead to higher fat oxidation in humans, while a number of polyphenols obtained from tea extracts (e.g. L-epicatechin, epicatechin-3-gallate, epigallocatechin, and epigallocatechin-3-gallate) have demonstrated strong inhibitory effects against pancreatic lipase, thereby leading to weight loss [3941].

It was previously demonstrated that rats that consumed a HFD gained weight faster than those that consumed a low-fat diet [42, 43]. In the present study, the rats were fed a HFD that consisted of 60% fat for 10 weeks. After 8 weeks of consuming an obesity-inducing diet, the rats that showed a body weight increase of at least 20% when compared to the control group were regarded as obese [44, 45]. The present study found that the rats fed a HFD weighed 40% more than the rats in the control group. This finding was consistent with other research. For example, one study found that mice that were fed a HFD diet for 8 weeks weighed approximately 50% more than those in the control group, which were fed a normal diet [46], while another study reported that weight gain was significantly higher in rats fed a HFD for 4 weeks than in the rats in the control group [47]. Taken together, these results indicated that increases in body weight may be related to HFDs [48, 49].

Obesity treatments are considered successful if they prevent further weight gain, reduce initial weight by 5–10%, and provide sustained long-term weight loss [2]. However, the efficiency of new obesity treatments should first be evaluated by their effects on body weight [50]. In the present study, weight gain was suppressed by 26% in the rats in the UD + HFD group when compared to the rats in the HFD group. It can therefore be concluded that the UD extract was successful in treating obesity because it prevented further weight gain.

UD can control obesity and its complications [51]. Aqueous ethanolic extracts of UD are demonstrated to be effective for weight reduction in those with obesity by reducing the pre-inflammatory factor of chemerin and obesity-related factors [52]. UD protects against HFD-induced obesity through mechanisms involving lipid accumulation and glucose metabolism in skeletal muscle, liver, and adipose tissue [53]. Madadi Jaberi et al. reported that hydro-alcoholic extract of UD significantly reduces the levels of apelin and high sensitivity C-reactive protein, which points to its effective role in controlling body fat percentage and obesity [54]. UD plant attenuates HFD-induced weight gain through its effects on gut microbiota composition and diversity. A high proportion of soluble and insoluble fibre and phytochemicals in UD may serve as substrates for gut bacteria, resulting in proliferation of beneficial bacterial taxa or metabolites that affect host cellular mechanisms [55]. Based on results from the present study, it is believed that the reduction in body weight as a result of UD treatment is due to the above-mentioned mechanisms.

Hepatic steatosis is a well-known pathology in severely obese human patients, and it is particularly associated with visceral adiposity and diabetes [56]. Dietary fat intake is probably responsible for increased adipocytes [43]. Simple steatosis, steatohepatitis, severe fibrosis, and cirrhosis are typically observed clinicopathologically in patients with fatty liver disease [57], which is diagnosed via histopathological examination and is defined as the presence of fatty vacuoles in more than 5% of hepatocytes [58].

Hepatic steatosis has also been reported in rats [56]. For instance, Xu et al. [24] reported that Grade 1 hepatic steatosis (defined as less than 33% steatosis of the hepatic parenchyma) occurred in the fourth week of a HFD and Grade 2 hepatic steatosis (i.e. more than 33% steatosis of the hepatic parenchyma) developed in the eighth week. Moreover, hepatic steatosis continued to gradually increase from the 12th week to the 48th week. In addition, mononuclear cell infiltrations, vascular dilatation [56], and congestion [59, 60] have also been reported in rats fed a HFD. The results of the present study were consistent with these previous findings.

Recent research has reported that some plants have prevented hepatic steatosis in an experimentally generated fatty liver model with a HFD [61]. Consistent with this, in the present study, significantly more hepatic steatosis was observed among rats in the HFD group than among the rats in the HFD + UD group.

Studies have also found that the immunomodulatory and antioxidant effects of the UD extract provide some protection via immunomodulatory and antioxidant effects against coagulative necrosis, lipid peroxidation, and the liver degeneration and fibrosis associated with carbon tetrachloride toxicity. In addition, UD extract causes a significant reduction in the number of SMA-positive perisinusoidal cells with myofibroblastic transformation and lysosomal enzyme activity suggesting fibrogenesis [62]. Yener et al. [9] found that UD extract significantly improved the hydropic degeneration, necrosis, fat degeneration, bile duct proliferation, and periportal fibrosis caused by aflatoxicosis through a decrease in MDA, enhancement in the activities of CAT, GR, and SOD, decreases in the levels and activities of serum AST, ALT, and GGT, and prevention of the formation of ROS or scavenges. In this study, similar findings were decreased as a result of the UD extract treatment.

Increased hepatic triglyceride levels have been reported to cause hepatic steatosis in some obese individuals [63]. Natural products, such as pistachio nuts [31], psyllium fibre [64], black Chinese tea [39], Camellia sinensis [65], yacon syrup [66], olive oil [30], and fenugreek seed [67], have all been shown to reduce triglyceride levels. An anti-hyperlipidaemic effect of UD extract has been demonstrated by many studies in rats [6871]. The presence of antioxidants in UD extract components may play a role in the hypolipidaemic effect. It has been stated that this hypothesis can be considered as one of the mechanisms by which this extract can regulate lipid homeostasis [51, 72]. Consistent with these findings, the present study saw significantly decreased triglyceride levels in the rats treated with UD extracts, suggesting that UD extracts cause histopathological changes in the liver.

Previous research has shown that the serum levels of AST and ALT were significantly higher in obese rats than in rats with normal body weight [48]. These increased levels, as well as the increased LDH activity, can be attributed to the changing structure of liver cells, which are intracellular enzymes that are present in only a small amount of serum [73]. This is because when liver cells are damaged by autolytic destruction or cellular necrosis they leak into the plasma [74]. However, various doses of methanolic UD extracts have been reported to reduce serum ALT, AST, and LDH in mice with cisplatin-induced toxicity [73]. Similarly, another study found that UD extracts significantly reduced serum AST and ALT values in hypercholesterolaemic mice, which was attributed to the antihepatotoxic potential of the UD extract [75]. UD extract has no apparent negative effects on liver enzymes and has also been shown to decrease enzyme levels in rats fed a HFD [76]. Consistent with these results, the present study found that serum ALT and ALP levels were highest in the HFD group and second highest in the HFD + UD group. However, in contrast to previous studies, no significant difference was found in the serum AST and LDH levels in any of the groups. It is possible that the duration of the study may have affected the serum ALT level findings. As a matter of fact, one study observed significantly increased serum ALT levels in rats fed a HFD in the 4th, 12th, and 16th weeks of the study, but no significant changes were observed in the 8th, 36th, or 48th weeks [24].

A HFD causes dyslipidaemic changes by increasing the levels of serum triglycerides, total cholesterol, and LDL cholesterol and lowering the serum HDL levels. Dyslipidaemic changes in obesity may be due to the increased entry of unesterified fatty acids into the liver caused by increased triglycerides [77]. It has been shown that serum triglyceride, total cholesterol, LDL cholesterol, and very-LDL cholesterol levels increase, while HDL cholesterol levels decrease in rats fed an HFD [78]. Similarly, Amin and Nagy [48] reported that serum triglyceride, total cholesterol, and LDL cholesterol levels increased, and HDL cholesterol levels decreased in rats fed an HFD. Consistent with these findings, the present study observed that the serum LDL, cholesterol, and triglyceride levels were significantly higher, and the HDL cholesterol level was significantly lower in the rats in the HFD group than in the control group, while in the HFD + UD group, the serum LDL and triglyceride levels were lower and HDL levels were higher than in the HFD group.

Serum cholesterol levels were higher in the HFD + UD group than in the HFD group, suggesting that the cholesterol levels increased as a result of the UD extract treatment. Although the cause of these unwanted results is unknown, a connection between the type of rats, the presence of diabetes, the method of extract preparation, and the duration of the study has been hypothesised [59]. In a study conducted in fish, different doses of UD given for 4 weeks did not cause a significant change in triglyceride and cholesterol levels. However, when the same doses were applied for 8 weeks, a decrease was observed in triglyceride levels, but no change was detected in cholesterol levels. The difference in serum cholesterol was attributed to the presence of plant sterols such as stigmasterol, campesterol, and phenolic compounds [79]. It has been stated that the reduction of triglycerides may be due to carvacrol in nettle, which can have a greater effect on lipogenesis than cholesterol biosynthesis [80]. As a result, the cholesterol level is likely to vary based on numerous parameters.


Efforts to combat obesity have typically been disappointing. Complex pathogenesis, misdiagnosis, mistreatment of the disease, and several unwanted effects associated with various treatment methods suggest that obesity cannot be widely treated with simple drug therapy. Moreover, approaches tailored to the needs of individual patients, and changes in eating habits and energy are typically necessary to help overweight or obese patients lose weight. In the present study, UD extract partially prevented obesity and its associated effects. UD extract decreased weight gain, decreased hepatic steatosis, and significantly improved serum triglyceride, HDL, and LDL levels in rats fed an HFD. However, the UD extract also increased the cholesterol levels of the rats; hence, by itself, it is presumably an insufficient treatment for obesity due to the complex and multifactorial nature of the disease.


This study was funded by the Van Yuzuncu Yil University Scientific Research Projects Foundation (Grant number TYL-2018-7381). This study was prepared from Kenan KAÇAK’s master’s thesis

Conflict of interest

The authors declare no conflict of interest.



Altunkaynak BZ, Özbek E. Obesity: causes and treatment alternatives. Van Med J 2006; 13: 138-142.


Alarcon-Aguilar FJ, Zamilpa A, Perez-Garcia MD, et al. Effect of Hibiscus sabdariffa on obesity in MSG mice. J Ethnopharmacol 2007; 114: 66-71.


Eckel RH, York DA, Rössner S, et al. Prevention Conference VII: obesity, a worldwide epidemic related to heart disease and stroke: executive summary. Circulation 2004; 110: 2968-75.


Hasani-Ranjbar S, Larijani B, Abdollahi M. A systematic review of the potential herbal sources of future drugs effective in oxidant-related diseases. Inflamm Allergy Drug Targets 2009; 8: 2-10.


Abdollahi M, Afshar-Imani B. A review on obesity and weight loss measures. Middle East Pharmacy 2003; 11: 6-10.


Barnes PM, Powell-Griner E, McFann K, Nahin RL. Complementary and alternative medicine use among adults: United States, 2002. Semin Integrative Med 2004; 2: 54-71.


Moro C, Basile G. Obesity and medicinal plants. Fitoterapia 2000; 71: 73-82.


Hanl K, Kimura Y, Okuda H. Anti-obesity effects of natural products. Stud Nat Prod Chem 2005; 30: 79-110.


Yener Z, Celik I, Ilhan F, Bal R. Effects of Urtica dioica L. seed on lipid peroxidation, antioxidants and liver pathology in aflatoxin-induced tissue injury in rats. Food Chem Toxicol 2009; 47: 418-24.


Chaurasia N, Wichtl M. Flavonol glycosides aus Urtica Dioica. Planta Med 1987; 53: 432-4.


Ganßer D, Spiteller G. Aromatase inhibitors from Urtica dioica roots. Planta Med 1995; 61: 138-40.


Chaurasia N, Wichtl M. Scopoletin, 3-b-sitosterin und sitosterin 3-b-Dglucoside aus Brennesselwurzel (Urticae radix). Dtsch Apoth Ztg 1987; 126: 81-3.


Wagner H, Willer F, Kreher B. Biologically active compounds from the aqueous extract of Urtica dioica. Planta Med 1989; 55: 452-4.


Glusker JP, Rossi M. Molecular aspects of chemical carcinogens and bioflavonoids. Prog Clin Biol Res 1986; 213: 395-410.


Akbay P, Basaran AA, Undeger U, Basaran N. In vitro immunomodulatory activity of flavonoid glycosides from Urtica dioica L. Phytother Res 2003; 17: 34-7.


Riehemann K, Behnke B, Schulze-Osthoff K. Plant extracts from stinging nettle (Urtica dioica), an antirheumatic remedy, inhibit the proinflammatory transcription factor NF-κB. FEBS Letters 1999; 442: 89-94.


Tahri A, Yamani S, Legssyer A, et al. Acute diuretic, natriuretic and hypotensive effects of a continuous perfusion of aqueous extract of Urtica dioica in the rat. J Ethnopharmacol 2000; 73: 95-100.


Sezik E, Yeşilada E, Honda G, et al. Traditional medicine in Turkey X. Folk medicine in central Anatolia. J Ethnopharmacol 2001; 75: 95-115.


Yeşilada E, Honda G, Sezik E, et al. Traditional medicine in Turkey IV. Folk medicine in the Mediterranean subdivision. J Ethnopharmacol 1993; 39: 31-8.


Sezik E, Yeşilada E, Tabata M, et al. Traditional medicine in Turkey viii. folk medicine in east Anatolia; Erzurum, Erzíncan, Ağri, Kars, Iğdir provinces. Econ Bot 1997; 51: 195-211.


Nassiri-Asl M, Zamansoltani F, Abbasi E, et al. Effects of Urtica dioica extract on lipid profile in hypercholesterolemic rats. Zhongxiyi Jiehe Xuebao 2009; 7: 428-33.


Dar SA, Ganai FA, Yousuf AR, et al. Pharmacological and toxicological evaluation of Urtica dioica. Pharma Biol 2013; 51: 170-80.


Uyar A, Esim E. Histopathological and biochemical investigation of the effects of Mate (Ilex paraguariensis) tea on antiobesity effect in rats fed with high fat diet. Harran Üniv Vet Fak Derg 2018; 7: 154-61.


Xu ZJ, Fan JG, Ding XD, et al. Characterization of high-fat, diet-induced, non-alcoholic steatohepatitis with fibrosis in rats. Dig Dis Sci 2010; 55: 931-40.


Ghibaudi L, Cook J, Farley C, et al. Fat intake affects adiposity, comorbidity factors, and energy metabolism of Sprague–Dawley rats. Obes Res 2002; 10: 956-63.


Hill JO, Melanson EL, Wyatt HT. Dietary fat intake and regulation of energy balance: implications for obesity. J Nutr 2000; 130: 284-8.


Hasani-Ranjbar S, Jouyandeh Z, Abdollahi M. A systematic review of anti-obesity medicinal plants-an update. Diabetes Metab Syndr 2013; 12: 28.


Bloch AS. Nutrition for health promotion: phytochemicals, functional foods, and alternative approaches to combat obesity. Dent Clin N Am 2003; 47: 411-23.


Datau EA, Surachmanto EE, Pandelaki K, Langi JA. Efficacy of Nigella sativa on serum free testosterone and metabolic disturbances in central obese male. Acta Med Indones 2010; 42: 130-4.


Razquin C, Martinez JA, Martinez-Gonzalez MA, et al. A 3 years follow-up of a Mediterranean diet rich in virgin olive oil is associated with high plasma antioxidant capacity and reduced body weight gain. Eur J Clin Nutr 2009; 63: 1387-93.


Li Z, Song R, Nguyen C, et al. Pistachio nuts reduce triglycerides and body weight by comparison to refined carbohydrate snack in obese subjects on a 12-week weight loss program. J Am Coll Nutr 2010; 29: 198-203.


Kobayashi Y, Nakano Y, Kizaki M, et al. Capsaicin-like anti-obese activities of evodiamine from fruits of Evodia rutaecarpa, a vanilloid receptor agonist. Planta Med 2001; 67: 628-33.


Park YS, Yoon Y, Ahn HS. Platycodon grandiflorum extract represses up-regulated adipocyte fatty acid binding protein triggered by a high fat feeding in obese rats. World J Gastroenterol 2007; 13: 3493-9.


Kim SJ, Jung JY, Kim HW, Park T. Anti-obesity effects of Juniperus chinensis extract are associated with increased AMP-activated protein kinase expression and phosphorylation in the visceral adipose tissue of rats. Biol Pharm Bull 2008; 31: 1415-21.


Urias-Silvas JE, Cani PD, Delmée E, et al. Physiological effects of dietary fructans extracted from Agave tequilana Gto. and Dasylirion spp. Br J Nutr 2008; 99: 254-61.


Yun JW. Possible anti-obesity therapeutics from nature–a review. Phytochemistry 2010; 71: 1625-41.


Snitker S, Fujishima Y, Shen H, et al. Effects of novel capsinoid treatment on fatness and energy metabolism in humans: possible pharmacogenetic implications. Am J Clin Nutr 2010; 89: 45-50.


Amagase H, Nance DM. Lycium barbarum increases caloric expenditure and decreases waist circumference in healthy overweight men and women: pilot study. J Am Coll Nutr 2011; 30: 304-9.


Thielecke F, Boschmann M. The potential role of green tea catechins in the prevention of the metabolic syndrome–a review. Phytochemistry 2009; 70: 11-24.


Wang H, Wen Y, Du Y, et al. Effects of catechin enriched green tea on body composition. Obesity 2009; 18: 773-9.


Kubota K, Sumi S, Tojo H, Sumi-Inoue Y. Improvements of mean body mass index and body weight in preobese and overweight Japanese adults with black Chinese tea [Pu-Erh] water extract. Nutr Res 2011; 31: 421-8.


Buettner R, Schölmerich J, Bollheimer LC. High-fat diets: modeling the metabolic disorders of human obesity in rodents. Obesity 2007; 15: 798-808.


Hariri N, Thibault L. High-fat diet-induced obesity in animal models. Nutr Res Rev 2010; 23: 270-99.


Widdowson PS, Upton R, Buckingham R, et al. Inhibition of food response to intracerebroventricular injection of leptin is attenuated in rats with diet-induced obesity. Diabetes 1997; 46: 1782-5.


Kaya MS, Bayiroglu F, Mis L, et al. In case of obesity, longevity-related mechanisms lead to anti-inflammation. Age 2014; 36: 677-87.


Cho AS, Jeon SM, Kim MJ, et al. Chlorogenic acid exhibits anti-obesity property and improves lipid metabolism in high-fat diet-induced-obese mice. Food Chem Toxicol 2010; 48: 937-43.


Choi BK, Park SB, Lee DR, et al. Green coffee bean extract improves obesity by decreasing body fat in high-fat diet-induced obese mice. Asian Pac J Trop Dis 2016; 9: 635-43.


Amin KA, Nagy MA. Effect of Carnitine and herbal mixture extract on obesity induced by high fat diet in rats. Diabetol Metab Syndr 2009; 1: 17.


Lee JS, Lee MK, Ha TY, et al. Supplementation of whole persimmon leaf improves lipid profiles and suppresses body weight gain in rats fed high-fat diet. Food Chem Toxicol 2006; 44: 1875-83.


Campfield LA, Smith FJ, Burn P. Strategies and potential molecular targets for obesity treatment. Science 1998; 280: 1383-7.


Samakar B, Mehri S, Hosseinzadeh H. A review of the effects of Urtica dioica (nettle) in metabolic syndrome. Iran J Basic Med Sci 2022; 25: 543-53.


Ashtiani ARA, Vahidian-Rezazadeh M, Jafari M, et al. Study of changes in the plasma levels of chemerin of women with overweight and obese during a period of endurance training on a cycle-ergometer using hydroalcoholic extract of urtica. Pharmacophore 2018; 9: 72-9.


Fan S, Raychaudhuri S, Kraus O, et al. Urtica dioica whole vegetable as a functional food targeting fat accumulation and insulin resistance–a preliminary study in a mouse pre-diabetic model. Nutrients 2020; 12: 1059.


Madadi Jaberi M, Vahidian Rezazadeh M, Mogharnasi M, Karaji Bani M. The effect of 8 weeks of aerobic training and consumption of hydro-alcoholic extract of nettle on apelin and hs-CRP plasma levels of overweight and obese women. Armaghan Danesh 2016; 21: 846-59.


Fan S, Raychaudhuri S, Page R, et al. Metagenomic insights into the effects of Urtica dioica vegetable on the gut microbiota of C57BL/6J obese mice, particularly the composition of Clostridia. J Nutr Biochem 2021; 91: 108594.


Altunkaynak Z. Effects of high fat diet ınduced obesity on female rat livers (a histochemical study). Eur J Gen Med 2005; 2: 100-9.


Tiniakos DG. Nonalcoholic fatty liver disease/nonalcoholic steatohepatitis: histological diagnostic criteria and scoring systems. Eur J Gastroenterol Hepatol 2010; 22: 643-50.


Adams LA, Lymp JF, Sauver JS, et al. The natural history of nonalcoholic fatty liver disease: a population-based cohort study. Gastroenterology 2005; 129: 113-21.


Chan LL, Chen Q, Go AG, et al. Reduced adiposity in bitter melon (Momordica charantia)–fed rats is associated with increased lipid oxidative enzyme activities and uncoupling protein expression. J Nutr 2005; 135: 2517-23.


Wang Y, Ausman LM, Russell RM, et al. Increased apoptosis in high-fat diet-induced nonalcoholic steatohepatitis in rats is associated with c-Jun NH2-terminal kinase activation and elevated proapoptotic Bax. J Nutr 2008; 138: 1866-71.


Sharma SK, Vij AS, Sharma S. Mechanisms and clinical uses of capsaicin. Eur J Pharmacol 2013; 720: 55-62.


Turkdogan MK, Ozbek H, Yener Z, et al. The role of Urtica dioica and Nigella sativa in the prevention of carbon tetrachloride-induced hepatotoxicity in rats. Phytother Res 2003; 17: 942-6.


Roden M, Anderwald C, Furnsinn C, et al. Effects of short-term leptin exposure on triglyceride deposition in rat liver. Hepatology 2000; 32: 1045-9.


Pal S, Khossousi A, Binns C, et al. The effect of a fibre supplement compared to a healthy diet on body composition, lipids, glucose, insulin and other metabolic syndrome risk factors in overweight and obese individuals. Br J Nutr 2011; 105: 90-100.


Lenon GB, Li KX, Chang YH, et al. Efficacy and safety of a Chinese herbal medicine formula (RCM-104) in the management of simple obesity: a randomized, placebo-controlled clinical trial. Evid Based Complementary Alternat Med 2012; 2012: 435702.


Genta S, Cabrera W, Habib N, et al Yacon syrup: beneficial effects on obesity and insulin resistance in humans. Clin Nutr 2009; 28: 182-7.


Raju J, Bird RP. Alleviation of hepatic steatosis accompanied by modulation of plasma and liver TNF-α levels by Trigonella foenum graecum (fenugreek) seeds in Zucker obese (fa/fa) rats. Int J Obes 2006; 30: 1298-307.


Gaballu FA, Gaballu YA, Khyavy OM, et al. Effects of a triplex mixture of Peganum harmala, Rhus coriaria, and Urtica dioica aqueous extracts on metabolic and histological parameters in diabetic rats. Pharm Biol 2015; 53: 1104-9.


Mehran MM, Norasfard MR, Abedinzade M, Khanaki K. Lamium album or Urtica dioica? which is more effective streptozotocin induced diabetic rats: a comparative study. Afr J Tradit Complement Altern Med 2015; 12: 84-8.


Ghorbani A, Shafiee-Nick R, Rakhshandeh H, Borji A. Antihyperlipidemic effect of a polyherbal mixture in streptozotocin-induced diabetic rats. J Lipids 2013: 675759.


Das M, Sarma B, Rokeya B, et al. Antihyperglycemic and antihyperlipidemic activity of Urtica dioica on type 2 diabetic model rats. J Diabetol 2011; 2: 1-6.


Mahjoub S, Davari S, Moazezi Z, Qujeq D. Hypolipidemic effects of ethanolic and aqueous extracts of Urtica dioica in rats. World Appl Sci J 2012; 17: 1345-8.


Özkol H, Musa D, Tuluce Y, Koyuncu I. Ameliorative influence of Urtica dioica L against cisplatin-induced toxicity in mice bearing Ehrlich ascites carcinoma. Drug Chem Toxicol 2012; 35: 251-7.


Recknagel RO, Glende EA, Dolak JA, Waller RL. Mechanisms of carbon tetrachloride toxicity. Pharmacol Ther 1989; 43: 139-54.


Avcı G, Kupeli E, Eryavuz A, et al. Antihypercholesterolaemic and antioxidant activity assessment of some plants used as remedy in Turkish folk medicine. J Ethnopharmacol 2006; 107: 418-23.


Daher CF, Baroody KG, Baroody GM. Effect of Urtica dioica extract intake upon blood lipid profile in the rats. Fitoterapia 2006; 77: 183-8.


Grundy SM. Obesity, metabolic syndrome, and cardiovascular disease. J Clin Endocrinol Metab 2004; 89: 2595-600.


Noeman SA, Hamooda HE, Baalash AA. Biochemical study of oxidative stress markers in the liver, kidney and heart of high fat diet induced obesity in rats. Diabetol Metab Syndr 2011; 3: 17.


Binaii M, Ghiasi M, Farabi SMV, et al. Biochemical and hemato-immunological parameters in juvenile beluga (Huso huso) following the diet supplemented with nettle (Urtica dioica). Fish Shellfish Immunol 2014; 36: 46-51.


Lee KW, Everts H, Beyen AC. Dietary carvacrol lowers body gain but improves feed conversion in female broiler chickens. J Appl Poult Res 2003; 12: 394.e9.

Copyright: © 2023 Termedia Sp. z o. o. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License (http://creativecommons.org/licenses/by-nc-sa/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
© 2024 Termedia Sp. z o.o.
Developed by Bentus.