Increased β-cell volume in mice fed a high-fat diet: A dynamic study over 12 months

Ahrén, Jonatan; Åhrén, Bo; Wierup, Nils

doi:10.4161/isl.2.6.13619

Cited by 88 publications

(55 citation statements)

References 23 publications

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“…Contrary to cell area measured in conventional optical microscopy, "brightfield area" provides a more accurate estimation of cell size (or volume). In agreement with previous observations showing that β cell size can decrease during the first 3 months of exposure to a HFD, and later followed by β cell hyperthrophy after 6 and 12 months of HFD feeding (43), our ImageStream analysis suggests that even a short-term exposure to a HFD may have a significant impact on the overall homeostasis of β cell volume. Interestingly, results from this analysis also revealed that the geometric mean intensity of insulin-specific immunoreactivity detected in cells gated from the "in focus" population was decreased by ~45% (from 305,362 to 173,261 ImageStream X Mark II arbitrary units) in β cells from ZDF-HFD ( Figure 4, B and E).…”

Section: Body Weights Plasma Insulin Ip Glucose Tolerance Test (Isupporting

confidence: 78%

Nrf2/antioxidant pathway mediates β cell self-repair after damage by high-fat diet–induced oxidative stress

Abebe¹,

Mahadevan²,

Bogachus³

et al. 2017

JCI Insight

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Section: Body Weights Plasma Insulin Ip Glucose Tolerance Test (Isupporting

confidence: 78%

Nrf2/antioxidant pathway mediates β cell self-repair after damage by high-fat diet–induced oxidative stress

Abebe¹,

Mahadevan²,

Bogachus³

et al. 2017

JCI Insight

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“…Consistent with previous reports (20), pathological findings indicated that the numbers of ␤-cells were significantly enhanced in HFD-fed WT mice (Fig. 6A).…”

Section: Resultssupporting

confidence: 81%

Impaired Oxidative Endoplasmic Reticulum Stress Response Caused by Deficiency of Thyroid Hormone Receptor α

Takahashi

Furuya

Shimura

et al. 2014

Journal of Biological Chemistry

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Background: Endoplasmic reticulum (ER) stress is involved in ␤-cell failure and apoptotic death. Results: Upon endogenous TR␣ knockdown, ER stress significantly enhanced apoptosis in pancreatic ␤-cells. Conclusion: TR␣ facilitates reduced apoptosis in pancreatic ␤-cells under ER stress. Significance: TR␣ is coupled to stress response modulation and improved survival of pancreatic ␤-cells.

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“…Increased islet size has previously been reported in animal models of obesity and insulin resistance (Gepts et al 1960, Rafacho et al 2009, Ahren et al 2010 and this was also evident in this model with GC excess. Both pancreatic insulin content and islet volume were increased in mice exposed to corticosterone.…”

Section: Effects Of Corticosterone On Pancreatic Islet Adaptationmentioning

confidence: 70%

β-cell adaptation in a mouse model of glucocorticoid-induced metabolic syndrome

Fransson¹,

Franzén²,

Rosengren³

et al. 2013

Journal of Endocrinology

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Glucocorticoids (GCs) are stress hormones primarily responsible for mobilizing glucose to the circulation. Due to this effect, insulin resistance and glucose intolerance are concerns in patients with endogenous overproduction of GCs and in patients prescribed GC-based therapy. In addition, hypercortisolemic conditions share many characteristics with the metabolic syndrome. This study reports on a thorough characterization, in terms of glucose control and lipid handling, of a mouse model where corticosterone is given via the drinking water. C57BL/6J mice were treated with corticosterone (100 or 25 mg/ml) or vehicle in their drinking water for 5 weeks after which they were subjected to insulin or glucose tolerance tests. GC-treated mice displayed increased food intake, body weight gain, and central fat deposit accumulations. In addition, the GC treatment led to dyslipidemia as well as accumulation of ectopic fat in the liver and skeletal muscle, having a substantial negative effect on insulin sensitivity. Also glucose intolerance and hypertension, both part of the metabolic syndrome, were evident in the GC-treated mice. However, the observed effects of corticosterone were reversed after drug removal. Furthermore, this study reveals insights into b-cell adaptation to the GC-induced insulin resistance. Increased pancreatic islet volume due to cell proliferation, increased insulin secretion capacity, and increased islet chaperone expression were found in GC-treated animals. This model mimics the human metabolic syndrome. It could be a valuable model for studying the complex mechanisms behind the development of the metabolic syndrome and type 2 diabetes, as well as the multifaceted relations between GC excess and disease.

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Increased β-cell volume in mice fed a high-fat diet: A dynamic study over 12 months

Cited by 88 publications

References 23 publications

Nrf2/antioxidant pathway mediates β cell self-repair after damage by high-fat diet–induced oxidative stress

Nrf2/antioxidant pathway mediates β cell self-repair after damage by high-fat diet–induced oxidative stress

Impaired Oxidative Endoplasmic Reticulum Stress Response Caused by Deficiency of Thyroid Hormone Receptor α

β-cell adaptation in a mouse model of glucocorticoid-induced metabolic syndrome

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