The DOI matches its Crossref record; 119 of the 119 references it cites were found in a registry or an index.
Mouse models of the metabolic syndrome
Open accessAbstract
The metabolic syndrome (MetS) is characterized by obesity concomitant with other metabolic abnormalities such as hypertriglyceridemia, reduced high-density lipoprotein levels, elevated blood pressure and raised fasting glucose levels. The precise definition of MetS, the relationships of its metabolic features, and what initiates it, are debated. However, obesity is on the rise worldwide, and its association with these metabolic symptoms increases the risk for diabetes and cardiovascular disease (among many other diseases). Research needs to determine the mechanisms by which obesity and MetS increase the risk of disease. In light of this growing epidemic, it is imperative to develop animal models of MetS. These models will help determine the pathophysiological basis for MetS and how MetS increases the risk for other diseases. Among the various animal models available to study MetS, mice are the most commonly used for several reasons. First, there are several spontaneously occurring obese mouse strains that have been used for decades and that are very well characterized. Second, high-fat feeding studies require only months to induce MetS. Third, it is relatively easy to study the effects of single genes by developing transgenic or gene knockouts to determine the influence of a gene on MetS. For these reasons, this review will focus on the benefits and caveats of the most common mouse models of MetS. It is our hope that the reader will be able to use this review as a guide for the selection of mouse models for their own studies.
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Cites
Positional cloning of the mouse obese gene and its human homologue
Zhang, Y., Proenca, R., Maffei, M., Barone, M., Leopold, L., & Friedman, J. M. (1994) · Nature · doi:10.1038/372425a0 · Cited by 13,419
Role of Insulin Resistance in Human Disease
Reaven, G. M. (1988) · Diabetes · doi:10.2337/diab.37.12.1595 · Cited by 12,154
Genetics of Food Intake Self-Regulation in Childhood: Literature Review and Research Opportunities
Faith, M. S., Carnell, S., & Kral, T. V. E. (2013) · Human Heredity · doi:10.1159/000353879 · Cited by 7,601
Paradoxical Decrease of an Adipose-Specific Protein, Adiponectin, in Obesity
Arita, Y., Kihara, S., Ouchi, N., Takahashi, M., Maeda, K., Miyagawa, J.-I., Hotta, K., Shimomura, I., Nakamura, T., Miyaoka, K., et al. (1999) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1999.0255 · Cited by 4,856
Banting lecture 1988. Role of insulin resistance in human disease
Reaven, G. M. (1988) · Diabetes · doi:10.2337/diabetes.37.12.1595 · Cited by 3,811
Targeted disruption of the melanocortin-4 receptor results in obesity in mice
Huszar, D., Lynch, C. A., Fairchild-Huntress, V., Dunmore, J. H., Fang, Q., Berkemeier, L. R., Gu, W., Kesterson, R. A., Boston, B. A., Cone, R. D., et al. (1997) · Cell · doi:10.1016/s0092-8674(00)81865-6 · Cited by 3,030
Plump, A. S., Smith, J. D., Hayek, T., Aalto-Setälä, K., Walsh, A., Verstuyft, J. G., Rubin, E. M., & Breslow, J. L. (1992) · Cell · doi:10.1016/0092-8674(92)90362-g · Cited by 2,263
Spontaneous Hypercholesterolemia and Arterial Lesions in Mice Lacking Apolipoprotein E
Zhang, S. H., Reddick, R. L., Piedrahita, J. A., & Maeda, N. (1992) · Science · doi:10.1126/science.1411543 · Cited by 2,237
Diet-induced insulin resistance in mice lacking adiponectin/ACRP30
Maeda, N., Shimomura, I., Kishida, K., Nishizawa, H., Matsuda, M., Nagaretani, H., Furuyama, N., Kondo, H., Takahashi, M., Arita, Y., et al. (2002) · Nature Medicine · doi:10.1038/nm724 · Cited by 2,088
Role of melanocortinergic neurons in feeding and the agouti obesity syndrome
Fan, W., Boston, B. A., Kesterson, R. A., Hruby, V. J., & Cone, R. D. (1997) · Nature · doi:10.1038/385165a0 · Cited by 1,902
Cited by
Metabolic Syndrome: Updates on Pathophysiology and Management in 2021
Fahed, G., Aoun, L., Bou Zerdan, M., Allam, S., Bou Zerdan, M., Bouferraa, Y., & Assi, H. I. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23020786 · Cited by 1,441
The impact of obesity on the immune response to infection
Milner, J. J., & Beck, M. A. (2012) · Proceedings of The Nutrition Society · doi:10.1017/s0029665112000158 · Cited by 439
Large animal models of cardiovascular disease
Tsang, H. G., Rashdan, N. A., Whitelaw, C. B. A., Corcoran, B. M., Summers, K. M., & MacRae, V. E. (2016) · Cell Biochemistry and Function · doi:10.1002/cbf.3173 · Cited by 154
A rodent model of rapid-onset diabetes (ROD) induced by glucocorticoids and high-fat feeding
Shpilberg, Y., Beaudry, J. L., D'Souza, A., Campbell, J. E., Peckett, A., & Riddell, M. C. (2011) · Disease Models & Mechanisms · doi:10.1242/dmm.008912 · Cited by 77
Greenfield, J. R. (2011) · Journal of Neuroendocrinology · doi:10.1111/j.1365-2826.2010.02088.x · Cited by 72
Metadata
- Authors
- Kennedy, A. J., Ellacott, K. L. J., King, V. L., & Hasty, A. H.
- Venue
- Disease Models & Mechanisms
- Publisher
- The Company of Biologists
- Published
- 2010-03-08
- Volume
- 3
- Issue
- 3-4
- Pages
- 156-166
- ISSN
- 1754-8403 (ISSN-L)
- 1754-8411
- OpenAlex
- W2120902612
- Cited by
- 264
- References
- 119
- FWCI
- 9.91
- Type
- journal article
- Language
- en
- Open access
- green
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