Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1
Charalampos Proestos
 -- 2718 2022-08-29 08:47:15 |
2 format correct
Vivi Li
 -5 word(s) 2713 2022-08-30 04:01:24 |

Video Upload Options

Do you have a full video?
Send video materials Upload full video

Confirm

Are you sure to Delete?
Yes No
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Kumar, M.;  Kaushik, D.;  Kaur, J.;  Proestos, C.;  Oz, F.;  Oz, E.;  Gupta, P.;  Kundu, P.;  Kaur, A.;  Anisha, A.; et al. Herbal Approach, Bioactive Compounds, and Mechanism of Obesity. Encyclopedia. Available online: https://encyclopedia.pub/entry/26587 (accessed on 08 August 2024).
Kumar M,  Kaushik D,  Kaur J,  Proestos C,  Oz F,  Oz E, et al. Herbal Approach, Bioactive Compounds, and Mechanism of Obesity. Encyclopedia. Available at: https://encyclopedia.pub/entry/26587. Accessed August 08, 2024.
Kumar, Mukul, Deepika Kaushik, Jasjit Kaur, Charalampos Proestos, Fatih Oz, Emel Oz, Prerna Gupta, Priyanka Kundu, Anmol Kaur, Anisha Anisha, et al. "Herbal Approach, Bioactive Compounds, and Mechanism of Obesity" Encyclopedia, https://encyclopedia.pub/entry/26587 (accessed August 08, 2024).
Kumar, M.,  Kaushik, D.,  Kaur, J.,  Proestos, C.,  Oz, F.,  Oz, E.,  Gupta, P.,  Kundu, P.,  Kaur, A.,  Anisha, A., & Ritika, R. (2022, August 29). Herbal Approach, Bioactive Compounds, and Mechanism of Obesity. In Encyclopedia. https://encyclopedia.pub/entry/26587
Kumar, Mukul, et al. "Herbal Approach, Bioactive Compounds, and Mechanism of Obesity." Encyclopedia. Web. 29 August, 2022.
Herbal Approach, Bioactive Compounds, and Mechanism of Obesity
Edit
This entry is adapted from the peer-reviewed paper 10.3390/app12168342

Obesity is arising as a global pandemic throughout the world. Obesity has tripled worldwide, creating an alarming situation. The majority of people nowadays are suffering from obesity and overweight. It affects health of people of all age groups, ethnicity, gender, and sex, and is linked to a sedentary lifestyle of people, poor eating habits, and disturbed sleeping patterns. It causes several diseases such as diabetes mellitus type 2, hypertension, cardiovascular diseases, asthma, gallstones, and colon cancer. Many synthetic anti-obesity drugs such as orlistat, lorcaserin, phentermine, bupropion, and liraglutide are already available on the market. However, these drugs have side effects, including dry mouth and sleeping disorders, dizziness, blood pressure, heart rate elevation, constipation, and headache. Humans have a long and ancient history of dependency on traditional medicinal plants and their major bioactive antioxidant components, such as quercetin, anthocyanins, and ellagic acid, for treating such diseases and disorders. 

anti-obesity drugs body mass index antioxidants medicinal plants obesity

1. Introduction

Obesity is defined as an elevation of the fat tissue mass in the body, which is not limited to any age group. It is characterized by increased body and fat mass, hormonal disturbances, food intake (eating pattern), and genetic factors [1]. Obesity is a significant contributor to the global burden of several chronic diseases such as diabetes mellitus type 2, cardiovascular diseases, asthma, etc., which affect the human body. It has been proclaimed a global pandemic with a death rate of approximately 2.8 million people annually [2][3]. Since fat is present all over the body, it is not possible to measure it directly. Therefore, body mass index (BMI) is used to observe the relationship between weight and height. Whereas waist circumference, waist/hip ratio, skinfold thickness, and bioimpedance help to assess obesity and overweight [4].
Suppose the BMI of the person lies in the range of overweight, the chances of getting affected by other diseases such as diabetes mellitus type 2, hypertension, cardiovascular diseases, gallstones, etc., increase. For obesity class 1, the chances are moderate, while in the case of obesity class 2, the chances are severe. In the case of extreme obesity, the chances are very high, particularly if the person is affected by other obesity-related diseases [5][6]. Figure 1 summarizes the BMI classification recommended by WHO and the National Institute of Health in the United States.
Figure 1. Classification of weight according to body mass index (BMI).
There are two types of fats, visceral and subcutaneous. The fat deposited over visceral organs such as the kidney, abdomen, liver, intestines, heart, and pancreas is known as visceral fat. The other name for visceral fat is active fat because research has proved that it significantly affects our hormonal activity, resulting in metabolic syndrome and insulin resistance. The hormonal activity influences metabolism, body fat distribution, and appetite [7]. Moreover, the fat underneath the skin is known as subcutaneous fat and can be felt underarm and legs [8]. The body attains two types of shapes, apple, and pear, due to fat deposition in certain body areas [9]. In the case of an apple shape (Android), fat accumulation occurs in the upper area of the waist and abdomen. Some deposition also appears on the neck, arms, and shoulders. The main reason behind this body shape is visceral fat, which is associated with the health risk of type 2 diabetes [10]. In the pear shape (Gynoid), fat deposition occurs on the thighs and buttocks. The amount of visceral fat is low in this type of body shape, resulting in low chances of weight-related diseases [11].
Obesity also causes several complications such as reproductive (women and men), respiratory, cardiovascular diseases, pancreas, and gastrointestinal, as shown in Figure 2.
Figure 2. Several complications as a result of obesity.
According to the survey performed by the Organisation for Economic Co-operation and Development (OECD) in 2017, the United States of America is ranked first, followed by China and India in obesity. From 1999 to 2000 and 2015 to 2016, there has been a remarkable increase in obesity [12]. In 2016, the World Health Organization (WHO) reported that over 1.9 billion adults who were either 18 years old or above were overweight, and among these 1.9 billion, 650 million were suffering from obesity [2]. According to a survey, 25 million people die annually because of obesity or being overweight [12]. According to another study by WHO (World Health Organization) in 2019, 38.2 million children under the age of 5 were either suffering from obesity or overweight [13].
Even in India, the prevalence of obesity varies from urban to rural and state-wise. It was reported that the prevalence of obesity in males was higher in urban areas (37.5%) compared to rural areas (20.78%) [14]. Some of the states of India affected by obesity are Jharkhand, Kerala, Pondicherry, Chhattisgarh, Madhya Pradesh, Bihar, and Andhra Pradesh [14][15].
The vital factor that plays a headway role in the case of obesity is the person’s lifestyle and eating habits [16]. Most food items with high fat and sugar are responsible for increasing body weight, and such food materials have low micronutrients [17][18]. Consumption of excessive refined grains, junk foods, and soft drinks can lead to a big waist:hip ratio, and the person’s fat mass also increases [19].

2. Hormones Related to Obesity

2.1. Leptin

Leptin is a significant hormone that is related to an increase in body weight [20]. Leptin, the result of the ob (obese) gene product, is the first adipose hormone that links the central regulation of metabolism with peripheral adipose fat mass. In the arcuate nucleus of the hypothalamus, leptin suppresses appetite by either decreasing the activity of orexigenic neuropeptides (NPY and AgRP) or boosting the activity of anorexigenic neuropeptides (α-MSH and CART) [21][22]. As adiposity increases, serum leptin concentrations increases along with it. Higher circulating levels of leptin reduce energy intake and increase energy expenditure in a homeostatic system, but this is not the case in those who are suffering from obesity or overweight, thus, indicating a condition of leptin resistance. Circulating soluble leptin receptor (SLR) levels decline with obesity. These receptors are blood-circulating proteins that directly support leptin activity. This combination of high levels of leptin and low SLR may contribute to the leptin resistance seen in obese people [7]. Clinical investigations have demonstrated that the administration of leptin has minimal effect on the body weight of obese participants, despite enthusiastic research on the use of leptin in the treatment of obesity [21][22]. If there is a deficiency of leptin, it can lead to extreme obesity [23].

2.2. Ghrelin

A 28-amino acid peptide hormone called ghrelin is mainly produced in the stomach. Ghrelin increases the growth hormone release by directly interacting with the GH secretagogue receptor at the pituitary level [24][25]. Ghrelin seems to have a role in neuroendocrine and metabolic responses to food intake. Its circulating levels are elevated in anorexia and cachexia and lowered in obesity [26][27][28]. Plasma ghrelin levels are inversely related to body fat mass, body mass index, plasma leptin levels, insulin, and glucose levels [29]. Various studies imply that ghrelin may be crucial in controlling appetite and weight. GH secretion, food intake, and obesity are all controlled by the GH secretagogue receptor (GHS-R1a) in the arcuate nucleus [30][31].

2.3. Insulin

Excess body weight is frequently linked to insulin resistance, a condition in which tissues, particularly skeletal muscle, the liver, and adipose tissue, are less receptive to the physiological effects of insulin [32][33]. Plasma insulin levels are persistently increased in insulin-resistant conditions, even while fasting. Increased plasma concentrations of free fatty acids, continually produced from adipose tissue, are the leading cause of insulin resistance by excess weight. Increased hepatic and muscle fatty acid absorption and oxidation due to increased free fatty acid concentrations result in metabolic changes that reduce these tissues’ ability to absorb and utilize glucose for energy metabolism. Reduced insulin receptor levels and post-receptor abnormalities in insulin signaling are included in these adaptations. Increases in intra-abdominal body fat storage, which release free fatty acids into the circulation more quickly than other adipose tissue compartments, are most significantly associated with insulin resistance [34][35][36]. Weight reduction often increases insulin sensitivity and normalizes plasma insulin concentrations in obese patients [37].

2.4. Adiponectin

Mature adipocytes release adiponectin, and its circulating levels are lower in obese and diabetic people. The plasma level of adiponectin is increased by anti-diabetic and anti-obesity medications such PPARagonists (thiazolidinediones) and CB1 antagonists (rimonabant). Through the activation of AMP kinases, which have been linked with the adiponectin receptors R1 and R2 in animal models and human studies, adiponectin increases insulin sensitivity [38][39]. In humans, atherosclerosis, dyslipidemia, and insulin resistance have been linked to lower adiponectin levels in obesity. With an increase in insulin sensitivity, plasma adiponectin levels considerably rise with weight reduction [7]. As a result, treating insulin resistance associated with obesity and type 2 diabetes may include targeting adiponectin and adiponectin receptors.

3. Synthetic Drugs

Many anti-obesity synthetic drugs such as orlistat, lorcaserin, phentermine/topiramate, bupropion/naltrexone, and liraglutide are already available on the market. These drugs target obesity by increasing noradrenaline, dopamine, and serotonin. However, they have many side effects related to cardiovascular health, increased blood pressure, and affect the central nervous system by causing changes in sleep patterns and affecting hormonal secretion [40][41].

3.1. Orlistat

Orlistat, approved in 1998, is a synthetic derivative of lipstatin [42], a potent and reversible inhibitor of gastrointestinal lipase that inhibits pancreatic and stomach lipase to reduce dietary fat absorption by 30% [43]. Orlistat was produced as one of the lipstatin analogs and is known as an anti-obesity medication due to its ability to suppress pancreatic lipase activity selectively. Orlistat works by reducing fat absorption by permanently inhibiting lipase activity in the gastrointestinal tract, which reduces energy intake [42]. The most common side effects include diarrhea, abdominal pain, bloating, flatulence, oily stools, dyspepsia, reduced absorption of fat-soluble vitamins, and in some rare cases, it can cause severe liver and kidney injury [43].

3.2. Lorcaserin

Lorcaserin, approved in 2012 in the USA, is a selective serotonin 2C (5-HT2C) receptor agonist that decreases body weight by reducing food intake [43]. Serotonin (5-HT) is released when lorcaserin interacts with the 5-hydroxytryptamine 2C (5-HT2C) receptor, and serotonin uptake is subsequently inhibited [44]. Because lorcaserin has a low specificity for the 5-HT2B receptor (about 100 times lower than that of the 5-HT2C receptor), there is a limited chance that long-term use of lorcaserin may result in heart-valve abnormalities [6][45]. The side effects of lorcaserin include serotonin syndrome or neuroleptic malignant syndrome-like reactions: headache, dizziness, nausea, fatigue, dry mouth, constipation, low blood sugar (hypoglycemia), headache, cough, back pain, and fatigue in diabetic patients [46].

3.3. Phentermine/Extended-Release Topiramate (Qnexa)

A combination treatment of phentermine and extended-release (ER) topiramate, developed by Vivus, is known as Qnexa. Although the exact mode of action is unknown, phentermine is believed to stimulate the release of catecholamines (including dopamine and noradrenaline) in the hypothalamus. In contrast, topiramate enhances the activity of the neurotransmitter gamma-aminobutyrate, regulates voltage-gated ion channels, and inhibits carbonic anhydrase and AMPA/kainite excitatory glutamate receptors [47][48]. The side effects reported include dizziness, paresthesia (tingling in the hands and feet), changed taste perception, dry mouth, dysgeusia, insomnia, and constipation, without increased risk of serious cardiovascular problems [48].

3.4. Bupropion/Naltrexone (Contrave)

The combination of bupropion and naltrexone synergistically enhances neuronal activity and decreases food uptake by stimulating satiety [42]. Although bupropion is a relatively poor inhibitor of dopamine and norepinephrine uptake, it stimulates the hypothalamic pro-opiomelanocortin (POMC) system, which activates melanocortin receptors and induces weight reduction through appetite suppression and increased energy expenditure. Naltrexone functions as an antagonist of the opioid receptor that generally causes a negative feedback-mediated inhibition of POMC activation and thus acts synergistically to prolong the bupropion’s action on metabolism [49]. The most common adverse effects (AEs) reported are nausea, headache, dizziness, vomiting, insomnia, constipation, and dry mouth [50].

3.5. Liraglutide

An analog of glucagon-like peptide (GLP)-1, liraglutide has a half-life of 13 h, which significantly prolongs its activation of the GLP-1 receptor (the half-life of native GLP-1 is about 1.5 min), increasing stimulation of glucose-dependent insulin secretion and exerting a more substantial effect on glucagon suppression [51]. Native GLP-1 has central effects that control appetite and feeding centers in the brain [52]; hence, liraglutide may potentially have the ability to influence energy intake. A 5-week partial crossover trial with liraglutide demonstrated that liraglutide caused weight reduction most likely mediated by lowering appetite and decreasing food consumption. It did not enhance energy expenditure, as measured by appetite scores, post-prandial satiety, and fullness ratings [53]. The most common side effects reported include nausea, diarrhea, vomiting, constipation, decreased appetite, and low blood sugar (hypoglycemia) [54].

4. Herbs That Control Obesity

Herbs have always proved to be an essential and functional source for many chronic diseases, and obesity is one of them. Other than a few allergic reactions in susceptible individuals, herbs have fewer adverse effects than single-compound drugs. Medicinal herbs such as Nigella sativa, Hibiscus sabdariffa, Ilex paraguariensis, Coffea arabica, Caralluma fimbriata, Panax ginseng, and many others have shown positive effects on obesity by different mechanisms such as suppressing appetite; reducing triglyceride levels; increasing the metabolic rate; inhibiting pancreatic lipase, etc. Hence, they facilitate the process of weight loss [55][56].

4.1. Nigella sativa

The herb is a member of the Ranunculaceae family, also known as black seed. The origin of the herb belongs to south European countries, including Albania, Bosnia, Bulgaria, and Cyprus, as well as some southwest Asian countries such as Indonesia, Thailand, and Singapore. It is also grown in India, Pakistan, Turkey, and Syria [57][58]. The herb contains vitamins and minerals such as copper, potassium, zinc, and iron [59]. It treats various diseases and disorders related to liver, cardiovascular health, inflammation, gastrointestinal health, and diabetes. It has antioxidant, anti-inflammatory, anti-bacterial, and anti-fungal properties [60][61]. The herb is a potent anti-obesity agent. The main bioactive compound, Thymoquinone (TQ), is mainly responsible for anti-obesity activity. It targets obesity by suppressing the appetite and reducing triglyceride levels. It also plays a significant role in adiponectin hormone level, which plays a vital role in protecting against insulin obstinacy in the body [62][63].

4.2. Hibiscus sabdariffa

The other name for the herb is roselle; it is a sub-shrub that can grow up to 8 ft in height. It is a native plant of India and Malaysia but is grown in other parts of the world, such as China, Thailand, Sudan, Nigeria, Jamaica, etc. [64][65]. It is a vital source of vitamins and minerals such as calcium, iron, phosphorus, riboflavin, and vitamin C. Hibiscus sabdariffa helps to fight against many diseases related to kidney stones, gastrointestinal disorders, and liver damage. It has antioxidant, antimicrobial, anti-inflammatory, anti-carcinogenic, anti-obesity, and anti-diabetic properties [66]. The main bioactive compounds, such as anthocyanins, flavonoids, and organic acids, are responsible for the anti-obesity activity of the herb [67]. The extract of Hibiscus sabdariffa has the potential to enhance insulin sensitivity and resistance while lowering lipid accumulation and oxidative stress. An increase in lipoprotein lipase activity and a decrease in the expression of the adipogenesis genes are two ways that anthocyanin suppresses lipid accumulation and decreases fat mass in high-fat diet-induced obese rats. The loss of visceral adipose tissue reduces inflammatory cytokines and oxidative state, which reduces insulin resistance and enhances insulin sensitivity in obese rats [68].

4.3. Ilex paraguariensis

The herb’s common name is yerba mate; it belongs to the Aquifoliaceae family. It is a native plant of South America (Brazil, Argentina, etc.) [69]. The height of the plant can be up to 20 m. It is one of the richest sources of flavonoids (quercetin and rutin) and phenolic acids such as chlorogenic and caffeic acid. It also contains saponins and caffeine. It has many pharmacological properties such as antioxidant activity, anti-obesity, anti-diabetic, anti-tumor, neuroprotective, and anti-inflammatory [70]. It helps in the regulation of insulin as well as targets obesity by inhibiting the expression of genes that regulate adipogenesis, improve the lipid profile, and act as an appetite suppressant. It also inhibits the inflammatory action in adipose tissue caused by obesity. It enhances peripheral insulin sensitivity [71] and modulates the leptin release by adipose tissue [72].

4.4. Rosmarinus officinalis

The other name of the herb is rosemary; it belongs to Lamiaceae Mint family. The herb is native to the Mediterranean region. The leaves are a vital part of the herb used for medicinal purposes [73]. Anti-bacterial, antioxidant, anti-cancer, anti-diabetic, anti-inflammatory, anti-thrombotic, neuroprotective, and hepatoprotective are some of the herb’s uses [74]. It also has an anti-viral effect and helps to regulate blood pressure [75][76]. Certain studies revealed a significant anti-obesity impact with the help of carnosic acids that alter the activity of 3T3-L1 preadipocytes differentiation [77][78]. Evidence of the inhibitory effect of rosemary extract on pancreatic lipase activity, a crucial enzyme in the digestion and absorption of fat, as well as on gastric lipase activity, suggests that limiting lipid absorption is the primary mechanism by which rosemary extract lowered weight gain and adiposity index [79].

References

  1. Apovian, C.M.; Aronne, L.J.; Bessesen, D.H.; McDonnell, M.E.; Murad, M.H.; Pagotto, U.; Still, C.D. Pharmacological management of obesity: An Endocrine Society clinical practice guideline. J. Clin. Endocrinol. Metab. 2015, 100, 342–362.
  2. World Health Organization. Noncommunicable Diseases Country Profiles 2022; World Health Organization: Geneva, Switzerland, 2022.
  3. Forse, R.A.; Betancourt-Garcia, M.M.; Kissee, M.C. Epidemiology and Discrimination in Obesity. In The ASMBS Textbook of Bariatric Surgery; Springer: Cham, Switzerland, 2020; pp. 3–14.
  4. Smith, K.B.; Smith, M.S. Obesity Statistics. Prim. Care 2016, 43, 121–135, ix.
  5. James, P.T.; Leach, R.; Kalamara, E.; Shayeghi, M. The worldwide obesity epidemic. Obes. Res. 2001, 9, 228S–233S.
  6. Smith, S.R.; Weissman, N.J.; Anderson, C.M.; Sanchez, M.; Chuang, E.; Stubbe, S. Behavioral Modification and Lorcaserin for Overweight and Obesity Management (BLOOM) Study Group. Multicenter, placebo-controlled trial of lorcaserin for weight management. N. Engl. J. Med. 2010, 363, 245–256.
  7. Sidhu, S.; Parikh, T.; Burman, K.D. Endocrine Changes in Obesity. In Endotext; Feingold, K.R., Ed.; MDText.com, Inc.: South Dartmouth, MA, USA, 2017.
  8. Zhang, Y.; Yu, L.; Cai, W.; Fan, S.; Feng, L.; Ji, G.; Huang, C. Protopanaxatriol, a novel PPARγ antagonist from Panax ginseng, alleviates steatosis in mice. Sci. Rep. 2014, 4, 7375.
  9. Miranda, J.; Vázquez-Polo, M.; Pérez-Junkera, G.; Fernández-Gil, M.D.P.; Bustamante, M.Á.; Navarro, V.; Martínez, O. FODMAP intake in Spanish population: Open approach for risk assessment. Int. J. Environ. Res. Public Health 2020, 17, 5882.
  10. Pollex, R.L.; Hanley, A.J.; Zinman, B.; Harris, S.B.; Khan, H.M.; Hegele, R.A. Metabolic syndrome in aboriginal Canadians: Prevalence and genetic associations. Atherosclerosis 2006, 184, 121–129.
  11. Kumar, M.; Guleria, S.; Chawla, P.; Khan, A.; Modi, V.K.; Kumar, N.; Kaushik, R. Anti-obesity efficacy of the selected high altitude Himalayan herbs: In vitro studies. J. Food Sci. Technol. 2020, 57, 3081–3090.
  12. Ogden, C.L.; Carroll, M.D.; Curtin, L.R.; McDowell, M.A.; Tabak, C.J.; Flegal, K.M. Prevalence of overweight and obesity in the United States, 1999–2004. JAMA 2006, 295, 1549–1555.
  13. Pimpley, V.; Patil, S.; Srinivasan, K.; Desai, N.; Murthy, P.S. The chemistry of chlorogenic acid from green coffee and its role in attenuation of obesity and diabetes. Prep. Biochem. Biotechnol. 2020, 50, 969–978.
  14. Mishra, D.; Naorem, K.; Saraswathy, K.N. Angiotensin-Converting Enzyme Gene Insertion/Deletion Polymorphism and Cardiometabolic Risk Factors: A Study Among Bhil Tribal Population from Two Environmental Settings. Biochem. Genet. 2018, 56, 295–314.
  15. Kandpal, V.; Sachdeva, M.P.; Saraswathy, K.N. An assessment study of CVD-related risk factors in a tribal population of India. BMC Public Health 2016, 16, 434.
  16. Cameron, A.J.; Zimmet, P.Z.; Dunstan, D.W.; Dalton, M.; Shaw, J.E.; Welborn, T.A.; Jolley, D. Overweight and obesity in Australia: The 1999–2000 Australian diabetes, obesity, and lifestyle study (AusDiab). Med. J. Aust. 2003, 178, 427–432.
  17. Ruxton, C.H.S. Nutritional implications of obesity and dieting. Nutr. Bull. 2011, 36, 199–211.
  18. Mendez, M.A.; Popkin, B.M.; Buckland, G.; Schroder, H.; Amiano, P.; Barricarte, A.; González, C.A. Alternative methods of accounting for underreporting and overreporting when measuring dietary intake-obesity relations. Am. J. Epidemiol. 2011, 173, 448–458.
  19. Paradis, A.M.; Godin, G.; Pérusse, L.; Vohl, M.C. Associations between dietary patterns and obesity phenotypes. Int. J. Obes. 2009, 33, 1419–1426.
  20. Paz-Filho, G.; Mastronardi, C.A.; Licinio, J. Leptin treatment: Facts and expectations. Metabolism 2015, 64, 146–156.
  21. Heymsfield, S.B.; Greenberg, A.S.; Fujioka, K.; Dixon, R.M.; Kushner, R.; Hunt, T.; Lubina, J.A.; Patane, J.; Self, B.; Hunt, P.; et al. Recombinant leptin for weight loss in obese and lean adults: A randomized, controlled, dose-escalation trial. JAMA 1999, 282, 1568–1575.
  22. Fogteloo, A.J.; Pijl, H.; Frölich, M.; McCamish, M.; Meinders, A.E. Effects of recombinant human leptin treatment as an adjunct of moderate energy restriction on body weight, resting energy expenditure and energy intake in obese humans. Diabetes Nutr. Metab. 2003, 16, 109–114.
  23. Ahima, R.S.; Flier, J.S. Leptin. Annu. Rev. Physiol. 2000, 62, 413–437.
  24. Cordido, F.; Penalva, A.; Dieguez, C.; Casanueva, F.F. Massive growth hormone (GH) discharge in obese subjects after the combined administration of GH-releasing hormone and GHRP-6: Evidence for a marked somatotroph secretory capability in obesity. J. Clin. Endocrinol. Metab. 1993, 76, 819–823.
  25. Alvarez-Castro, P.; Isidro, M.L.; Garcia-Buela, J.; Leal-Cerro, A.; Broglio, F.; Tassone, F. Marked GH secretion after ghrelin alone or combined with GH-releasing hormone (GHRH) in obese patients. Clin. Endocrinol. 2004, 61, 250–255.
  26. Kojima, M.; Hosoda, H.; Matsuo, H.; Kangawa, K. Ghrelin: Discovery of the natural endogenous ligand for the growth hormone secretagogue receptor. Trends Endocrinol. Metab. 2001, 12, 118–122.
  27. Tschop, M.; Weyer, C.; Tataranni, P.A.; Devanarayan, V.; Ravussin, E.; Heiman, M.L. Circulating ghrelin levels are decreased in human obesity. Diabetes 2001, 50, 707–709.
  28. Otto, B.; Cuntz, U.; Fruehauf, E.; Wawarta, R.; Folwaczny, C.; Riepl, R.L. Weight gain decreases elevated plasma ghrelin concentrations of patients with anorexia nervosa. Eur. J. Endocrinol. 2001, 145, 669–673.
  29. Ukkola, O. Ghrelin and insulin metabolism. Eur. J. Clin. Investig. 2003, 33, 183–185.
  30. Shuto, Y.; Shibasaki, T.; Otagiri, A.; Kuriyama, H.; Ohata, H.; Tamura, H. Hypothalamic growth hormone secretagogue receptor regulates growth hormone secretion, feeding, and adiposity. J. Clin. Investig. 2002, 109, 1429–1436.
  31. Cummings, D.E.; Frayo, R.S.; Marmonier, C.; Aubert, R.; Chapelot, D. Plasma ghrelin levels and hunger scores in humans initiating meals voluntarily without time- and food-related cues. Am. J. Physiol. Endocrinol. Metab. 2004, 287, E297–E304.
  32. Abate, N. Insulin resistance and obesity. The role of fat distribution pattern. Diabetes Care 1996, 19, 292–294.
  33. Bjorntorp, P. Metabolic abnormalities in visceral obesity. Ann. Med. 1992, 24, 3–5.
  34. Flier, J.S. Insulin receptors and insulin resistance. Annu. Rev. Med. 1983, 34, 145–160.
  35. Kahn, C.R. Role of insulin receptors in insulin-resistant states. Metabolism 1980, 29, 455–466.
  36. Moller, D.E.; Flier, J.S. Insulin resistance-mechanisms, syndromes, and implications. N. Engl. J. Med. 1991, 325, 938–948.
  37. Kaaks, R.; Lukanova, A.; Kurzer, M.S. Obesity, endogenous hormones, and endometrial cancer risk: A synthetic review. Cancer Epidemiol. Biomark. Prev. 2002, 11, 1531–1543.
  38. Rabe, K.; Lehrke, M.; Parhofer, K.G.; Broedl, U.C. Adipokines and insulin resistance. Mol. Med. 2008, 14, 741–751.
  39. Guerre-Millo, M. Adiponectin: An update. Diabetes Metab. 2008, 34, 12–18.
  40. Cruickshank, C.C.; Dyer, K.R. A review of the clinical pharmacology of methamphetamine. Addiction 2009, 104, 1085–1099.
  41. Frohmader, K.S.; Pitchers, K.K.; Balfour, M.E.; Coolen, L.M. Mixing pleasures: Review of the effects of drugs on sex behavior in humans and animal models. Horm. Behav. 2010, 58, 149–162.
  42. Oh, S.; Kim, K.S.; Chung, Y.S.; Shong, M.; Park, S.B. Anti-obesity agents: A focused review on the structural classification of therapeutic entities. Curr. Top Med. Chem. 2009, 9, 466–481.
  43. Kang, J.G.; Park, C.Y. Anti-Obesity Drugs: A Review about Their Effects and Safety. Diabetes Metab. J. 2012, 36, 13–25.
  44. United States Food and Drug Administration. Lorcaserin Briefing Information: Endocrinologic and Metabolic Drugs Advisory Committee. 2012. Available online: http://www.fda.gov/AdvisoryCommittees/CommitteesMeetingMaterials/Drugs/EndocrinologicandMetabolicDrugsAdvisoryCommittee/ucm225628.htm (accessed on 28 October 2015).
  45. Weissman, N.J.; Sanchez, M.; Koch, G.G.; Smith, S.R.; Shanahan, W.R.; Anderson, C.M. Echocardiographic assessment of cardiac valvular regurgitation with lorcaserin from analysis of 3 phase 3 clinical trials. Circ. Cardiovasc. Imaging 2013, 6, 560–567.
  46. Fidler, M.C.; Sanchez, M.; Raether, B.; Weissman, N.J.; Smith, S.R.; Shanahan, W.R.; Anderson, C.M. A one-year randomized trial of lorcaserin for weight loss in obese and overweight adults: The BLOSSOM trial. J. Clin. Endocrinol. Metab. 2011, 96, 3067–3077.
  47. Scozzafava, A.; Supuran, C.T.; Carta, F. Antiobesity carbonic anhydrase inhibitors: A literature and patent review. Expert. Opin. Ther. Pat. 2013, 23, 725–735.
  48. Gadde, K.M.; Allison, D.B.; Ryan, D.H.; Peterson, C.A.; Troupin, B.; Schwiers, M.L.; Day, W.W. Effects of low-dose, controlled-release, phentermine plus topiramate combination on weight and associated comorbidities in overweight and obese adults (CONQUER): A randomised, placebo-controlled, phase 3 trial. Lancet 2011, 377, 1341–1352.
  49. Unites States Food and Drug Administration. Contrave (Naltrexone 4 mg, 8 mg/Bupropion HCL 90 mg Extended Release Tablet) Briefing Document, NDA 200063. 2010. Available online: http://www.fda.gov/downloads/advisorycommittees/committeesmeetingmaterials/drugs/endocrinologicandmetabolicdrugsadvisorycommitee/ucm235671.pdf (accessed on 28 October 2015).
  50. Wadden, T.A.; Foreyt, J.P.; Foster, G.D. Weight loss with naltrexone SR/bupropion SR combination therapy as an adjunct to behavior modification: The COR-BMOD trial. Obesity 2011, 19, 110–120.
  51. European Medicines Agency. Victoza Summary of Product Characteristics. Available online: http://www.ema.europa.eu/docs/en_GB/document_library/EPAR_-_Product_Information/human/001026/WC500050017.pdf (accessed on 28 October 2015).
  52. Turton, M.D.; O’Shea, D.; Gunn, I. A role for glucagon-like peptide-1 in the central regulation of feeding. Nature 1996, 379, 69–72.
  53. Van Can, J.; Sloth, B.; Jensen, C.B. Effects of the once-daily GLP-1 analog liraglutide on gastric emptying, glycemic parameters, appetite and energy metabolism in obese, non-diabetic adults. Int. J. Obes. 2014, 38, 784–793.
  54. United States Food and Drug Administration. FDA Approves Weight-Management Drug Saxenda. 2014. Available online: http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm427913.htm (accessed on 28 October 2015).
  55. Bahmani, M.; Eftekhari, Z.; Saki, K.; Fazeli-Moghadam, E.; Jelodari, M.; Rafieian-Kopaei, M. Obesity phytotherapy: Review of native herbs used in traditional medicine for obesity. J. Evid.-Based Complement. Altern. Med. 2016, 21, 228–234.
  56. Yun, J.W. Possible anti-obesity therapeutics from nature—A review. Phytochemistry 2010, 71, 1625–1641.
  57. Dessie, A.B.; Abate, T.M.; Adane, B.T.; Tesfa, T.; Getu, S. Estimation of technical efficiency of black cumin (Nigella sativa L.) farming in northwest Ethiopia: A stochastic frontier approach. J. Econ. Struct. 2020, 9, 18.
  58. Goreja, W.G. Black Seed: Nature’s Miracle Remedy; Karger Publishers: Basel, Switzerland, 2003.
  59. Cheikh-Rouhou, S.; Besbes, S.; Lognay, G.; Blecker, C.; Deroanne, C.; Attia, H. Sterol composition of black cumin (Nigella sativa L.) and Aleppo pine (Pinus halepensis Mill.) seed oils. J. Food Compos. Anal. 2008, 21, 162–168.
  60. Mehta, B.K.; Verma, M.; Gupta, M. Novel lipid constituents identified in seeds of Nigella sativa (Linn). J. Braz. Chem. Soc. 2008, 19, 458–462.
  61. Nickavar, B.; Mojab, F.; Javidnia, K.; Amoli, M.A.R. Chemical composition of the fixed and volatile oils of Nigella sativa L. from Iran. Z. Nat. C 2003, 58, 629–631.
  62. Morikawa, T.; Xu, F.; Ninomiya, K.; Matsuda, H.; Yoshikawa, M. Nigellamines A3, A4, A5, and C, new dolabellane-type diterpene alkaloids, with lipid metabolism-promoting activities from the Egyptian medicinal food black cumin. Chem. Pharm. Bull. 2004, 52, 494–497.
  63. Datau, E.A.; Surachmanto, E.E.; Pandelaki, K.; Langi, J.A. Efficacy of Nigella sativa on serum free testosterone and metabolic disturbances in central obese male. Acta Med. Indones. 2010, 42, 130–134.
  64. Adebayo-Tayo, B.C.; Samuel, U.A. Microbial Quality and Proximate Composition of Dried Hibiscus sabdariffa Calyxes in Uyo, Eastern Nigeria. Malays. J. Microbiol. 2009, 5, 13–18.
  65. Hirunpanich, V.; Utaipat, A.; Morales, N.P.; Bunyapraphatsara, N.; Sato, H.; Herunsale, A.; Suthisisang, C. Hypocholesterolemic and antioxidant effects of aqueous extracts from the dried calyx of Hibiscus sabdariffa L. in hypercholesterolemic rats. J. Ethnopharmacol. 2006, 103, 252–260.
  66. Sheba, A.L.; Ilakkia, A. Anti-obesity effect of hibiscus Sabdariffa L.—A review. Int. J. Pharma Bio Sci. 2016, 7, 13.
  67. Ojulari, O.V.; Lee, S.G.; Nam, J.O. Beneficial Effects of Natural Bioactive Compounds from Hibiscus sabdariffa L. on Obesity. Molecules 2019, 24, 210.
  68. Janson, B.; Prasomthong, J.; Malakul, W.; Boonsong, T.; Tunsophon, S. Hibiscus sabdariffa L. calyx extract prevents the adipogenesis of 3T3-L1 adipocytes, and obesity-related insulin resistance in high-fat diet-induced obese rats. Biomed. Pharmacother. 2021, 138, 111438.
  69. Mosimann, A.L.P.; Wilhelm-Filho, D.; Da Silva, E.L. Aqueous extract of Ilex paraguariensis attenuates the progression of atherosclerosis in cholesterol-fed rabbits. Biofactors 2006, 26, 59–70.
  70. Kim, S.Y.; Oh, M.R.; Kim, M.G.; Chae, H.J.; Chae, S.W. Anti-obesity effects of Yerba Mate (Ilex paraguariensis): A randomized, double-blind, placebo-controlled clinical trial. BMC Complement. Altern. Med. 2015, 15, 338.
  71. Hussein, G.M.; Matsuda, H.; Nakamura, S.; Akiyama, T.; Tamura, K.; Yoshikawa, M. Protective and ameliorative effects of maté (Ilex paraguariensis) on metabolic syndrome in TSOD mice. Phytomedicine 2011, 19, 88–97.
  72. Kang, Y.R.; Lee, H.Y.; Kim, J.H.; Moon, D.I.; Seo, M.Y.; Park, S.H.; Cho, S.W. Anti-obesity and anti-diabetic effects of Yerba Mate (Ilex paraguariensis) in C57BL/6J mice fed a high-fat diet. Lab. Anim. Res. 2012, 28, 23–29.
  73. Al-Mukhtar, E.; Selman, S.; Sahib, Z.; Naji, H. Antidepressant-Like Effect of Rosmarinus officinalis Extract in Male Mice. Med. J. Babylon 2013, 10, 803–808.
  74. Hussain, A.; Anwar, F.; Chatha, S.A.S.; Jabbar, A.; Mahboob, S.; Nigam, P. Rosmarinus officinalis essential oil: Antiproliferative, antioxidant and anti-bacterial activities. Braz. J. Microbiol. 2010, 41, 1070–1078.
  75. Karthik, D.; Viswanathan, P.; Anuradha, C.V. Administration of rosmarinic acid reduces cardiopathology and blood pressure through inhibition of p22phox NADPH oxidase in fructose-fed hypertensive rats. J. Cardiovasc. Pharmacol. 2011, 58, 514–521.
  76. Amaral, G.P.; de Carvalho, N.R.; Barcelos, R.P.; Dobrachinski, F.; de Lima Portella, R.; da Silva, M.H.; Athayde, M.L. Protective action of ethanolic extract of Rosmarinus officinalis L. in gastric ulcer prevention induced by ethanol in rats. Food Chem. Toxicol. 2013, 55, 48–55.
  77. Gaya, M.; Repetto, V.; Toneatto, J.; Anesini, C.; Piwien-Pilipuk, G.; Moreno, S. Antiadipogenic effect of carnosic acid, a natural compound present in Rosmarinus officinalis, is exerted through the C/EBPs and PPARγ pathways at the onset of the differentiation program. Biochim. Biophys. Acta—Gen. Subj. 2013, 1830, 3796–3806.
  78. Bustanji, Y.; Issa, A.; Mohammad, M.; Hudaib, M.; Tawah, K.; Alkhatib, H.; Al-Khalidi, B. Inhibition of hormone sensitive lipase and pancreatic lipase by Rosmarinus officinalis extract and selected phenolic constituents. J. Med. Plant Res. 2010, 4, 2235–2242.
  79. Shatla, I.M.; Abdel-Hamid, A.M.; Metwally, M. The Effect of Rosmarinus officinalis L. Extract on High Fat Diet-Induced Obesity in Adult Male Albino Rats. Al-Azhar Med. J. 2017, 46, 749–764.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Upload a video for this entry
Information
Subjects: Nutrition & Dietetics
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Mukul Kumar
,
Deepika Kaushik
,
Jasjit Kaur
,
Charalampos Proestos
,
Fatih Oz
,
Emel Oz
,
Prerna Gupta
,
Priyanka Kundu
,
Anmol Kaur
,
Anisha Anisha
,
Ritika Ritika
View Times: 816
Revisions: 2 times (View History)
Update Date: 30 Aug 2022
Table of Contents
    1000/1000
    Hot Most Recent
    Video Production Service
    Feedback