You're using an outdated browser. Please upgrade to a modern browser for the best experience.
Obesity Rodent Models Applied to Research: History
View Latest Version
Please note this is an old version of this entry, which may differ significantly from the current revision.
Contributor: Tânia Martins , Tiago Ferreira , Elisabete Nascimento-Gonçalves , Catarina Ribeiro ,
, Luis Antunes , Paula Oliveira

Obesity is a disease whose incidence has increased over the last few decades. Despite being a multifactorial disease, obesity results essentially from excessive intake of high-calorie foods associated with low physical activity. The demand for a pharmacological therapy using natural compounds as an alternative to synthetic drugs has increased. Natural compounds may have few adverse effects and high economic impact, as most of them can be extracted from underexploited plant species and food by-products. To test the potential anti-obesogenic effects of new natural substances, the use of preclinical animal models of obesity has been an important tool, among which rat and mouse models are the most used. Some animal models are monogenic, such as the db/db mice, ob/ob mice, Zucker fatty rat and Otsuka Long-Evans Tokushima fatty rat. There are also available chemical models using the neurotoxin monosodium glutamate that induces lesions in the ventromedial hypothalamus nucleus, resulting in the development of obesity. However, the most widely used are the obesity models induced by high-fat diets. 

  • fatness
  • overweight
  • animal model
  • diet-induced obesity
  • high-fat diet
  • bioactive compounds

1. db/db Mice

The db/db mouse (db stands for diabetes) [1] can be used to study the molecular basis of obesity; however, it is commonly used for studies concerning type 2 diabetes [2]. These db/db mice were developed by investigators from the Jackson Laboratories in 1966 and are phenotypically similar to the ob/ob mouse model. They exhibit a mutation in leptin receptor gene, in an autosomal recessive trait that encodes for a G-to-T point mutation, leading to defective leptin signaling [2][3]. The predominant mouse strain in which this mutation is maintained is the C57BL/KS [2][4]. The db/db mice are characterized by hyperphagia, a consequence of impaired leptin signing in the hypothalamus, develop early-onset obesity due to low energy expenditure, are insulin resistant, have decreased insulin levels and are hypothermic. Moreover, they develop dyslipidemia, hypogonadism, hyperglycemia, have growth hormone (GH) deficiency, and are infertile [1][3]. Regarding the analysis of natural products on obesity development, this model can become an option, especially when the compounds that are tested, such as Artemisia extract (artemether) and barley (Table 1), have supposedly a double effect on both obesity and diabetes [5][6].

2. ob/ob Mice

Developed at Jackson Laboratories in 1966, the ob/ob mice are homozygous for the obese spontaneous mutation in the leptin gene that prevents the secretion of bioactive leptin resulting in leptin deficiency [1][4][7]. Leptin is a hormone derived from adipocytes, and its deficiency leads to an increase in appetite and the development of severe obesity [8][9][10]. The homozygous mutant mice are typically of the C57BL/6J strain. These mice present a pronounced obese phenotype characterized by uncontrollable food intake, type 2 diabetes, hyperphagia, hyperleptinemia, insulin resistance and fatty liver, hepatic steatosis, hypogonadism, and hypothyroidism [2][3]. The ob/ob mice are a better model for studying obesity than db/db mice because they have a longer lifetime and fewer clinical signs [11]. The effects of natural compounds such as celastrol, genistein, cannabinoid Δ9-tetrahydrocannabivarin and cinnamon extract on the ob/ob mouse model can be analyzed in Table 1 [12][13][14][15].

3. Zucker Fatty Rat

The Zucker fatty rat (ZFR), or Zucker (fa/fa), has a similar phenotype to ob/ob and db/db mice, as it has a homozygous missense mutation (fatty, fa) in the long form of the leptin receptor, which makes it insensitive to leptin [16][17]. Defects in the leptin receptor caused by this mutation result in the development of early-onset obesity due to hyperphagia, reducing the energy expenditure and leading to morbid obesity [4]. These rats are less likely to acquire diabetes, although ZFR has a high level of insulin resistance and fertility is reduced [3][4]
The ZFR is the most used model for studying several genetic characteristics associated with obesity [18][19], although it has also been used to study the anti-obesogenic effects of natural compounds such as the extracts of red wine [20], rosemary [21], green tea [22], bilberries, and purple potatoes [23] (Table 1).

4. Otsuka Long-Evans Tokushima Fatty Rat

The Otsuka Long-Evans Tokushima fatty (OLETF) rat is a spontaneous cholecystokinin type A (CCK-A) receptor knockout and does not respond to CCK, a peptide-derived hormone that functions as a peripheral satiety signal [3][24]. As a result, these rats are hyperphagic beginning several weeks after birth and develop mild obesity [19], which is a consequence of increased food intake and meal sizes, leading to an increase in body weight [25]. Moreover, OLETF rats develop diabetes, which manifests as polyuria and polydipsia [3]. At approximately 8 weeks of age, OLETF rats display hyperinsulinemia, and insulin resistance is observed at 12 weeks of age. Later, hyperplasia of pancreatic islets and hypertriglyceridemia develop [1].
The effects of gambigyeongsinhwan [26], gyeongshingangjeehwan [27], fermented mushroom milk-supplemented dietary fiber [28], or soy β-conglycinin [29] on obesity were evaluated in this animal model (Table 1).

5. Monosodium Glutamate (MSG)-Induced Obesity Model

The VMH nucleus, located in the hypothalamus, is associated with the regulation of eating behavior and satiety, with the use of rats with VMH lesions being one of the first models developed to induce obesity in rodents [3][4][30]. Bilateral lesions of the VMH nucleus lead to the development of hyperphagia, vagal hyperactivity, sympathetic hypoactivity, enlarged pancreatic islets, and hyperinsulinemia and can be caused by using the neurotoxin MSG [31][32]. MSG administration also causes lesions in the arcuate nucleus of the hypothalamus and circumventricular neurons. To induce obesity, MSG can be administered subcutaneously or intraperitoneally (2–4 mg/g of body weight) during the neonatal period, 4–10 times [33]. Adult rats who received MSG in the neonatal period developed endocrine dysfunction syndromes, which are characterized by obesity development, disturbances in the regulation of caloric balance, reduced growth, behavioral changes, and hypogonadism [32][34]. This obesity model was used to study the anti-obesogenic effects of Roselle (Hibiscus sabdariffa L.) [35] (Table 1).
Table 1. Anti-obesity effects of natural products in monogenic and neurotoxin monosodium glutamate (MSG)-induced obesity models.
Food Product/Plant Bioactive Compounds Strain/Obesity Model Dose and Treatment Observed Effects References
Artemisia extract Artemether C57BL/KsJ db/db mice ♂ 200 mg/kg (oral gavage), for 2 weeks ↓ Food intake and weight increase rate [5]
↓ Fasting blood glucose levels
↑ Tolerance to glucose
↑ Insulin sensitivity
↑ Insulin secretion
Improved hyperinsulinemia
Ameliorated islet vacuolar degeneration and hepatic steatosis
↓ Apoptosis of pancreatic beta cells
Barley N.A. db/db mice (BKS.Cg-+Leprdb/+Leprdb/OlaHsd—fat, black, homozygous) ♂ 88% (w/w; mixed with the diet), for 8 weeks ↓ Plasma insulin and resistin levels [6]
↓ TC levels in the liver
Bilberries (Vaccinium myrtillus) Nonacylated anthocyanin extract Zucker (fa/fa) rats ♂, fed with HFD 25 mg/kg/day (oral gavage), for 8 weeks ↓ Fasting plasma glucose level [23]
↓ Levels of branched-chain amino acids
Improved lipid profiles
Cannabis sativa Cannabinoid
Δ9-tetrahydrocannabivarin		 C57BL/6 ob/ob mice ♀ 0.1, 0.5, 2.5 and 12.5 mg/kg/day (oral gavage), for 30 days ↓ Liver TG concentration (only for 12.5 mg/kg) [12]
Cinnamon extract (Cinnamomum zeylanicum) N.A. B6.V-Lepob/J mice [on a C57BL/6J background (ob/ob)] ♂ 4.5 mL/kg (equates to 0.8 g/kg) (in drinking water), for 6 weeks ↑ Insulin sensitivity and glucose tolerance [13]
↓ Hepatic levels of TG
↓ Fat accumulation in the liver
↑ Liver glycogen content
Improvement of insulin-stimulated locomotor activity
Celastraceae family members (including Tripterygium wilfordii) Celastrol (tripterine) C57BL/6J ob/ob mice ♂, fed with HFD 3 mg/kg/day (mixed with the HFD), for 6 weeks ↓ B.w. [15]
↓ Liver weight
↓ TG levels in the liver
↑ Glucose clearance
Downregulation of intestinal lipid transporters
↑ Lipid excretion in feces
Green tea Polyphenols Zucker (fa/fa) rats ♂, fed with HFD 200 mg/kg/day (oral gavage), for 8 weeks ↓ B.w. gain [22]
↓ Visceral fat
↓ Fasting serum insulin, glucose and lipids levels
Liriope platyphylla (dry roots) Aqueous extract OLETF rats 5 or 10% (15 mL/g b.w./day; oral gavage), for 2 weeks ↓ Abdominal fat mass [36]
↓ Glucose concentration
↑ Insulin production (only for 10% concentration)
↓ Expression of Glut-1
Mix of Curcuma longa L., Alnus japonica and Massa Medicata Fermentata Gambigyeongsinhwan OLETF rats ♂ 250 or 500 mg/kg/day (oral gavage), for 8 weeks ↓ B.w. gain [26]
↓ Adipose tissue weight and visceral adipocyte size
↑ mRNA levels PPARα in adipose tissue
Mix of edible mushrooms (Lentinus edodes, Ganoderma lucidum, Pleurotus ostreatus and Flammulina velutipes) in fermented milk N.A. OLETF rats ♂ 10 and 20% (v/w; mixed with the diet), for 6 weeks ↓ B.w., [28]
↓ Perirenal fat, visceral and epididymal fat (only for 20% concentration),
↓TG and FFA levels
Mix of Liriope platyphylla, Platycodon grandiflorum, Schisandra chinensis, and Ephedra sinica Gyeongshingangjeehwan OLETF rats ♂ 121.7 mg/kg/day (oral gavage), for 8 weeks ↓ Visceral WAT weight [27]
↓ Size adipocytes in mesenteric WAT
↓ mRNA expression levels of adipocyte marker genes (PPARγ, aP2 and leptin) in visceral WAT
↑ mRNA expression levels of PPARα target genes in visceral WAT
↓ Plasma levels of FFA, TG, insulin and glucose
Purple Potato (Solanum tuberosum) Acylated anthocyanin extract Zucker (fa/fa) rats ♂, fed with HFD 25 mg/kg/day (oral gavage), for 8 weeks ↓ Levels of branched-chain amino acids [23]
improved lipid profiles
↑ Glutamine/glutamate ratio
↓ Glycerol levels and metabolites involved in glycolysis
Red Wine (ProvinolsTM) Polyphenol extract (70% Polyphenols) Zucker (fa/fa) rats 20 mg/kg/day (mixed with the diet), for 8 weeks ↓ Plasma levels of glucose, fructosamine, TG, TC and LDL-cholesterol [20]
↑ NO
↑ eNOS activity
↓Superoxide anion
Roselle (Hibiscus sabdariffa L.) aqueous extract Anthocyanins Swiss Webster (CFW) mice ♂ induced by MSG 120 mg/kg/day (60 mg/kg/day by oral gavage plus 60 mg/kg/day dissolved in tap water given ad libitum), for 60 days ↓ B.w. gain [35]
↓ Glycemia
↑ ALT levels
Rosemary (Rosmarinus officinalis L.) extract Carnosic acid and carnosol Zucker (fa/fa) rats ♀ 0.5% (w/w; mixed with the diet), for 64 days ↓ B.w. gain, [21]
↓ Serum TG, TC and insulin levels
Lipase activity inhibition in the stomach
Soy products, grains and legumes Genistein ob/ob mice ♀ 0.06% (w/w; mixed with the diet), for 4 weeks ↓B.w. gain [10]
Downregulation of SOD activity
↑ iNOS expression in mesenteric artery perivascular adipose tissue
♂, male; ♀, female; ↓, decrease; ↑, increase; ALT, alanine aminotransferase; aP2, adipocyte fatty acid-binding protein; B.w., body weight; eNOS, endothelial nitric oxide-synthase; FFA, free fatty acids; Glut-1, glucose transporter 1; iNOS, inducible nitric oxide synthase; LDL, low density lipoprotein; MSG, monosodium glutamate; N.A., not applicable; NO, nitric oxide; PPAR-α, peroxisome proliferator-activated receptor alpha; PPARγ, peroxisome proliferator-activated receptor gamma; SOD, superoxide dismutase; TC, total cholesterol; TG, triglycerides; WAT, white adipose tissue; weeks, weeks.

6. Diet-Induced Obesity Models

Diet-induced obesity (DIO) rodent models are achieved by exposing rats and mice to specific diets that induce obesity, thereby reproducing dietary imbalances that are often the main cause of obesity in humans [3][37][38][39]. The main advantage of diets is that they can be standardized and control the nutrient percentages. There are a variety of diets that can be used for this purpose, such as high-fat diets (HFD), high-sugar diets (HSD), and high-sugar and high-fat (HSHF) diets, known as Western diets [40]. The HFD-induced obesity mouse model is one of the most used to understand the relationship between hyperlipidemic diets and the pathophysiology of obesity [38]. Within mouse strains, there are some more susceptible to DIO than others [37][41]; for example, the inbred C57BL/6 mouse strain is highly susceptible in contrast to SWR/J, A/J and CAST/Ei mouse strains, which tend to be resistant to these diets. In fact, the C57BL/6J mouse strain is the most used since when they are fed with HFD, these animals develop characteristics similar to humans with complex metabolic syndrome, such as obesity, high fat accumulation, insulin resistance, hyperglycemia, hyperlipidemia, hypertension, non-alcoholic fatty liver disease, and endothelium damage associated with cardiovascular diseases [1][3][38][42][43]. Some rat strains can also be used as models of HFD-induced obesity, such as the outbred Sprague Dawley, Wistar, or Long Evans rats [4]. However, Sprague Dawley rats showed diverse responses, with some animals showing DIO, while others showed resistance to the diet [37].

This entry is adapted from the peer-reviewed paper 10.3390/obesities2020015

References

  1. Kanasaki, K.; Koya, D. Biology of Obesity: Lessons from Animal Models of Obesity. J. Biomed. Biotechnol. 2011, 2011, 197636.
  2. Suleiman, J.B.; Mohamed, M.; Bakar, A.B.A. A Systematic Review on Different Models of Inducing Obesity in Animals: Advantages and Limitations. J. Adv. Vet. Anim. Res. 2020, 7, 103–114.
  3. Kleinert, M.; Clemmensen, C.; Hofmann, S.M.; Moore, M.C.; Renner, S.; Woods, S.C.; Huypens, P.; Beckers, J.; de Angelis, M.H.; Schürmann, A.; et al. Animal Models of Obesity and Diabetes Mellitus. Nat. Rev. Endocrinol. 2018, 14, 140–162.
  4. Lutz, T.A.; Woods, S.C. Overview of Animal Models of Obesity. Curr. Protoc. Pharmacol. 2012, 58, 5.61.1–5.61.18.
  5. Guo, Y.; Fu, W.; Xin, Y.; Bai, J.; Peng, H.; Fu, L.; Liu, J.; Li, L.; Ma, Y.; Jiang, H. Antidiabetic and Antiobesity Effects of Artemether in Db/Db Mice. BioMed Res. Int. 2018, 2018, 8639523.
  6. Garcia-Mazcorro, J.F.; Mills, D.A.; Murphy, K.; Noratto, G. Effect of Barley Supplementation on the Fecal Microbiota, Caecal Biochemistry, and Key Biomarkers of Obesity and Inflammation in Obese Db/Db Mice. Eur. J. Nutr. 2018, 57, 2513–2528.
  7. Speakman, J.; Hambly, C.; Mitchell, S.; Król, E. The Contribution of Animal Models to the Study of Obesity. Lab. Anim. 2008, 42, 413–432.
  8. Crujeiras, A.B.; Carreira, M.C.; Cabia, B.; Andrade, S.; Amil, M.; Casanueva, F.F. Leptin Resistance in Obesity: An Epigenetic Landscape. Life Sci. 2015, 140, 57–63.
  9. Liu, J.; Lee, J.; Andres, M.; Hernandez, S.; Mazitschek, R.; Ozcan, U.; Hospital, G. Treatment of Obesity with Celastrol. Treatment 2016, 161, 999–1011.
  10. Smith, J.T.; Acohido, B.V.; Clifton, D.K.; Steiner, R.A. KiSS-1 Neurones Are Direct Targets for Leptin in the Ob/Ob Mouse. J. Neuroendocrinol. 2006, 18, 298–303.
  11. Ritskes-Hoitinga, M.; Tobin, G.; Jensen, T.L.; Mikkelsen, L.F. Nutrition of the Laboratory Mouse. In The Laboratory Mouse; Elsevier: Amsterdam, The Netherlands, 2012; pp. 567–599. ISBN 978-0-12-382008-2.
  12. Wargent, E.T.; Zaibi, M.S.; Silvestri, C.; Hislop, D.C.; Stocker, C.J.; Stott, C.G.; Guy, G.W.; Duncan, M.; Di Marzo, V.; Cawthorne, M.A. The Cannabinoid Δ9-Tetrahydrocannabivarin (THCV) Ameliorates Insulin Sensitivity in Two Mouse Models of Obesity. Nutr. Diabetes 2013, 3, e68.
  13. Sartorius, T.; Peter, A.; Schulz, N.; Drescher, A.; Bergheim, I.; Machann, J.; Schick, F.; Siegel-Axel, D.; Schürmann, A.; Weigert, C.; et al. Cinnamon Extract Improves Insulin Sensitivity in the Brain and Lowers Liver Fat in Mouse Models of Obesity. PLoS ONE 2014, 9, e92358.
  14. Simperova, A.; Al-Nakkash, L.; Faust, J.J.; Sweazea, K.L. Genistein Supplementation Prevents Weight Gain but Promotes Oxidative Stress and Inflammation in the Vasculature of Female Obese ob/ob Mice. Nutr. Res. 2016, 36, 789–797.
  15. Hua, H.; Zhang, Y.; Zhao, F.; Chen, K.; Wu, T.; Liu, Q.; Huang, S.; Zhang, A.; Jia, Z. Celastrol Inhibits Intestinal Lipid Absorption by Reprofiling the Gut Microbiota to Attenuate High-Fat Diet-Induced Obesity. iScience 2021, 24, 102077.
  16. van der Spek, R.; Kreier, F.; Fliers, E.; Kalsbeek, A. Circadian Rhythms in White Adipose Tissue. In Progress in Brain Research; Elsevier: Amsterdam, The Netherlands, 2012; Volume 199, pp. 183–201. ISBN 978-0-444-59427-3.
  17. Kitada, M.; Ogura, Y.; Koya, D. Rodent Models of Diabetic Nephropathy: Their Utility and Limitations. Int. J. Nephrol. Renov. Dis. 2016, 9, 279–290.
  18. Yorek, M.A. Alternatives to the Streptozotocin-Diabetic Rodent, 1st ed.; Elsevier Inc.: Amsterdam, The Netherlands, 2016; Volume 127, ISBN 9780128039151.
  19. Owens, D.R. Spontaneous, Surgically and Chemically Induced Models of Disease. In The laboratory Rat; Academic Press: Cambridge, MA, USA, 2006; pp. 711–732.
  20. Agouni, A.; Lagrue-Lak-Hal, A.-H.; Mostefai, H.A.; Tesse, A.; Mulder, P.; Rouet, P.; Desmoulin, F.; Heymes, C.; Martínez, M.C.; Andriantsitohaina, R. Red Wine Polyphenols Prevent Metabolic and Cardiovascular Alterations Associated with Obesity in Zucker Fatty Rats (Fa/Fa). PLoS ONE 2009, 4, e5557.
  21. Romo Vaquero, M.; Yáñez-Gascón, M.-J.; García Villalba, R.; Larrosa, M.; Fromentin, E.; Ibarra, A.; Roller, M.; Tomás-Barberán, F.; Espín de Gea, J.C.; García-Conesa, M.-T. Inhibition of Gastric Lipase as a Mechanism for Body Weight and Plasma Lipids Reduction in Zucker Rats Fed a Rosemary Extract Rich in Carnosic Acid. PLoS ONE 2012, 7, e39773.
  22. Tan, Y.; Kim, J.; Cheng, J.; Ong, M.; Lao, W.-G.; Jin, X.-L.; Lin, Y.-G.; Xiao, L.; Zhu, X.-Q.; Qu, X.-Q. Green Tea Polyphenols Ameliorate Non-Alcoholic Fatty Liver Disease through Upregulating AMPK Activation in High Fat Fed Zucker Fatty Rats. World J. Gastroenterol. 2017, 23, 3805.
  23. Chen, K.; Wei, X.; Zhang, J.; Pariyani, R.; Jokioja, J.; Kortesniemi, M.; Linderborg, K.M.; Heinonen, J.; Sainio, T.; Zhang, Y.; et al. Effects of Anthocyanin Extracts from Bilberry (Vaccinium Myrtillus L.) and Purple Potato (Solanum Tuberosum L. Var. ‘Synkeä Sakari’) on the Plasma Metabolomic Profile of Zucker Diabetic Fatty Rats. J. Agric. Food Chem. 2020, 68, 9436–9450.
  24. Bi, S.; Moran, T.H. Actions of CCK in the Controls of Food Intake and Body Weight: Lessons from the CCK-A Receptor Deficient OLETF Rat. Neuropeptides 2002, 36, 171–181.
  25. Schwarzer, M. Models to Investigate Cardiac Metabolism Michael. In The Scientist’s Guide to Cardiac Metabolism; Elsevier Inc.: Amsterdam, The Netherlands, 2016; Volume 45, p. 114. ISBN 9780128023945.
  26. Sung Roh, J.; Lee, H.; Woo, S.; Yoon, M.; Kim, J.; Dong Park, S.; Shik Shin, S.; Yoon, M. Herbal Composition Gambigyeongsinhwan (4) from Curcuma Longa, Alnus Japonica, and Massa Medicata Fermentata Inhibits Lipid Accumulation in 3T3-L1 Cells and Regulates Obesity in Otsuka Long-Evans Tokushima Fatty Rats. J. Ethnopharmacol. 2015, 171, 287–294.
  27. Shin, S.S.; Jung, Y.S.; Yoon, K.H.; Choi, S.; Hong, Y.; Park, D.; Lee, H.; Seo, B., II; Lee, H.Y.; Yoon, M. The Korean Traditional Medicine Gyeongshingangjeehwan Inhibits Adipocyte Hypertrophy and Visceral Adipose Tissue Accumulation by Activating PPARα Actions in Rat White Adipose Tissues. J. Ethnopharmacol. 2010, 127, 47–54.
  28. Jeon, B.S.; Park, J.W.; Kim, B.K.; Kim, H.K.; Jung, T.S.; Hahm, J.R.; Kim, D.R.; Cho, Y.S.; Cha, J.Y. Fermented Mushroom Milk-Supplemented Dietary Fibre Prevents the Onset of Obesity and Hypertriglyceridaemia in Otsuka Long-Evans Tokushima Fatty Rats. Diabetes Obes. Metab. 2005, 7, 709–715.
  29. Wanezaki, S.; Tachibana, N.; Nagata, M.; Saito, S.; Nagao, K.; Yanagita, T.; Kohno, M. Soy β-Conglycinin Improves Obesity-Induced Metabolic Abnormalities in a Rat Model of Nonalcoholic Fatty Liver Disease. Obes. Res. Clin. Pract. 2015, 9, 168–174.
  30. Sun, H.; Zhao, P.; Liu, W.; Li, L.; Ai, H.; Ma, X. Ventromedial Hypothalamic Nucleus in Regulation of Stress-Induced Gastric Mucosal Injury in Rats. Sci. Rep. 2018, 8, 10170.
  31. Kiba, T.; Tanaka, K.; Numata, K.; Hoshino, M.; Misugi, K.; Inoue, S. Ventromedial Hypothalamic Lesion-Induced Vagal Hyperactivity Stimulates Rat Pancreatic Cell Proliferation. Gastroenterology 1996, 110, 885–893.
  32. Parasuraman, S.; Wen, L.E. Animal Model for Obesity-An Overview. Syst. Rev. Pharm. 2016, 6, 9–12.
  33. Von Diemen, V.; Trindade, E.N.; Trindade, M.R.M. Experimental Model to Induce Obesity in Rats. Acta Cir. Bras. 2006, 21, 425–429.
  34. Miśkowiak, B.; Partyka, M. Effects of Neonatal Treatment with MSG (Monosodium Glutamate) on Hypothalamo-Pituitary-Thyroid Axis in Adult Male Rats. Histol. Histopathol. 1993, 8, 731–734.
  35. Alarcon-Aguilar, F.J.; Zamilpa, A.; Perez-Garcia, M.D.; Almanza-Perez, J.C.; Romero-Nuñez, E.; Campos-Sepulveda, E.A.; Vazquez-Carrillo, L.I.; Roman-Ramos, R. Effect of Hibiscus Sabdariffa on Obesity in MSG Mice. J. Ethnopharmacol. 2007, 114, 66–71.
  36. Kim, J.-E.; Hwang, I.-S.; Choi, S.-I.; Hye-Ryun, L.; Young-Ju, L.; Jun-Seo, G.; Hee-Seob, L.; Son, H.-J.; Jang, M.-J.; Lee, S.-H.; et al. Aqueous Extract of Liriope Platyphylla, a Traditional Chinese Medicine, Significantly Inhibits Abdominal Fat Accumulation and Improves Glucose Regulation in OLETF Type II Diabetes Model Rats. Lab Anim. Res 2012, 28, 181–191.
  37. Speakman, J.; Hambly, C.; Mitchell, S.; Król, E. Animal Models of Obesity. Obes. Rev. 2007, 8, 55–61.
  38. Hernández-Granados, M.J.; Ramírez-Emiliano, J.; Franco-Robles, E. Rodent Models of Obesity and Diabetes. In Experimental Animal Models of Human Diseases—An Effective Therapeutic Strategy; Bartholomew, I., Ed.; InTech: London, UK, 2018; ISBN 978-1-78923-164-9.
  39. Geiger, B.M.; Pothos, E.N. Translating Animal Models of Obesity and Diabetes to the Clinic. In Handbook of Behavioral Neuroscience; Elsevier: Amsterdam, The Netherlands, 2019; Volume 29, pp. 1–16. ISBN 978-0-12-803161-2.
  40. Preguiça, I.; Alves, A.; Nunes, S.; Fernandes, R.; Gomes, P.; Viana, S.D.; Reis, F. Diet-induced Rodent Models of Obesity-related Metabolic Disorders—A Guide to a Translational Perspective. Obes. Rev. 2020, 21, e13081.
  41. Panchal, S.K.; Brown, L. Rodent Models for Metabolic Syndrome Research. J. Biomed. Biotechnol. 2011, 2011, 1–14.
  42. Yang, Y.; Smith, D.L.; Keating, K.D.; Allison, D.B.; Nagy, T.R. Variations in Body Weight, Food Intake and Body Composition after Long-Term High-Fat Diet Feeding in C57BL/6J Mice: Variations in Diet-Induced Obese C57BL/6J Mice. Obesity 2014, 22, 2147–2155.
  43. Glastras, S.J.; Chen, H.; Teh, R.; McGrath, R.T.; Chen, J.; Pollock, C.A.; Wong, M.G.; Saad, S. Mouse Models of Diabetes, Obesity and Related Kidney Disease. PLoS ONE 2016, 11, e0162131.
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.
This entry is offline, you can click here to edit this entry!
Academic Video Service
Feedback