Potential of an Interorgan Network Mediated by Toxic Advanced Glycation End-Products in a Rat Model

Inoué, Shinya; Takata, Takanobu; Nakazawa, Yusuke; Nakamura, Yuka; Guo, Xin; Yamada, Sohsuke; Ishigaki, Yasuhito; Takeuchi, Masayoshi; Miyazawa, Katsuhito

doi:10.3390/nu13010080

Cited by 6 publications

(28 citation statements)

References 58 publications

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“…In a transcriptome analysis of renal cortex comparing diabetic mice with diabetic post-menopausal mice, Usp2 expression was slightly enhanced in the menopause model [ 130 ]. By contrast, high-fructose corn syrup supplementation downregulated Usp2 mRNA in the kidney via humoral factors derived from the liver [ 131 ]. Further studies are required to clarify the role of USP2 in the pathogenesis of diabetic nephropathy.…”

Section: Diabetes-associated Disordersmentioning

confidence: 99%

Ubiquitin-Specific Proteases (USPs) and Metabolic Disorders

Kitamura

2023

IJMS

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Ubiquitination and deubiquitination are reversible processes that modify the characteristics of target proteins, including stability, intracellular localization, and enzymatic activity. Ubiquitin-specific proteases (USPs) constitute the largest deubiquitinating enzyme family. To date, accumulating evidence indicates that several USPs positively and negatively affect metabolic diseases. USP22 in pancreatic β-cells, USP2 in adipose tissue macrophages, USP9X, 20, and 33 in myocytes, USP4, 7, 10, and 18 in hepatocytes, and USP2 in hypothalamus improve hyperglycemia, whereas USP19 in adipocytes, USP21 in myocytes, and USP2, 14, and 20 in hepatocytes promote hyperglycemia. In contrast, USP1, 5, 9X, 14, 15, 22, 36, and 48 modulate the progression of diabetic nephropathy, neuropathy, and/or retinopathy. USP4, 10, and 18 in hepatocytes ameliorates non-alcoholic fatty liver disease (NAFLD), while hepatic USP2, 11, 14, 19, and 20 exacerbate it. The roles of USP7 and 22 in hepatic disorders are controversial. USP9X, 14, 17, and 20 in vascular cells are postulated to be determinants of atherosclerosis. Moreover, mutations in the Usp8 and Usp48 loci in pituitary tumors cause Cushing syndrome. This review summarizes the current knowledge about the modulatory roles of USPs in energy metabolic disorders.

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Section: Diabetes-associated Disordersmentioning

confidence: 99%

Ubiquitin-Specific Proteases (USPs) and Metabolic Disorders

Kitamura

2023

IJMS

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“…Finally, Solution A and Solution B were mixed together (9:1) (Solution C, Table 1). The components of Solution C were 27 mM Tris, 6.3 M urea, 1.8 M thiourea, and 3.6% CHAPS, making up the lysis buffer used for our novel slot blot analysis [15,[22][23][24][25][26][27]29]. The final components of Solution D were based on the preparation of Solution C. When Tris, urea, thiourea, and CHAPS were dissolved in ultra-pure water, Solution B was added to it (Table 1) [20,21,28,30].…”

Section: Preparation and Application Of Lysis Buffermentioning

confidence: 99%

“…Solution C [15,[22][23][24][25][26][27]29] Solution D [20,21,28,30] Table 3. References for the cell types lysed with Solution C and D.…”

Section: Solution Referencesmentioning

confidence: 99%

“…From 2017 to 2022, we quantified the intracellular content of TAGE, which was calculated using TAGE-BSA in the human hepatic cell line HepG2 [20,21], hepatocyte-like cells differentiated from human induced pluripotent stem cells (hiPS-HLC) [22], rat primary hepatocytes [23], rat primary cardiomyocytes [24], human normal cardiac fibroblasts [25], the human pancreatic islet β-cell line 1.4E7 [26], a human pancreatic ductal cell line [15], the murine skeletal muscle myoblast cell line C2C12 [27], the murine osteoblastic cell line MC3T3-E1 [28], and rat hepatic tissue [23,29]. In addition, in 2019, we suggested that human hepatocytes might produce 1,5-anhydro-D-fructose-derived AGEs (1,5-AF-AGEs) [30].…”

Section: Introductionmentioning

confidence: 99%

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Is the Novel Slot Blot a Useful Method for Quantification of Intracellular Advanced Glycation End-Products?

Takata

2023

Metabolites

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Various types of advanced glycation end-products (AGEs) have been identified and studied. I have reported a novel slot blot analysis to quantify two types of AGEs, glyceraldehyde-derived AGEs, also called toxic AGEs (TAGE), and 1,5-anhydro-D-fructose AGEs. The traditional slot blot method has been used for the detection and quantification of RNA, DNA, and proteins since around 1980 and is one of the more commonly used analog technologies to date. However, the novel slot blot analysis has been used to quantify AGEs from 2017 to 2022. Its characteristics include (i) use of a lysis buffer containing tris-(hydroxymethyl)-aminomethane, urea, thiourea, and 3-[3-(cholamidopropyl)-dimetyl-ammonio]-1-propane sulfonate (a lysis buffer with a composition similar to that used in two-dimensional gel electrophoresis-based proteomics analysis); (ii) probing of AGE-modified bovine serum albumin (e.g., standard AGE aliquots); and (iii) use of polyvinylidene difluoride membranes. In this review, the previously used quantification methods of slot blot, western blot, immunostaining, enzyme-linked immunosorbent assay, gas chromatography–mass spectrometry (MS), matrix-associated laser desorption/ionization–MS, and liquid chromatography–electrospray ionization–MS are described. Lastly, the advantages and disadvantages of the novel slot blot compared to the above methods are discussed.

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“…We recently demonstrated that the excess consumption of 10% HFCS 55 (Fru 55%/Glu 45%) increased intracellular TAGE levels in normal rat livers and serum TAGE levels [ 55 , 56 ]. The HFCS-induced promotion of TAGE generation in normal rat livers may increase the risk of NAFLD/NASH.…”

Section: The Intracellular Generation and Accumulation Of Tage In The...mentioning

confidence: 99%

Involvement of Intracellular TAGE and the TAGE–RAGE–ROS Axis in the Onset and Progression of NAFLD/NASH

2023

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The repeated excessive intake of sugar, a factor that contributes to the onset of nonalcoholic fatty liver disease (NAFLD) and its progression to the chronic form of nonalcoholic steatohepatitis (NASH), markedly increases the hepatocyte content of glyceraldehyde (GA), a glucose/fructose metabolic intermediate. Toxic advanced glycation end-products (toxic AGEs, TAGE) are synthesized by cross-linking reactions between the aldehyde group of GA and the amino group of proteins, and their accumulation has been implicated in the development of NAFLD/NASH and hepatocellular carcinoma (HCC). Our previous findings not only showed that hepatocyte disorders were induced by the intracellular accumulation of TAGE, but they also indicated that extracellular leakage resulted in elevated TAGE concentrations in circulating fluids. Interactions between extracellular TAGE and receptor for AGEs (RAGE) affect intracellular signaling and reactive oxygen species (ROS) production, which may, in turn, contribute to the pathological changes observed in NAFLD/NASH. RAGE plays a role in the effects of the extracellular leakage of TAGE on the surrounding cells, which ultimately promote the onset and progression of NAFLD/NASH. This review describes the relationships between intracellular TAGE levels and hepatocyte and hepatic stellate cell (HSC) damage as well as the TAGE–RAGE–ROS axis in hepatocytes, HSC, and HCC cells. The “TAGE theory” will provide novel insights for future research on NAFLD/NASH.

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Potential of an Interorgan Network Mediated by Toxic Advanced Glycation End-Products in a Rat Model

Cited by 6 publications

References 58 publications

Ubiquitin-Specific Proteases (USPs) and Metabolic Disorders

Ubiquitin-Specific Proteases (USPs) and Metabolic Disorders

Is the Novel Slot Blot a Useful Method for Quantification of Intracellular Advanced Glycation End-Products?

Involvement of Intracellular TAGE and the TAGE–RAGE–ROS Axis in the Onset and Progression of NAFLD/NASH

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