Genetic models
Mouse overexpressing neuropeptide Y under the promoter of dopamine-beta-hydroxylase in adrenergic and noradrenergic neurons presents with a Metabolic Syndrome -like phenotype with increased fat mass and impaired glucose tolerance without hyperphagia. The mice are susceptible to induction of vascular hypertrophy.
Vähätalo et al, Acta Physiol 2015
Salomäki-Myftari et al, PloS One 2016
Ailanen et al, J Endocrinol 2017
Diet-induced models
Diets high in fat and/or sucrose content are used to induce fat mass gain, insulin resistance, hyperlipidemia, hypercholesterolemia, hepatosteatosis and impaired vascular function. Effects of pharmacological, dietary and exercise interventions can be studied in the diet-induced mouse models of obesity and impaired glucose tolerance.
Heinonen I et al Acta Physiol 2014
Ailanen et al, Front Pharmacol 2018
Ruohonen et al, Neurondocrinology 2018
Type 1 Diabetes
Non-obese diabetic (NOD) mice develop an autoimmune diabetes spontaneously with age. The model can be used to study pathogenesis and prevention of type 1 diabetes.
Sysi-Aho M et al Metabolic regulation in progression to type 1 diabetes, PLoS Computational Biology 7:e1002257, 2011.
Alam CM et al. Keratin 8 modulates ß-cell stress responses and normoglyceamia. J. Cell Sci. 126:5635-5644, 2013.
Chemically induced model of diabetes
Streptozotocin (STZ) is used to destroy pancreatic β-cells, reduce the production of insulin leading to hyperglycemia and a commonly used model for of Type I diabetes. Acute and chronic diabetic phenotypes are studied. Combining low-dose STZ with diet-induced insulin release is used to model type 2 diabetes.
Alam CM et al. Keratin 8 modulates ß-cell stress responses and normoglyceamia. J. Cell Sci. 126:5635-5644, 2013.