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Amir Najafi, Mohammad Amin Momeni-Moghaddam, Dr Davoud Salarbashi, Narges Amini Beidokhti, Marziye Rahmani, Milad Khorasani,
Volume 27, Issue 3 (7-2024)
Abstract

Introduction: Type 2 diabetes is a non-communicable disease that imposes a significant financial burden on the healthcare system each year. Numerous studies have demonstrated the involvement of inflammatory factors in the initiation and progression of this condition. The primary goal of this study is to compare the polymorphism of the interleukin 1 receptor antagonist gene among individuals with type 2 diabetes and those in the control group.
Methods: Following approval from the Ethics Committee of Gonabad University of Medical Sciences, blood samples were collected from 100 participants at Bohlool Hospital in Gonabad. These individuals were categorized into two groups: cases (individuals with type 2 diabetes) and controls (healthy individuals). DNA extraction was carried out using the salting out method. To examine the polymorphism, the specific segment was initially amplified through PCR with designated primers and then identified via gel electrophoresis. The data were analyzed using  subjected to the Chi-square test at a significance level below 5%.
Results: Findings from the polymorphism analysis revealed a notable contrast in the genotype 2/1 (P = 0.001) and 2/2 (P = 0.004) within the case group when compared to the healthy participants. Specifically, individuals with genotype 2/1 exhibited a heightened risk of developing type 2 diabetes by up to 15 times.
Conclusions: Within the examined population, the polymorphism of the interleukin 1 receptor antagonist gene substantially influenced the predisposition to type 2 diabetes, amplifying the likelihood of developing this ailment. Individuals harboring allele 2 are at an increased susceptibility to type 2 diabetes.
Sahar Khalvati, Tahereh Foroutan, Madjid Momeni-Moghaddam, Toktam Hajjar,
Volume 28, Issue 1 (3-2025)
Abstract

Introduction: This study aimed to investigate the effects of insulin drug therapy on the kidney structure of offspring of insulin-treated diabetic mice.
Methods: After pregnancy, female Sprague-Dawley rats were divided into control, sham, diabetics induced by streptozotocin, and diabetics receiving insulin groups. Diabetic rat offspring were sacrificed on the 10th day after natural childbirth, and the left kidneys were studied for morphometric and histological studies.
Results: The weight of children of diabetic mothers showed a significant decrease compared to children of healthy mothers (P < 0.001). The weight of the offspring of diabetic mothers receiving insulin did not show a substantial change compared to the offspring of diabetic mothers. The weight of the kidneys of the offspring of diabetic mothers showed a significant decrease compared to the control group. However, the weight of the kidneys of the offspring of diabetic mothers receiving insulin did not increase compared to those of diabetic mothers. The results of the kidney sections stained with hematoxylin-eosin and trichrome Masson showed that the offspring of diabetic mothers treated with insulin did not show a significant improvement compared to the control group.
Conclusions: Although the use of insulin is one of the momentous therapeutic ways to control blood glucose in diabetics, it cannot significantly lead to the normal health of the kidneys of the offspring of diabetic mothers under insulin treatment.

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