Insulin resistance contributes to aberrant stress responses in the Tg2576 mouse model of Alzheimer's disease
Open accessAbstract
We previously reported aberrant stress responses and impaired glucose tolerance in transgenic Tg2576 mice, a model of Alzheimer's disease (AD). Here we report that by 8 months of age, Tg2576 mice had lower basal serum insulin concentrations and exhibited a delayed insulin-induced reduction in blood glucose levels relative to wild-type mice. However, the basal levels of blood glucose and percent glycosylated hemoglobin (%HbA1c) were similar between the two groups of mice. While the basal levels of serum corticosterone were similar between Tg2576 and wild-type mice, an overnight fasting caused a greater rise in serum corticosterone levels and an excessive reduction in serum insulin concentrations in the transgenics. At 9 months of age, we began administering Tg2576 mice rosiglitazone, an agonist of peroxisome proliferator-activated receptor-gamma that increases peripheral insulin sensitivity, and after 6 weeks of administration the Tg2576 mice had the same response to insulin and increase in serum corticosterone levels after an overnight fast as did wild-type mice. By 13 months of age, untreated Tg2576 mice had become hyperinsulinemic, in contrast to Tg2576 mice administered rosiglitazone for 4 months where the serum insulin concentrations were maintained at levels observed in wild-type mice. These results provide evidence for a relationship between insulin resistance, impaired regulation of insulin and glucose levels, and aberrant stress responses in Tg2576 mice.
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Sustained PPARγ or LXR activation results in amelioration of AD-related pathophysiology in AD mouse models.
“Sustained PPARγ or LXR activation results in amelioration of AD-related pathophysiology in AD mouse models (Yan et al., 2003; Pedersen and Flynn, 2004; Heneka et al., 2005; Koldamova et al., 2005a; Riddell et al., 2007; Zelcer et al., 2007; Jiang et al., 2008; Donkin et al., 2010; Fitz et al., 2010; Toledo and Inestrosa, 2010).”
From Mechanisms Underlying the Rapid Peroxisome Proliferator-Activated Receptor-γ-Mediated Amyloid Clearance and Reversal of Cognitive Deficits in a Murine Model of Alzheimer's Disease (2012) · cites this paper as Pedersen and Flynn, 2004
There has been no consensus on the mechanisms of action of PPARγ agonists in AD mouse models.
“however, there has been no consensus on the mechanisms of action”
From Mechanisms Underlying the Rapid Peroxisome Proliferator-Activated Receptor-γ-Mediated Amyloid Clearance and Reversal of Cognitive Deficits in a Murine Model of Alzheimer's Disease (2012) · cites this paper as Pedersen and Flynn, 2004
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- Authors
- PEDERSEN, W., & FLYNN, E.
- Affiliations
- CHI Health Creighton University Medical Center - Bergan Mercy (US)
- Corresponding author
- PEDERSEN, W
- ORCID
- FLYNN, E
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2004-12
- Volume
- 17
- Issue
- 3
- Pages
- 500-506
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W2043841065
- Cited by
- 108
- References
- 36
- Citations by year
- 2025: 3 · 2024: 2 · 2023: 4 · 2022: 2 · 2021: 3 · 2020: 2 · 2019: 2 · 2018: 5 · 2017: 1 · 2016: 4 · 2015: 5 · 2014: 5 · 2013: 7 · 2012: 13
- FWCI
- 3.66
- Type
- journal article
- Language
- en
- Open access
- green
- doaj.org
- Licence
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Creighton University
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- insulin resistance, Alzheimer's disease, Tg2576 mice, stress response, corticosterone, glucose tolerance, hyperinsulinemia, rosiglitazone, PPARγ agonists, insulin sensitivity
- MeSH terms
- Rosiglitazone, Alzheimer Disease, Animals, Blood Glucose, Disease Models, Animal, Glycated Hemoglobin, Humans, Hypoglycemic Agents, Insulin, Insulin Resistance, Mice, Transgenic, Reference Values, Stress, Physiological, Thiazolidinediones, Mice
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