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Favorable outcomes of hydroxychloroquine in insulin resistance may be accomplished by adjustment of the endothelial dysfunction as well as the skewed balance of adipokines
•Hydroxychloroquine has a favorable effect on the endocrine pancreas in insulin resistance.•This effect may be attained by suppression of the endothelial stress markers.•This is accompanied by the correction of the skewed adipokines balance.•The favorable outcome is reflected on the glucose homeosta...
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Published in: | Acta histochemica 2016-07, Vol.118 (6), p.560-573 |
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Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | •Hydroxychloroquine has a favorable effect on the endocrine pancreas in insulin resistance.•This effect may be attained by suppression of the endothelial stress markers.•This is accompanied by the correction of the skewed adipokines balance.•The favorable outcome is reflected on the glucose homeostasis parameters.
Hydroxychloroquine (HCQ) has been demonstrated to reduce the risk to develop diabetes mellitus (DM). However no previous experimental study had investigated its effect on the structure of the endocrine pancreas, islets of Langerhans (IOL), in insulin resistance (IR). In addition, the mechanism by which HCQ can prevent DM is not well understood. In this study, we hypothesized that the possible favorable outcome of HCQ may be partly achieved by its molecular effect on the endothelial stress markers as well as on the imparied balance of the adipokines that usually accompanies IR.
A total of 54 rats were divided equally into; control, high fat diet (HFD) and HFD+HCQ groups (received standard chow, HFD and HFD+HCQ respectively). After 12 weeks, samples from pancreas as well as visceral adipose tissue (VAT) were histologically studied for the consequent changes.
In the HFD group, there were mild degenerative changes and expansion of the IOL accompanied with a significantly increased (p |
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ISSN: | 0065-1281 1618-0372 |
DOI: | 10.1016/j.acthis.2016.06.002 |