Toxic AGEs (TAGE) Cause Lifestyle-Related Diseases
Abstract
:1. Introduction
2. Glycation and AGEs, the History of Glycation Research
3. Overview of AGEs Formation Pathway in the Body
- (i)
- GA is produced by nonenzymatic dephosphorylation of glyceraldehyde-3-phosphate (GA-3-P), a glycolytic intermediate. Glycolysis is a fundamental metabolic pathway involving the conversion of Glu to pyruvate. When GA-3-P metabolism shifts to another route, the amount of GA increases, promoting the formation of GA-AGEs.
- (ii)
- GA is directly produced from Fru by the action of fructokinase (FK) and aldolase B, which are key enzymes in fructolysis [40,41]. FK accumulates in the liver after a meal, and Fru is phosphorylated by a specific FK to form Fru-1-phosphate (F-1-P), which is then cleaved by aldolase B, producing dihydroxyacetone-phosphate (DHA-P) and GA.
- (iii)
- GA is produced by fructolysis but from Fru produced in the polyol pathway [42,43], an alternative pathway of glycolysis, under hyperglycemic conditions. Aldose reductase catalyzes the reduction of Glu to sorbitol, which is then converted to Fru by sorbitol dehydrogenase. Under hyperglycemic conditions, Glu concentrations are elevated in insulin-independent tissues, enhancing the activity of the polyol pathway.
4. Origin of the Name TAGE
5. The TAGE-RAGE Axis
6. Structures and Formation Pathway of TAGE
6.1. Formation Pathways of Known GA-AGEs and TAGE
6.2. Structure of TAGE
7. TAGE as a Cytotoxic Factor
7.1. Association with Neuronal Damage
7.2. Association with Hepatocellular Damage
7.3. Association with Cardiomyocyte Damage
7.4. Summary
8. Blood TAGE as a Predictive Marker for LSRD
8.1. Association with NASH
8.2. Association with CRC
8.3. Association with CVD and Heart Failure
8.4. Association with Infertility Treatment
8.5. Summary
9. Strategies to Prevent LSRD by Suppressing TAGE
9.1. Sugar Intake and TAGE
9.2. dAGEs Intake and TAGE
9.3. Summary
10. Degradation Pathway of TAGE
11. Therapeutic Drugs of TAGE in LSRD
- (i)
- When healthy individuals took collagen tripeptide [95,96,97], which has TAGE inhibitory effects, the blood TAGE levels as well as the cardio–ankle vascular index decreased, which indicates the stiffness of the blood vessel walls. It is expected that an “improvement of TAGE levels will restore the elasticity of blood vessels and prevent arteriosclerosis” [4].
- (ii)
- When water chestnut (Trapa bispinosa Roxb.) extract [98,99,100] was administered to elderly patients with intractable infertility, the birth rate significantly increased with the decrease in blood TAGE levels [4]. Water chestnut extract significantly enhanced oocyte developmental potential, improved endometrial receptivity in natural cycles, and decreased blood and follicular fluid TAGE levels [4].
- (iii)
- Blood TAGE levels in NASH patients with dyslipidemia were reduced by treatment with atorvastatin. A 6-month treatment with atorvastatin decreased the activities of liver alanine aminotransferase and γ-glutamyl transpeptidase in all patients. Moreover, plasma adiponectin levels increased, and plasma TNF-α levels decreased in NASH and NAFL patients, while blood TAGE levels decreased [4].
- (iv)
- We demonstrated significant reductions in blood TAGE levels in DM patients treated with acarbose for 12 weeks [2]. We also found that blood TAGE levels were significantly reduced by a DPP-4 inhibitor, sulfonylurea, and insulin, and these decreases were associated with reductions in the biomarker levels of organ damage in DM patients [2,4]. Furthermore, we observed decreases in blood TAGE levels in DM patients treated with atorvastatin [2,4].
- (v)
- (vi)
- Yamamoto et al. found that an anti-TAGE monoclonal antibody inhibited eye angiogenesis in diabetic mice [WO2020045646A1].
- (vii)
- We recently reported on the protective role of pyridoxamine, which has TAGE inhibitory effects against the GA-mediated suppression of axonal outgrowth in zymosan-induced axonal elongation following nerve injury in mice [5].
12. Conclusions
Funding
Conflicts of Interest
References
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Takeuchi, M. Toxic AGEs (TAGE) Cause Lifestyle-Related Diseases. Antioxidants 2024, 13, 1372. https://doi.org/10.3390/antiox13111372
Takeuchi M. Toxic AGEs (TAGE) Cause Lifestyle-Related Diseases. Antioxidants. 2024; 13(11):1372. https://doi.org/10.3390/antiox13111372
Chicago/Turabian StyleTakeuchi, Masayoshi. 2024. "Toxic AGEs (TAGE) Cause Lifestyle-Related Diseases" Antioxidants 13, no. 11: 1372. https://doi.org/10.3390/antiox13111372
APA StyleTakeuchi, M. (2024). Toxic AGEs (TAGE) Cause Lifestyle-Related Diseases. Antioxidants, 13(11), 1372. https://doi.org/10.3390/antiox13111372