Histone deacetylase 3 inhibition improves glycaemia and insulin secretion in obese diabetic rats

Publikation: Bidrag til tidsskrift › Letter › Forskning › fagfællebedømt

Standard

Histone deacetylase 3 inhibition improves glycaemia and insulin secretion in obese diabetic rats. / Lundh, Morten; Galbo, Thomas; Poulsen, Steen Seier; Mandrup-Poulsen, Thomas.

I: Diabetes, Obesity and Metabolism, Bind 17, Nr. 7, 07.2015, s. 703-7.

Publikation: Bidrag til tidsskrift › Letter › Forskning › fagfællebedømt

Harvard

Lundh, M, Galbo, T, Poulsen, SS & Mandrup-Poulsen, T 2015, 'Histone deacetylase 3 inhibition improves glycaemia and insulin secretion in obese diabetic rats', Diabetes, Obesity and Metabolism, bind 17, nr. 7, s. 703-7. https://doi.org/10.1111/dom.12470

APA

Lundh, M., Galbo, T., Poulsen, S. S., & Mandrup-Poulsen, T. (2015). Histone deacetylase 3 inhibition improves glycaemia and insulin secretion in obese diabetic rats. Diabetes, Obesity and Metabolism, 17(7), 703-7. https://doi.org/10.1111/dom.12470

Vancouver

Lundh M, Galbo T, Poulsen SS, Mandrup-Poulsen T. Histone deacetylase 3 inhibition improves glycaemia and insulin secretion in obese diabetic rats. Diabetes, Obesity and Metabolism. 2015 jul.;17(7):703-7. https://doi.org/10.1111/dom.12470

Author

Lundh, Morten ; Galbo, Thomas ; Poulsen, Steen Seier ; Mandrup-Poulsen, Thomas. / Histone deacetylase 3 inhibition improves glycaemia and insulin secretion in obese diabetic rats. I: Diabetes, Obesity and Metabolism. 2015 ; Bind 17, Nr. 7. s. 703-7.

Bibtex

@article{b6a3d4b62a984b24a1e581458bdc99a6,
title = "Histone deacetylase 3 inhibition improves glycaemia and insulin secretion in obese diabetic rats",
abstract = "Failure of pancreatic β cells to compensate for insulin resistance is a prerequisite for the development of type 2 diabetes. Sustained elevated circulating levels of free fatty acids and glucose contribute to β-cell failure. Selective inhibition of Histone deacetylase (HDAC)-3 protects pancreatic β cells against inflammatory and metabolic insults in vitro. Here we tested the ability of a selective HDAC3 inhibitor, BRD3308, to reduce hyperglycemia and increase insulin secretion in an animal model of type 2 diabetes. At diabetes onset, an ambulatory hyperglycemic clamp was performed. HDAC3 inhibition improved hyperglycemia over the study period without affecting weight gain. At the end of the hyperglycemic clamp, circulating insulin levels were significantly higher in BRD3308-treated animals. Pancreatic insulin staining and contents were also significantly higher. These findings highlight HDAC3 as a key therapeutic target for β-cell protection in type 2 diabetes.",
author = "Morten Lundh and Thomas Galbo and Poulsen, {Steen Seier} and Thomas Mandrup-Poulsen",
note = "This article is protected by copyright. All rights reserved.",
year = "2015",
month = jul,
doi = "10.1111/dom.12470",
language = "English",
volume = "17",
pages = "703--7",
journal = "Diabetes, Obesity and Metabolism",
issn = "1462-8902",
publisher = "Wiley-Blackwell",
number = "7",

}

RIS

TY - JOUR

T1 - Histone deacetylase 3 inhibition improves glycaemia and insulin secretion in obese diabetic rats

AU - Lundh, Morten

AU - Galbo, Thomas

AU - Poulsen, Steen Seier

AU - Mandrup-Poulsen, Thomas

N1 - This article is protected by copyright. All rights reserved.

PY - 2015/7

Y1 - 2015/7

N2 - Failure of pancreatic β cells to compensate for insulin resistance is a prerequisite for the development of type 2 diabetes. Sustained elevated circulating levels of free fatty acids and glucose contribute to β-cell failure. Selective inhibition of Histone deacetylase (HDAC)-3 protects pancreatic β cells against inflammatory and metabolic insults in vitro. Here we tested the ability of a selective HDAC3 inhibitor, BRD3308, to reduce hyperglycemia and increase insulin secretion in an animal model of type 2 diabetes. At diabetes onset, an ambulatory hyperglycemic clamp was performed. HDAC3 inhibition improved hyperglycemia over the study period without affecting weight gain. At the end of the hyperglycemic clamp, circulating insulin levels were significantly higher in BRD3308-treated animals. Pancreatic insulin staining and contents were also significantly higher. These findings highlight HDAC3 as a key therapeutic target for β-cell protection in type 2 diabetes.

AB - Failure of pancreatic β cells to compensate for insulin resistance is a prerequisite for the development of type 2 diabetes. Sustained elevated circulating levels of free fatty acids and glucose contribute to β-cell failure. Selective inhibition of Histone deacetylase (HDAC)-3 protects pancreatic β cells against inflammatory and metabolic insults in vitro. Here we tested the ability of a selective HDAC3 inhibitor, BRD3308, to reduce hyperglycemia and increase insulin secretion in an animal model of type 2 diabetes. At diabetes onset, an ambulatory hyperglycemic clamp was performed. HDAC3 inhibition improved hyperglycemia over the study period without affecting weight gain. At the end of the hyperglycemic clamp, circulating insulin levels were significantly higher in BRD3308-treated animals. Pancreatic insulin staining and contents were also significantly higher. These findings highlight HDAC3 as a key therapeutic target for β-cell protection in type 2 diabetes.

U2 - 10.1111/dom.12470

DO - 10.1111/dom.12470

M3 - Letter

C2 - 25846481

VL - 17

SP - 703

EP - 707

JO - Diabetes, Obesity and Metabolism

JF - Diabetes, Obesity and Metabolism

SN - 1462-8902

IS - 7

ER -

ID: 135222112