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

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Fransson, LiselotteKarolinska Institutet (author)

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

Article/chapterEnglish2013

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BioScientifica,2013
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LIBRIS-ID:oai:DiVA.org:liu-102775
https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-102775URI
https://doi.org/10.1530/JOE-13-0189DOI
https://urn.kb.se/resolve?urn=urn:nbn:se:hig:diva-38202URI
http://kipublications.ki.se/Default.aspx?queryparsed=id:127845513URI

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Language:English
Summary in:English

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Subject category:ref swepub-contenttype
Subject category:art swepub-publicationtype

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Funding Agencies|Diabetes Research and Wellness Foundation||Swedish Diabetes Foundation (Diabetesfonden)||Tore Nilsson Foundation||Swedish Society for Medical Research||KID (Karolinska Institutet)||
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 mu g/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 beta-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.

Subject headings and genre

MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin hsv//swe
MEDICAL AND HEALTH SCIENCES Clinical Medicine hsv//eng
glucocorticoid
diabetes
insulin secretion
obesity
islet cells
MEDICINE
MEDICIN

Added entries (persons, corporate bodies, meetings, titles ...)

Franzén, StephanieLinköpings universitet,Avdelningen för läkemedelsforskning,Hälsouniversitetet,Linköpings universitet, Avdelningen för läkemedelsforskning(Swepub:liu)stefr34 (author)
Rosengren, VictoriaKarolinska Institutet (author)
Wolbert, PetraSoder Sjukhuset, Sweden (author)
Sjöholm, ÅkeSoder Sjukhuset, Sweden(Swepub:hig)akesjm (author)
Ortsater, HenrikSoder Sjukhuset, Sweden (author)
Karolinska InstitutetAvdelningen för läkemedelsforskning (creator_code:org_t)

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In:Journal of Endocrinology: BioScientifica219:3, s. 231-2410022-07951479-6805

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