Parathyroid hormone alleviates non-alcoholic liver steatosis via activating the hepatic cAMP/PKA/CREB pathway

Xu, Feng; Xiao, Yamei; Guo, Qi; Peng, Hui; Huang, Zhou; Wang, Jianping; Xia, Zhuying

doi:10.3389/fendo.2022.899731

Cited by 10 publications

(5 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In vitro, cAMP signaling pathway inhibited palmitic acid-induced intracellular lipid accumulation in PTH1R-dependent manner. cAMP signaling pathway activation upregulated the expression of the genes involved in lipid beta-oxidation and downregulated the expression of the genes related to lipid uptake and de novo lipogenesis [50]. In this study, we found that the overlapping DEGs among the 1st, 3rd and 5th day were involved in cAMP signaling pathway, which was consistent with previous studies [51,52].…”

Section: Discussionsupporting

confidence: 92%

“…In the present study, the DEGs in the livers between treated with and without MnCl 2 on the 3rd and 5th day were involved in AMPK signaling pathway (Fig. 3B-C), which was consistent with previous ndings [47][48][49][50]. AMPK signaling pathway induced by dapagli ozin reduced oxidative stress and in ammation in vitro model of NAFLD [47].…”

Section: Discussionsupporting

confidence: 91%

“…The activation of AMPK in hepatocytes effectively attenuated the effects of lambda-cyhalothrin-induced hepatic steatosis [49]. In addition, AMPK signaling pathway was linked to the effects of ferulic acid in upregulating the hepatic speci c markers (HNF4a, Foxa2, and Alb) [50].…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Unveiling the Hub Genes Associated with Manganese-Induced Hepatotoxicity

Yang

Wang

et al. 2023

Preprint

View full text Add to dashboard Cite

Excessive exposure to manganese (Mn) can cause severe toxicity in human and animal organs, particularly the liver. However, the specific mechanisms of Mn-induced hepatotoxicity remain unclear. Thus, the objective of this study was to identify the key genes associated with hepatotoxicity caused by Mn administration. We obtained the gene expression data set GSE59923 from the Gene Expression Omnibus, which included liver samples treated with manganese chloride (MnCl2) as well as control samples. Through our analysis, we identified 222, 351, and 494 differentially expressed genes (DEGs) in the livers treated with MnCl2 at 700 mg/kg on the 1st, 3rd, and 5th day, respectively. Notably, we found a total of 27 overlapping DEGs in the liver samples. Biological process analysis revealed that these common DEGs were associated with the response to xenobiotic stimulus, cellular calcium ion homeostasis, and ion transmembrane transport. Pathway analysis further indicated the involvement of cAMP, p53, PI3K-Akt, MAPK, and AMPK signaling pathways in Mn-induced hepatotoxicity. Furthermore, we identified several important genes, including CCR2, CDKN1A, CELSR2, LCN2, and PER2, which appeared to play a role in Mn-induced hepatotoxicity. Taken together, this study sheds light on the molecular mechanisms underlying Mn-induced hepatotoxicity, contributing to our overall understanding of this condition.

show abstract

Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 91%

See 1 more Smart Citation

Unveiling the Hub Genes Associated with Manganese-Induced Hepatotoxicity

Yang

Wang

et al. 2023

Preprint

View full text Add to dashboard Cite

show abstract

“…Regarding peptide hormones, parathyroid hormone (PTH), the only FDA-approved anabolic treatment for osteoporosis [ 125 ], is commonly utilized as a pharmaceutical agent for the treatment of osteoporosis [ 21 ]. Low calcium levels induce PTH production, which subsequently activates the Wnt-beta catenin pathway crucial for bone formation.…”

Section: Current Modifications Of Bone Repair Materialsmentioning

confidence: 99%

Advances in biomaterials for oral-maxillofacial bone regeneration: spotlight on periodontal and alveolar bone strategies

Li,

Wang,

Feng

et al. 2024

Regenerative Biomaterials

View full text Add to dashboard Cite

The intricate nature of oral-maxillofacial structure and function, coupled with the dynamic oral bacterial environment, presents formidable obstacles in addressing the repair and regeneration of oral-maxillofacial bone defects. Numerous characteristics should be noticed in oral-maxillofacial bone repair, such as irregular morphology of bone defects, homeostasis between hosts and microorganisms in the oral cavity, and complex periodontal structures that facilitate epithelial ingrowth. Therefore, oral-maxillofacial bone repair necessitates restoration materials that adhere to stringent and specific demands. This review starts with exploring these particular requirements by introducing the particular characteristics of oral-maxillofacial bones, and then summarizes the classifications of current bone repair materials in respect of composition and structure. Additionally, we discuss the modifications in current bone repair materials including improving mechanical properties, optimizing surface topography and pore structure, and adding bioactive components such as elements, compounds, cells, and their derivatives. Ultimately, we organize a range of potential optimization strategies and future perspectives for enhancing oral-maxillofacial bone repair materials, including physical environment manipulation, oral microbial homeostasis modulation, osteo-immune regulation, smart stimuli-responsive strategies and multifaceted approach for poly-pathic treatment, in the hope of providing some insights for researchers in this field. In summary, this review analyzes the complex demands of oral-maxillofacial bone repair, especially for periodontal and alveolar bone, concludes multifaceted strategies for corresponding biomaterials, and aims to inspire future research in the pursuit of more effective treatment outcomes.

show abstract

“…The expression of these genes lead to the activation of the cAMP/PKA/CREB pathway, and facilitates NAFLD steatosis. 108 NAFLD in pregnancy is a risk factor for maternal and child health. 109 In this context, PTH reduces insulin sensitivity and β-cell functions in pregnancy.…”

Section: Role Of Vitamin D In Diabetesmentioning

confidence: 99%

Molecular Crosstalk Between Vitamin D and Non-alcoholic Fatty Liver Disease

Sarkar¹

2023

Explor Res Hypothesis Med

View full text Add to dashboard Cite

Non-alcoholic fatty liver disease (NAFLD) is one of the leading causes of chronic liver disease. The worldwide increasing prevalence of NAFLD has become a cause of concern for clinicians. Furthermore, the molecular mechanism of NAFLD pathogenesis remains poorly understood. Moreover, therapeutic interventions are presently limited. Balanced diet, physical exercise and lifestyle modifications have been recommended. Several studies have revealed that vitamin D deficiency is correlated with NAFLD, and it's supplementation may play a vital role in this regard. Sufficient information was obtained from full articles written in the English language, and accessible in PubMed, Google Scholar, Web of Science, and Scopus. The increasing prevalence of vitamin D deficiency remains as a global health risk factor, and this is linked to NAFLD pathogenesis. In vitro and in vivo studies, and clinical trials have revealed the beneficial role of vitamin D supplementation to control NAFLD. Vitamin D potentially regulates the molecular pathways associated with NAFLD risk factors, such as obesity, insulin resistance, and diabetes. It acts on adipocytes to control free fatty acid (FFA) trafficking, lipogenesis, and inflammation. Similarly, vitamin D acts on hepatocytes to reduce de novo lipogenesis and cellular FFA trafficking. Furthermore, it acts on pancreatic β-cells to improve insulin secretion, cell survival, and cellular functions. Vitamin D supplementation improves glucose uptake and insulin sensitivity. In addition, it decreases inflammation and liver injury, and acts on mitochondria to control reactive oxygen species (ROS)-mediated cellular toxicity. Vitamin D deficiency is a major risk factor for NAFLD pathogenesis. Thus, there is an urgent need to conduct molecular level analysis for further discernments.

show abstract

Parathyroid hormone alleviates non-alcoholic liver steatosis via activating the hepatic cAMP/PKA/CREB pathway

Cited by 10 publications

References 47 publications

Unveiling the Hub Genes Associated with Manganese-Induced Hepatotoxicity

Unveiling the Hub Genes Associated with Manganese-Induced Hepatotoxicity

Advances in biomaterials for oral-maxillofacial bone regeneration: spotlight on periodontal and alveolar bone strategies

Molecular Crosstalk Between Vitamin D and Non-alcoholic Fatty Liver Disease

Contact Info

Product

Resources

About