Glucocorticoids and Type 2 Diabetes: From Physiology to Pathology
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 inabilit...
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| Format: | Article |
| Language: | English |
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Wiley
2012-01-01
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| Series: | Journal of Nutrition and Metabolism |
| Online Access: | http://dx.doi.org/10.1155/2012/525093 |
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| author | Guido Di Dalmazi Uberto Pagotto Renato Pasquali Valentina Vicennati |
| author_facet | Guido Di Dalmazi Uberto Pagotto Renato Pasquali Valentina Vicennati |
| author_sort | Guido Di Dalmazi |
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| description | 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. |
| format | Article |
| id | doaj-art-36a6c2b00ebc4701b2a4cc9eb611e1d1 |
| institution | OA Journals |
| issn | 2090-0724 2090-0732 |
| language | English |
| publishDate | 2012-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Nutrition and Metabolism |
| spelling | doaj-art-36a6c2b00ebc4701b2a4cc9eb611e1d12025-08-20T02:07:45ZengWileyJournal of Nutrition and Metabolism2090-07242090-07322012-01-01201210.1155/2012/525093525093Glucocorticoids and Type 2 Diabetes: From Physiology to PathologyGuido Di Dalmazi0Uberto Pagotto1Renato Pasquali2Valentina Vicennati3Division of Endocrinology, Department of Medical and Surgical Science, S. Orsola-Malpighi Hospital, University Alma Mater Studiorum, Via Massarenti 9, 40138 Bologna, ItalyDivision of Endocrinology, Department of Medical and Surgical Science, S. Orsola-Malpighi Hospital, University Alma Mater Studiorum, Via Massarenti 9, 40138 Bologna, ItalyDivision of Endocrinology, Department of Medical and Surgical Science, S. Orsola-Malpighi Hospital, University Alma Mater Studiorum, Via Massarenti 9, 40138 Bologna, ItalyDivision of Endocrinology, Department of Medical and Surgical Science, S. Orsola-Malpighi Hospital, University Alma Mater Studiorum, Via Massarenti 9, 40138 Bologna, ItalyType 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.http://dx.doi.org/10.1155/2012/525093 |
| spellingShingle | Guido Di Dalmazi Uberto Pagotto Renato Pasquali Valentina Vicennati Glucocorticoids and Type 2 Diabetes: From Physiology to Pathology Journal of Nutrition and Metabolism |
| title | Glucocorticoids and Type 2 Diabetes: From Physiology to Pathology |
| title_full | Glucocorticoids and Type 2 Diabetes: From Physiology to Pathology |
| title_fullStr | Glucocorticoids and Type 2 Diabetes: From Physiology to Pathology |
| title_full_unstemmed | Glucocorticoids and Type 2 Diabetes: From Physiology to Pathology |
| title_short | Glucocorticoids and Type 2 Diabetes: From Physiology to Pathology |
| title_sort | glucocorticoids and type 2 diabetes from physiology to pathology |
| url | http://dx.doi.org/10.1155/2012/525093 |
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