Biological Functions of RBP4 and Its Relevance for Human Diseases

Steinhoff, Julia; Lass, Achim; Schupp, Michael

doi:10.3389/fphys.2021.659977

Cited by 96 publications

(108 citation statements)

References 175 publications

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“…We further focused on the DEGs in this group of genes and applied PPI network analysis to distinguish hub genes, which are defined as genes with a high degree of connectivity that play an essential role in stabilizing the PPI network structure. Here, some star genes were identified, such as RBP4 20 , SPP2 21 and MAPK3 22 , those had been confirmed a role in pathological mechanisms. Fourth, DEGs specific to CCA subtypes were explored and compared.…”

Section: Discussionmentioning

confidence: 57%

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A comprehensive transcriptomic landscape of cholangiocarcinoma based on bioinformatics analysis from large cohort of patients

Zhang

et al. 2021

Sci Rep

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Cholangiocarcinoma (CCA) is a group of malignancies emerging in the biliary tree and is associated with a poor patient prognosis. Although the anatomical location is the only worldwide accepted classification basis, it still has bias. The current study integrates the whole-genome expression data from several big cohorts in the literature, to screen and provide a comprehensive bioinformatic analysis, in order to better classify molecular subtypes and explore an underlying cluster mechanism related to anatomy and geographical regions. Differentially expressed protein-coding genes (DEGs) were identified for CCA as well as subtypes. Biological function enrichment analysis—Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis—was applied and identified different DEGs enriched signaling pathways in CCA subtypes. A co-expression network was presented by Weighted gene co-expression network analysis package and modules related to specific phenotypes were identified. Combined with DEGs, hub genes in the given module were demonstrated through protein–protein interaction network analysis. Finally, DEGs which significantly related to patient overall survival and disease-free survival time were selected, including ARHGAP21, SCP2, UBIAD1, TJP2, RAP1A and HDAC9.

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Section: Discussionmentioning

confidence: 57%

“…Out of this module, 579 DEGs were extracted and hub genes were identified through PPI network analysis. The PPI network suggested that RBP4 20 , SPP2 21 , MAPK3 22 and another around 30 genes were hub genes (Fig. 3 d).…”

Section: Resultsmentioning

confidence: 97%

A comprehensive transcriptomic landscape of cholangiocarcinoma based on bioinformatics analysis from large cohort of patients

Zhang

et al. 2021

Sci Rep

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“…Although the involvement of TTR in the transport of thyroid hormones [ 37 ] and retinol through binding to RBP [ 38 ], as well as in the development of familial amyloidotic polyneuropathy (FAP) [ 39 ], is well established, its other roles, such as neuroprotective and metabolic roles, began to be explored only recently.…”

Section: Discussionmentioning

confidence: 99%

Exploring the Physiological Role of Transthyretin in Glucose Metabolism in the Liver

Alemi

Oliveira

Tavares

et al. 2021

IJMS

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Transthyretin (TTR), a 55 kDa evolutionarily conserved protein, presents altered levels in several conditions, including malnutrition, inflammation, diabetes, and Alzheimer’s Disease. It has been shown that TTR is involved in several functions, such as insulin release from pancreatic β-cells, recovery of blood glucose and glucagon levels of the islets of Langerhans, food intake, and body weight. Here, the role of TTR in hepatic glucose metabolism was explored by studying the levels of glucose in mice with different TTR genetic backgrounds, namely with two copies of the TTR gene, TTR+/+; with only one copy, TTR+/-; and without TTR, TTR-/-. Results showed that TTR haploinsufficiency (TTR+/-) leads to higher glucose in both plasma and in primary hepatocyte culture media and lower expression of the influx glucose transporters, GLUT1, GLUT3, and GLUT4. Further, we showed that TTR haploinsufficiency decreases pyruvate kinase M type (PKM) levels in mice livers, by qRT-PCR, but it does not affect the hepatic production of the studied metabolites, as determined by 1H NMR. Finally, we demonstrated that TTR increases mitochondrial density in HepG2 cells and that TTR insufficiency triggers a higher degree of oxidative phosphorylation in the liver. Altogether, these results indicate that TTR contributes to the homeostasis of glucose by regulating the levels of glucose transporters and PKM enzyme and by protecting against mitochondrial oxidative stress.

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“…RBP4 was identified in the 1960s by Kanai et al as the plasma transporter of retinol complexed with transthyretin (TTR). This 21 kDa lipocalin is mainly expressed in liver and adipose tissue, and various other tissues at lower levels, and is the main—if not the only—transporter of vitamin A in vivo [ 8 ]. Some gain-of-function mutations on RBP4 promoter were reported to be associated with a higher risk of developing obesity or type 2 diabetes [ 15 , 16 ] while a non-coding mutation in RBP4 promoter is associated with dyslipidemia [ 17 ].…”

Section: Rbp4mentioning

confidence: 99%

Adipose-Derived Lipid-Binding Proteins: The Good, the Bad and the Metabolic Diseases

Frances

Tavernier

Viguerie

2021

IJMS

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Adipose tissue releases a large range of bioactive factors called adipokines, many of which are involved in inflammation, glucose homeostasis and lipid metabolism. Under pathological conditions such as obesity, most of the adipokines are upregulated and considered as deleterious, due to their pro-inflammatory, pro-atherosclerotic or pro-diabetic properties, while only a few are downregulated and would be designated as beneficial adipokines, thanks to their counteracting properties against the onset of comorbidities. This review focuses on six adipose-derived lipid-binding proteins that have emerged as key factors in the development of obesity and diabetes: Retinol binding protein 4 (RBP4), Fatty acid binding protein 4 (FABP4), Apolipoprotein D (APOD), Lipocalin-2 (LCN2), Lipocalin-14 (LCN14) and Apolipoprotein M (APOM). These proteins share structural homology and capacity to bind small hydrophobic molecules but display opposite effects on glucose and lipid metabolism. RBP4 and FABP4 are positively associated with metabolic syndrome, while APOD and LCN2 are ubiquitously expressed proteins with deleterious or beneficial effects, depending on their anatomical site of expression. LCN14 and APOM have been recently identified as adipokines associated with healthy metabolism. Recent findings on these lipid-binding proteins exhibiting detrimental or protective roles in human and murine metabolism and their involvement in metabolic diseases are also discussed.

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Biological Functions of RBP4 and Its Relevance for Human Diseases

Cited by 96 publications

References 175 publications

A comprehensive transcriptomic landscape of cholangiocarcinoma based on bioinformatics analysis from large cohort of patients

A comprehensive transcriptomic landscape of cholangiocarcinoma based on bioinformatics analysis from large cohort of patients

Exploring the Physiological Role of Transthyretin in Glucose Metabolism in the Liver

Adipose-Derived Lipid-Binding Proteins: The Good, the Bad and the Metabolic Diseases

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