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Aim: Nonalcoholic fatty liver disease (NAFLD) is a significant health issue worldwide. This study investigated the effect of the adiponectin receptor 1 gene (ADIPOR1) polymorphism on susceptibility to NAFLD. Methods: Data from 330 participants, including 165 biopsy-proven NAFLD patients and 165 healthy controls, were collected. The PCR-RFLP method was used to detect the genotypes of ADIPOR1 rs2275738 or T-106C variant. Results: The "CC" genotype of the ADIPOR1 rs2275738 polymorphism, compared with the "TT" genotype and the "C" allele, compared with the "T" allele, are markers of increased NAFLD susceptibility (p = 0.018; OR = 2.07, 95% CI = 1.43–2.01 and p = 0.041; OR = 1.52, 95% CI = 1.24–2.35, respectively). Conclusion: This research suggests, for the first time, that the ADIPOR1 rs2275738 "CC" genotype is associated with a 107% increased risk for biopsy-proven NAFLD. Article highlights Nonalcoholic fatty liver disease (NAFLD) as the most common cause of liver dysfunction affects around 25% of the adult general population. More and more evidence indicate that adiponectin – a multifunctional adipocytokine – may contribute to the development and progression of NAFLD. To the best of our knowledge, this is the first demonstration of the association between adiponectin receptor 1 gene (ADIPOR1) variants and biopsy-proven NAFLD. The rs2275738 polymorphism in ADIPOR1 gene may be implicated in the pathogenesis of NAFLD. The rs2275738 "CC" genotype compared with the "TT" genotype had a 107% increased risk for NAFLD. The "C" allele of ADIPOR1 rs2275738 in comparison to the "T" allele was significantly overrepresented in the biopsy-proven NAFLD patients. Although these observations are relevant from a scientific viewpoint too, their replication in other populations is necessary to validate the role of ADIPOR1 gene SNPs in NAFLD. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC) stands as a significant global health issue, marked by elevated occurrence and mortality statistics. Despite the availability of various treatments, including chemotherapy, radiotherapy, and targeted therapy, CRC cells often exhibit resistance to these interventions. As a result, it is imperative to identify the disease at an earlier stage and enhance the response to treatment by acquiring a deeper comprehension of the processes driving tumor formation, aggressiveness, metastasis, and resistance to therapy. The Hippo pathway plays a critical role in facilitating the initiation of tumorigenesis and frequently experiences disruption within CRC because of genetic mutations and modified expression in its fundamental constituents. Targeting upstream regulators or core Hippo pathway components may provide innovative therapeutic strategies for modulating Hippo signaling dysfunction in CRC. To advance novel therapeutic techniques for CRC, it is imperative to grasp the involvement of the Hippo pathway in CRC and its interaction with alternate signaling pathways, noncoding RNAs, gut microbiota, and the immune microenvironment. This review seeks to illuminate the function and control of the Hippo pathway in CRC, ultimately aiming to unearth innovative therapeutic methodologies for addressing this ailment. [ABSTRACT FROM AUTHOR]