Emerging evidence suggests that the JAK/STAT/SOCS signaling pathway is crucial for maintaining homeostasis, and its dysregulation contributes to diabetes development. This study aimed to evaluate the roles of SOCS-1 and SOCS-3 in the pancreas, liver, and kidney and to explore the involvement of the JAK/STAT pathway in the molecular mechanisms underlying their effects on inflammation and apoptosis, as well as organ injury in a diabetes mellitus (DM) model. Additionally, we sought to elucidate the role of the JAK/STAT/SOCS pathway in mediating the effects of lycopene (LYC). Forty Sprague-Dawley rats were divided into control, DM, LYC, and LYC+DM groups. Diabetes was induced in the DM groups using streptozotocin. LYC was administered to the LYC and LYC+DM groups for 30 days. After the study, pancreas, liver, and kidney tissues were analyzed using histopathological, immunohistochemical, and PCR methods. Significant vacuolization and degenerative changes were observed in the DM group’s pancreatic islet cells. Kidney and liver tissues showed hyperemia, hemorrhage, and degenerative changes. Immunohistochemical analysis revealed increased expression of Cas-3, TNF-α, IFN-α, and IL-6, while IL-10 was significantly reduced in the DM group. PCR analysis showed elevated levels of TNF-α and Cas-3, with decreased SOCS-1 and SOCS-3 expression in the DM group. This study highlights the therapeutic potential of targeting the JAK/STAT/SOCS pathway with lycopene, demonstrating its promise in mitigating diabetes and related complications.

Although heavy metals are naturally occurring elements that are found throughout the Earth’s crust, most environmental contamination and human exposure result from anthropogenic activities, such as mining and smelting operations, industrial production and use, and the domestic and agricultural use of metals and metal-containing compounds. The accumulation of heavy metals eventually produces reactive oxygen species that can cause oxidative stress, which may lead to the production of various diseases. The aim of this study was to evaluate the possible effects of iron and zinc on kidney and liver tissues and the positive effects of juglone (5-hydroxy-1,4-naphthoquinone) antioxidant activity, using an immunohistochemical technique. The animals under study were randomly divided into five groups (seven in each group): group I, control; group II, iron (Fe) (600 ppm); group III, zinc (Zn) (400 ppm); group IV, Fe + antioxidant juglone; and group V, Zn + antioxidant juglone. Hematoxylin-eosin (H&E) was applied to determine the histological sides of the damage caused by the heavy metals in the liver and kidney tissues and the effects of the administration of juglone on reducing these damages. Furthermore, the immunohistochemical TUNEL method was applied to determine the DNA damages in the cells. The density of the damage in the liver and kidney tissues of the iron group was higher than in the other groups.

Obezite, genetik, çevresel faktörler ve bunların karmaşık etkileşimleri tarafından yönetilen birçok kronik hastalık ile ilişkilidir. Genetiğin obeziteye yatkınlıkta önemli rol oynadığı ve hastalık riskine %70'e kadar katkıda bulunabileceği tahmin edilmektedir. Yapılan genetik çalışmalar, genlerin obeziteye katkıda bulunduğunu doğrulamıştır. Genlerdeki anomaliler, Bardet- Biedl ve Prader-Willi sendromları gibi obezite ile ilişkili bozukluklardan doğrudan sorumludur. Genetik epidemiyolojik yaklaşımlar, özellikle genom çapında ilişkilendirme çalışmaları, insan obezitesinde önemli rol oynayan çok sayıda geni tanımlamıştır. Gelecekte, obezite genetiğinin daha fazla araştırılması, obezite tedavisi için yararlı teşhis testleri geliştirmeye yardımcı olabilir. Bu derleme ile obezite genetiği hakkında güncel literatür ile desteklenmiş bilgiler aktarılmıştır.

Tributyltin (TBT) is a persistent environmental endocrine disruptor with documented neurotoxic and reproductive effects, yet its impact on coordinated brain–ovary immune–endocrine regulation remains unclear. This study investigated whether subchronic, low-dose TBT exposure is associated with parallel alterations in these tissues. Female Wistar rats were exposed to TBT (50, 100, 300 ng/kg/day) with or without fucoxanthin (Fx, 20 mg/kg/day) for four weeks. Brain and ovarian tissues were assessed via histopathology, immunohistochemistry (NF‑κB, IL‑6, IL‑1β, IL‑10, ERα, PR), and RT‑qPCR (TNF‑α, Adipoq). TBT exposure was associated with reduced central IL‑10 alongside increased NF‑κB/IL‑1β/IL‑6 and neurodegenerative changes. Concurrently, ovaries showed NF‑κB/IL‑6 activation, altered TNF‑α/Adipoq expression, follicular degeneration, and disrupted ERα/PR signaling. These dose‑dependent, non‑linear effects occurred simultaneously in both tissues. Fx co‑treatment mitigated many alterations, partially restoring IL‑10, suppressing inflammatory markers, and improving ovarian histopathology. These findings indicate that subchronic low-dose TBT exposure is associated with parallel brain–ovary immune–endocrine-related alterations, supporting the concept that endocrine disruptors can perturb integrated central–peripheral immune–endocrine networks without implying direct endocrine dysfunction.