In:
Journal of Physics: Conference Series, IOP Publishing, Vol. 1853, No. 1 ( 2021-03-01), p. 012003-
Kurzfassung:
We aimed here to study the impact of leptin on insulin like growth factor-1 (IGF-1) level to imply its antidiabetic effect on Iraqi rheumatoid arthritis’s, who was with and without diabetes mellitus. Rheumatoid arthritis is a chronic inflammatory disease, primarily targets the synovium and articular cartilage, which causes joint damage. Although the role of adipocytokines in mediating damages of joint has recently suggested, it is still a matter of considerable debate. METHODS: Patients diagnosed as diabetic rheumatoid arthritis aged from 33-60 years and others diagnosed as non-diabetic rheumatoid arthritis were compared with healthy control (aged 33-46 years). Some biochemical parameters have determined, such as fasting serum glucose, glycated hemoglobin, lipid profile, serum fasting insulin, IGF-1, and leptin, using ELISA and immune radiometric assay. Results indicated an elevation in some biochemical parameters in diabetic rheumatoid arthritis’s when compared with patients without diabetes. There was a significant increase in fasting serum glucose and some of the lipid components in diabetic rheumatoid arthritis patients compared to that non-diabetic. A significant elevation of leptin in diabetic rheumatoid arthritis patients compared to control (p 〈 0.003). However, a non-significant difference of leptin was detected between diabetic rheumatoid arthritis and non-diabetic patients. In addition, some other parameters were significantly reduced in diabetic rheumatoid arthritis patients when compared to non-diabetic patients, such as high-density lipoprotein and IGF-1. This study highlights that leptin could act as pro-inflammatory mediator in rheumatoid arthritis. The negative correlation between leptin level and IGF-1 plays an important role in understanding the metabolic pathogenesis of rheumatoid arthritis.
Materialart:
Online-Ressource
ISSN:
1742-6588
,
1742-6596
DOI:
10.1088/1742-6596/1853/1/012003
Sprache:
Unbekannt
Verlag:
IOP Publishing
Publikationsdatum:
2021
ZDB Id:
2166409-2
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