ArticleJournal of molecular histology2024
Protective effects of ghrelin on pancreas in fructose diet and streptozotocin-induced diabetic rats.
Article in Journal of molecular histology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
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Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ghrelin, which is widely expressed in central and peripheral tissues, has several metabolic effects. It has been suggested that these effects may include anti-inflammatory, anti-oxidant, and anti-apoptotic effects. Therefore, we aimed to investigate the effects of ghrelin administered to diabetic rats on DNA repair and apoptosis mechanisms, and differences in oxidative stress (OS) and pancreatic hormone levels in the pancreas. Twenty-one rats were randomly divided into three groups: control, type 2 diabetes mellitus (T2DM), and T2DM treated with ghrelin (T2DM + ghrelin). We examined PCNA and PARP-1 to evaluate the effect of ghrelin on DNA repair, caspase-3 and caspase-9 to evaluate its effect on apoptosis, and insulin and glucagon to evaluate its role in regulating glucose homeostasis by immunohistochemistry in diabetic rats. Malondialdehyde, glutathione, and protein carbonyl levels, as well as catalase, glutathione-S-transferase, and superoxide dismutase (SOD) activities, were measured spectrophotometrically to detect the ghrelin effect on OS. Homeostasis model assessment for insulin resistance (HOMA-IR) and pancreatic insulin levels were assessed by ELISA method. Ghrelin may be a potential regulator of apoptosis as it significantly reduced the number of caspase-3 and caspase-9 immunopositive cells (p < 0.0001). In addition, ghrelin treatment reduced OS by decreasing glutathione (p < 0.001), malondialdehyde, and protein carbonyl, as well as the activity of SOD (p < 0.05) in diabetic rats. The results suggest that ghrelin is a potential apoptotic regulator and may be considered as a therapeutic agent due to its significant ability to suppress OS in T2DM.
Indexed as
Identifiers
39673670What Socratic holds
Registered trials
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