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PMID: 23316348 Published · ppublish English Journal Article

Glucocorticoids and type 2 diabetes: from physiology to pathology.

Journal of nutrition and metabolism ·Vol. 2012 ·2012-00-00 ·Pages 525093

Di Dalmazi G, Pagotto U, Pasquali R, Vicennati V

Abstract

Type 2 diabetes mellitus is the result of interaction between genetic and environmental factors, leading to heterogeneous and progressive pancreatic β-cell dysfunction. Overweight and obesity are major contributors to the development of insulin resistance and impaired glucose tolerance. The inability of β cells to secrete enough insulin produces type 2 diabetes. Abnormalities in other hormones such as reduced secretion of the incretin glucagon-like peptide 1 (GLP-1), hyperglucagonemia, and raised concentrations of other counterregulatory hormones also contribute to insulin resistance, reduced insulin secretion, and hyperglycaemia in type 2 diabetes. Clinical-overt and experimental cortisol excess is associated with profound metabolic disturbances of intermediate metabolism resulting in abdominal obesity, insulin resistance, and low HDL-cholesterol levels, which can lead to diabetes. It was therefore suggested that subtle abnormalities in cortisol secretion and action are one of the missing links between insulin resistance and other features of the metabolic syndrome. The aim of this paper is to address the role of glucocorticoids on glucose homeostasis and to explain the relationship between hypercortisolism and type 2 diabetes.

Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Di Dalmazi Guido
Division of Endocrinology, Department of Medical and Surgical Science, S. Orsola-Malpighi Hospital, University Alma Mater Studiorum, Via Massarenti 9, 40138 Bologna, Italy.
Pagotto Uberto
Pasquali Renato
Vicennati Valentina
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Article Info
Journal
Journal of nutrition and metabolism
Abbr.
J Nutr Metab
ISSN
2090-0732
DOI
10.1155/2012/525093
Published
2012-00-00
Epub
2012-00-18
Pages
525093
Language
English
Region
United States
NLM ID
101526296
PMCID
PMC3536319
External Links
PubMed source DOI: 10.1155/2012/525093 PMC Full Text View journal details
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