Treatment with an Interleukin 1 beta antibody improves glycemic control in diet-induced obesity

The proinflammatory cytokine Interleukin 1 beta (IL-1β) is elevated in obese individuals and rodents and it is implicated in impaired insulin secretion, decreased cell proliferation and apoptosis of pancreatic beta cells. In this study we describe the therapeutic effects by an IL-1β antibody to impr...

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Bibliographic Details
Published in:Cytokine (Philadelphia, Pa.) Pa.), 2008-10, Vol.44 (1), p.141-148
Main Authors: Osborn, O., Brownell, S.E., Sanchez-Alavez, M., Salomon, D., Gram, H., Bartfai, T.
Format: Article
Language:English
Subjects:
Animals
Antibodies - therapeutic use
Blood Glucose - metabolism
Diabetes
Diet
Glycated Hemoglobin A - metabolism
Hyperglycemia
Insulin Resistance - physiology
Interleukin 1 alpha
Interleukin 1 beta
Interleukin-1beta - immunology
Male
Mice
Obesity
Obesity - drug therapy
Obesity - physiopathology
Serum Amyloid A Protein - metabolism
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Summary:The proinflammatory cytokine Interleukin 1 beta (IL-1β) is elevated in obese individuals and rodents and it is implicated in impaired insulin secretion, decreased cell proliferation and apoptosis of pancreatic beta cells. In this study we describe the therapeutic effects by an IL-1β antibody to improve glucose control in hyperglycemic mice with diet-induced obesity. After 13 weeks of treatment the IL-1β antibody treated group showed reduced glycated hemoglobin ( ∗ P = 0.049), reduced serum levels of proinsulin ( ∗ P = 0.015), reduced levels of insulin and smaller islet size ( ∗ P = 1.65E-13) relative to the control antibody treated group. Neutralization of IL-1β also significantly reduced serum amyloid A (SAA) which is an indicator of inflammation-induced acute phase response ( ∗ P = 0.024). While there was no improvement of obesity, a significant improvement of glycemic control and of beta cell function is achieved by this pharmacological treatment which may slow/prevent disease progression in Type 2 Diabetes.
ISSN:1043-4666
1096-0023
DOI:10.1016/j.cyto.2008.07.004