The DOI matches its Crossref record; 106 of the 106 references it cites were found in a registry or an index; none of the 59 sources its claims cite is checked for support yet.
Glycation‐altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age‐related disease (in nondiabetics)
Open accessAbstract
Summary: Epidemiologic studies indicate that the risks for major age‐related debilities including coronary heart disease, diabetes, and age‐related macular degeneration (AMD) are diminished in people who consume lower glycemic index (GI) diets, but lack of a unifying physiobiochemical mechanism that explains the salutary effect is a barrier to implementing dietary practices that capture the benefits of consuming lower GI diets. We established a simple murine model of age‐related retinal lesions that precede AMD (hereafter called AMD‐like lesions). We found that consuming a higher GI diet promotes these AMD‐like lesions. However, mice that consumed the lower vs. higher GI diet had significantly reduced frequency (P < 0.02) and severity (P < 0.05) of hallmark age‐related retinal lesions such as basal deposits. Consuming higher GI diets was associated with > 3 fold higher accumulation of advanced glycation end products (AGEs) in retina, lens, liver, and brain in the age‐matched mice, suggesting that higher GI diets induce systemic glycative stress that is etiologic for lesions. Data from live cell and cell‐free systems show that the ubiquitin–proteasome system (UPS) and lysosome/autophagy pathway [lysosomal proteolytic system (LPS)] are involved in the degradation of AGEs. Glycatively modified substrates were degraded significantly slower than unmodified substrates by the UPS. Compounding the detriments of glycative stress, AGE modification of ubiquitin and ubiquitin‐conjugating enzymes impaired UPS activities. Furthermore, ubiquitin conjugates and AGEs accumulate and are found in lysosomes when cells are glycatively stressed or the UPS or LPS/autophagy are inhibited, indicating that the UPS and LPS interact with one another to degrade AGEs. Together, these data explain why AGEs accumulate as glycative stress increases.
Overview
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Written from the paper’s full text.
TL;DR
In a murine model, consuming a lower glycemic index diet delayed AMD-like retinal lesions and reduced tissue accumulation of advanced glycation end products (AGEs), while a higher GI diet increased glycative stress. Glycation impairs protein degradation by making substrates resistant and damaging ubiquitination machinery, with the ubiquitin-proteasome system and autophagic-lysosomal pathway cooperating to clear AGEs.
Key findings
- In 23.5-month-old mice fed low vs. high GI diets for 7 months, lower GI was associated with less deposition of basal laminar deposits (p=0.02) and smaller basal laminar deposits (p=0.05); the abstract reports reduced frequency (p<0.02) and severity (p<0.05) of hallmark age-related retinal lesions.
- Higher GI diets were associated with ~3-, 7-, 8-, and 34-fold higher levels of MG-H1 in retina, liver, lens, and brain, respectively, in age-matched mice; human lens showed 8-fold higher MG-H1 in a 76- vs. 22-year-old, and mouse brain showed 1.5-fold higher AGEs at 22 vs. 3 months.
- MGO exposure reduced intracellular protein degradation by 60% at 1.7 mM and >80% at 2.5 mM; glycated ubiquitin decreased degradation of αA162 by ~27% (G6P-modified) and ~40% (MGO-modified), whereas wild-type ubiquitin increased degradation by ≥20% and unmodified Ubc4 increased degradation by 80%.
- UPS and LPS/autophagy inhibitors delayed AGE clearance: at 14 h after 1 mM MGO, inhibitors retained ~2-fold higher MG-H1; 3MA increased AGE levels by >70%; blocking both UPS and LPS doubled the AGE/ubiquitin-conjugate ratio in the ubiquitin-conjugate pool.
Methods
- C57BL/6 mice (and some 129SvPas mice) were fed low- vs. high-GI diets; retinal lesions were assessed by electron microscopy (>84 fields in four low-GI and three high-GI 23.5-month-old mice after 7 months), alongside glucose tolerance, AGE/MG-H1 measurements, carbonyls, and immunohistochemistry in retina, lens, liver, and brain.
- Cultured RPE cells and cell-free lysates were exposed to glucose or MGO; analyses included intracellular proteolysis assays, UPS reporter Ub-G76V-GFP, ubiquitination/degradation assays with wild-type or glycated ubiquitin and Ubc4, proteasome activity, lysosomal fractionation, colocalization, and pulldown of ubiquitin conjugates, with inhibitors of the UPS, LPS, and autophagy (3MA).
- Experimental procedures are stated to be in Supporting Information.
Limitations
- Stated: small sample size meant some retinal differences (basal infoldings, cytoplasmic vacuoles) were not statistically significant; the possibility that some lysosomal AGEs are formed in situ could not be eliminated.
- Evident: mechanistic conclusions rely heavily on cultured RPE and cell-free systems, so the causal link in humans is not directly tested; high-GI mice had higher HOMA-IR than low-GI mice, although fasting insulin and glucose were within normal ranges, indicating diet effects were separable from diabetes but not metabolically identical.
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50 Own result · 39 Own interpretation · 29 Not checked yet · 6 No basis given · 3 Own method
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We established a simple murine model of age-related retinal lesions that precede AMD (hereafter called AMD-like lesions).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Abstract
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Consuming higher GI diets was associated with >3 fold higher accumulation of advanced glycation end products (AGEs) in retina, lens, liver and brain in the age-matched mice”
- Also stated in: § Consuming lower GI diets delays AMD-like lesions · plain
“We observed ∼3, 7, 8 and 34 fold higher levels of MG-H1 in retina, liver, lens and brain (primarily substantia nigra) from mice of the same age that consumed the higher –as opposed to the lower –GI diet (Figure 2 A-D).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Abstract
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § Consuming lower GI diets delays AMD-like lesions · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, mice that consumed the lower vs. higher GI diet had significantly reduced frequency (p<0.02) and severity (p<0.05) of hallmark age-related retinal lesions such as basal deposits.”
- Also stated in: § Consuming lower GI diets delays AMD-like lesions · plain
“Notably, eating the lower GI diet was associated with less deposition of basal laminar deposits (p=0.02) and smaller basal laminar deposits (p=0.05; Figure 1B, Figure S1A, B).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § Consuming lower GI diets delays AMD-like lesions · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Data from live cell and cell free systems show that the ubiquitin-proteasome system (UPS) and lysosome/autophagy pathway (LPS) are involved in the degradation of AGEs.”
- Also stated in: § A UPS and an autophagic-LPS collaborate to remove AGEs · hedged
“Taken together, these data provide the first indication that a UPS and LPS both play roles in the removal of AGEs and they indicate a dynamic flux of AGEs and ubiquitinated species between these compartments.”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § A UPS and an autophagic-LPS collaborate to remove AGEs · hedged
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Glycatively-modified substrates were degraded significantly slower than unmodified substrates by the UPS.”
- Also stated in: § Glycation induced reduction in UPS proteolytic activity · plain
“Consistent with findings that total proteolysis is depressed upon glycative stress, glycation of these substrates decreased their susceptibility to degradation (Figure 3D-H)”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § Glycation induced reduction in UPS proteolytic activity · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, mice that consumed the lower vs. higher GI diet had significantly reduced frequency (p<0.02) and severity (p<0.05) of hallmark age-related retinal lesions such as basal deposits.”
- Also stated in: § Consuming lower GI diets delays AMD-like lesions · plain
“Notably, eating the lower GI diet was associated with less deposition of basal laminar deposits (p=0.02) and smaller basal laminar deposits (p=0.05; Figure 1B, Figure S1A, B).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § Consuming lower GI diets delays AMD-like lesions · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Compounding the detriments of glycative stress, AGE-modification of ubiquitin and ubiquitin conjugating enzymes impaired UPS activities.”
- Also stated in: § Glycation induced reduction in UPS proteolytic activity · hedged
“Taken together, these data indicate that the degradation of AGE-modified proteins requires UPS capacities, and that glycation impairs the ability of ubiquitin and ubiquitin conjugating enzymes to catalyze ubiquitination.”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § Glycation induced reduction in UPS proteolytic activity · hedged
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Notably, eating the lower GI diet was associated with less deposition of basal laminar deposits (p=0.02) and smaller basal laminar deposits (p=0.05; Figure 1B, Figure S1A, B).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Results > Consuming lower GI diets delays AMD-like lesions
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Surprisingly, glycation is without effect on proteasomal activity (Figure 5E).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Results > Glycation induced reduction in UPS proteolytic activity
plain- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“and 1.5 fold higher levels of AGEs in 22 month old vs. 3 month old mouse brains from animals that consumed the same diet (Figure S1D, E).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Results > Consuming lower GI diets delays AMD-like lesions
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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- It may state two separate claims as one. 24
- Probably not a substantial claim. 6
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Furthermore, ubiquitin conjugates and AGEs accumulate and are found in lysosomes when cells are glycatively stressed or the UPS or LPS/autophagy are inhibited”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Whereas addition of unmodified Ubc4 increased degradation by 80%, addition of the same amount of AGE-modified Ubc4 was less efficient (Figure 5D).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Results > Glycation induced reduction in UPS proteolytic activity
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“When cells were not glycatively stressed GFP was cleared within 4hrs (Figure 4A, top). However, upon imposition of glycative stress the GFP was stabilized (Figure 4A, bottom).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Results > Glycation induced reduction in UPS proteolytic activity
plaindirect- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“we observed that additional Wt-Ub increased degradation by ≥20% whereas addition of ubiquitin modified by G6P or MGO, decreased degradation of αA162 by ∼27 and 40%, respectively (Figure 5B).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Results > Glycation induced reduction in UPS proteolytic activity
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Similar results were also obtained at 15 months of age (p=0.001 for difference between high and low GI groups, in another set of C57BL/6 mice and in 129SvPas mice (p=0.05)”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Results > Consuming lower GI diets delays AMD-like lesions
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
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In the paper
“As expected, exposure of the cells to MGO resulted in a vast increase in AGEs in the lysates (Figure 7, lanes 2 and 4 vs. 1 and 3, top), as well as in the ubiquitin conjugate isolates (lanes 5-8).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Results > A UPS and an autophagic-LPS collaborate to remove AGEs
plaindirect- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“By 14hrs levels of AGEs were declining (Figure 3B, Figure 6A lanes 7 vs. 2, Figure S6A lane 3 vs. 2) and this process continued such that by 20hrs relative levels of AGEs were only ≤70% the initial level (Figure 3B, Figure 6A lane 11 vs. 2).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Results > A UPS and an autophagic-LPS collaborate to remove AGEs
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“We also found evidence that the LPS, including an autophagic LPS, is involved and cooperates with the UPS in removal of AGEs (Figures 4-6).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Discussion
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“These include deposition of basal deposits and loss of basal infoldings (Figure 1).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Discussion
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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In the paper
“These, include AGEs that accumulated in lysosomes when the UPS was inhibited (Figure S7 panel 3 vs. 2) or when the LPS was inhibited (Figure S7 panel 4 vs. 2).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Results > A UPS and an autophagic-LPS collaborate to remove AGEs
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“we demonstrated that AGE-modification of UPS substrates attenuates their degradation and results in their accumulation in aggregates (Figures 3-7).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Discussion
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In contrast, when the LPS was inhibited there was 2.7 fold greater retention of AGEs in the NP40 insoluble fraction (lanes 6 vs. 4, right side) but only 25% more AGEs retained in the soluble fraction (lanes 6 vs. 4, left side).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Results > A UPS and an autophagic-LPS collaborate to remove AGEs
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“That the lesions delayed with dGI management are very early in the pathologic process is particularly attractive”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Discussion
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“However, it has been shown that relative to consuming higher GI diets, consuming lower GI diets is associated with attenuated blood glucose excursions, lower postprandial hypoglycemia/hyperlipidemia, lower insulinemia, less elevation of inflammatory markers and enhanced counter regulatory endocrine responses (Jenkins et al., 2002; Ludwig, 2002)”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Introduction
What the sources say
- Not checked yetcites Jenkins et al., 2002
- Not checked yetcites Ludwig, 2002
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Advanced glycation end products (AGEs) are formed when proteins are non enzymatically modified by carbohydrates or sugar metabolites, often with oxidative sequelle (Tessier et al., 1999; Ahmed et al., 2003; Thornalley et al., 2003; Glenn & Stitt, 2009).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Introduction
What the sources say
- Not checked yetcites Tessier et al., 1999
- Not checked yetcites Ahmed et al., 2003
- Not checked yetcites Thornalley et al., 2003
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“It has recently been demonstrated that the UPS and LPS collaborate in degradation of some proteins and that both proteolytic pathways are required to avoid protein insolubilization that is associated with neurodegeneration (Hara et al., 2006; Komatsu et al., 2006; Kwak et al., 2010; Hartl et al., 2011).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Results > A UPS and an autophagic-LPS collaborate to remove AGEs
What the sources say
- Not checked yetcites Hara et al., 2006
- Not checked yetcites Komatsu et al., 2006
- Not checked yetcites Kwak et al., 2010
boosteddirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“and that oxidative stress alters the function of the ubiquitin proteasome system (UPS) and limits cellular stress responses (Jahngen-Hodge et al., 1997; Shang et al., 1997; Shang et al., 2005; Shang & Taylor, 2011).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Introduction
What the sources say
- Not checked yetcites Jahngen-Hodge et al., 1997
- Not checked yetcites Shang et al., 1997
- Not checked yetcites Shang et al., 2005
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Compounding stress and proteolytic burden to the retina and RPE, the retina is the most oxygenated and metabolically active tissue in the body (Warburg, 1924).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Introduction
What the sources say
- Not checked yetcites Warburg, 1924
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Additional evidence that etiologically links accumulation of AGEs to dysfunction and aging is found in observations that maintaining a higher methylglyoxal (MGO) concentration is associated with shortened lifespan in C. elegans and increased apoptosis in cultured mammalian cells (Kuhla et al., 2006; Miller et al., 2006; Morcos et al., 2008; Guix et al., 2009; Ahmed et al., 2010).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Introduction
What the sources say
- Not checked yetcites Kuhla et al., 2006
- Not checked yetcites Miller et al., 2006
- Not checked yetcites Morcos et al., 2008
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“These data indicate that upon glycative stress some AGEs are being transferred to the lysosome. Most fail to enter it. Rather, they associate with the membrane fraction, akin to tau F1 (Wang et al., 2009).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Results > A UPS and an autophagic-LPS collaborate to remove AGEs
What the sources say
- Not checked yetcites Wang et al., 2009
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Protein editing is unperturbed and AGEs and ubiquitin conjugates do not accumulate.”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Discussion
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Taken together, these data provide the first indication that a UPS and LPS both play roles in the removal of AGEs and they indicate a dynamic flux of AGEs and ubiquitinated species between these compartments.”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Results > A UPS and an autophagic-LPS collaborate to remove AGEs
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Prolonged resistance to stress would appear essential for a postmitotic cell, such as the RPE, for which there are no options for replenishment.”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Discussion
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, upon chronic glycative stress and/or aging these capacities are insufficient to maintain the proteome, and may themselves be diminished.”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Discussion
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Prior literature and data from Figures 2-6, and S11, S8, S9 are consistent with glycative stress-induced accumulation of oligomers of AGEs, some of which are ubiquitinated or associated with ubiquitinated moieties.”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Results > A UPS and an autophagic-LPS collaborate to remove AGEs
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The autophagic pathway feeds into the LPS as autophagosomes fuse with lysosomes. (Klionsky et al., 2008).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Results > A UPS and an autophagic-LPS collaborate to remove AGEs
What the sources say
- Not checked yetcites Klionsky et al., 2008
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
In the paper
“it was predicted that consuming lower GI diets can save the sight of over 80,000 people in 5 years who would otherwise be blinded from AMD (Chiu et al., 2007c).”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Discussion
What the sources say
- Not checked yetcites Chiu et al., 2007c
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This situation is exacerbated by the accumulation of damaged proteins, which may diminish UPS efficacy, and induce oxidative stress, setting up a vicious cycle that results in additional stress and limited cellular function.”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Discussion
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The stress may also alter the interaction between the UPS or LPS as one or both pathways are attenuated, and proteopoise is perturbed.”
§ Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in non diabetics) > Discussion
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
No pathobiochemical mechanism explaining why lower GI diets have salutary advantages is currently available.
“Pathobiochemical mechanisms that indicate why such critical salutary advantage is derived from lower GI diets are currently unavailable.”
The paper relies on this without support.
To date, consuming high GI diets has been associated only with accumulation of AGEs in blood.
“To date consuming high GI diets has been associated only with accumulation of AGEs in blood.”
The paper relies on this without support.
Most prior work regarding the effects of AGEs focused on extracellular and signaling events, leaving intracellular activities poorly understood.
“Most prior work regarding the effects of AGEs focused on extracellular and signaling events, leaving intracellular activities poorly understood.”
The paper relies on this without support.
There have been no studies that investigated or modeled the effects of consuming low or high GI diets on proteopoise.
“However, there have been no studies which investigated or modeled the effects of consuming low or high GI diets on proteopoise: defined here as the combined effects to the proteome of protein modification and altered proteolytic capacities.”
The paper relies on this without support.
Literature describing roles for each pathway and interactions between these proteolytic systems with regard to degradation of glycated proteins is scanty.
“However, literature that describes roles for each pathway as well as interactions between these proteolytic systems with regard to degradation of glycated proteins is scanty.”
The paper relies on this without support.
Levels of AGEs are determined by rates of formation and removal.
“Levels of AGEs are determined by rates of formation and removal.”
The paper relies on this without support.
There is a lack of suitable animal models of GI-disease relationships.
“the lack of suitable animal models of GI-disease relationships”
The paper relies on this without support.
There is an absence of established intracellular biochemical mechanisms that link epidemiologic data to AMD and several other widely prevalent age-related diseases.
“the absence of established intracellular biochemical mechanisms that link the epidemiologic data that indicates that consuming higher GI diets is related to higher risk for AMD and several other widely prevalent age-related diseases.”
The paper relies on this without support.
Consuming higher GI diets is related to higher risk for AMD and several other widely prevalent age-related diseases.
“consuming higher GI diets is related to higher risk for AMD and several other widely prevalent age-related diseases.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Dietary AGEs promote AGE formation in the substantia nigra114.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [114]
Citations
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BackgroundGlycemic index of foods: a physiological basis for carbohydrate exchange
Jenkins, D. J., Wolever, T. M., Taylor, R. H., Barker, H., Fielden, H., Baldwin, J. M., Bowling, A. C., Newman, H. C., Jenkins, A. L., & Goff, D. V. (1981) · The American Journal of Clinical Nutrition · doi:10.1093/ajcn/34.3.362 · Cited by 3,857 · cited 2×
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Komatsu, M., Waguri, S., Chiba, T., Murata, S., Iwata, J.-I., Tanida, I., Ueno, T., Koike, M., Uchiyama, Y., Kominami, E., et al. (2006) · Nature · doi:10.1038/nature04723 · Cited by 3,500 · cited 1×
“…life-quality-limiting debilities including coronary heart disease (CHD), type 2 diabetes, and possibly age-related cataract even in nondiabetic subjects (Salmeron et al., 1997; Augustin et al., 2002; Chiu et al., 2007a,b, 2011; Krishnan et al., 2007; Mulholland et al., 2008; Chiu & Taylor, 2011).”
BackgroundMolecular chaperones in protein folding and proteostasis
Hartl, F. U., Bracher, A., & Hayer-Hartl, M. (2011) · Nature · doi:10.1038/nature10317 · Cited by 3,381 · cited 1×
“…recently been demonstrated that the UPS and LPS collaborate in degradation of some proteins and that both proteolytic pathways are required to avoid protein insolubilization that is associated with neurodegeneration (Hara et al., 2006; Komatsu et al., 2006; Kwak et al., 2010; Hartl et al., 2011).”
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“…is associated with attenuated blood glucose excursions, lower postprandial hypoglycemia ⁄ hyperlipidemia, lower insulinemia, less elevation of inflammatory markers, and enhanced counter regulatory endocrine responses (Jenkins et al., 2002; Ludwig, 2002), some of which have been related to AMD.”
Background
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Cited by
Sorted by citations
Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1
Klionsky, D. J., Abdel-Aziz, A. K., Abdelfatah, S., Abdellatif, M., Abdoli, A., Abel, S., Abeliovich, H., Abildgaard, M. H., Abudu, Y. P., Acevedo-Arozena, A., et al. (2021) · Autophagy · doi:10.1080/15548627.2020.1797280 · Cited by 2,897
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“N IH -PA Author M anuscript N IH -PA Author M anuscript N IH -PA Author M anuscript i.e. RPE and BrMb appear to be dysfunctional first.”
BackgroundChaudhuri, J., Bains, Y., Guha, S., Kahn, A., Hall, D., Bose, N., Gugliucci, A., & Kapahi, P. (2018) · Cell Metabolism · doi:10.1016/j.cmet.2018.08.014 · Cited by 669
Advanced glycation end products
Gkogkolou, P., & Böhm, M. (2012) · Dermato-Endocrinology · doi:10.4161/derm.22028 · Cited by 613
Consequences of oxidative stress in age-related macular degeneration
Jarrett, S. G., & Boulton, M. E. (2012) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2012.03.009 · Cited by 549
Aging and Autophagy in the Heart
Shirakabe, A., Ikeda, Y., Sciarretta, S., Zablocki, D., & Sadoshima, J. (2016) · Circulation Research · doi:10.1161/circresaha.116.307474 · Cited by 448
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“relationship with the disease etiology (Chiu et al., 2011; Handa et al., 1999; Uchiki et al., 2012; Weikel et al., 2012).”
Animal models of age related macular degeneration
Pennesi, M. E., Neuringer, M., & Courtney, R. J. (2012) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2012.06.003 · Cited by 391
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“Increased levels of advanced glycation end products (AGEs), i.e., covalent posttranslational oxidative and nonoxidative modifications of proteins by sugar-derived metabolites, were observed in the mice fed a high-glycemia (HG) diet (hereafter, “HG mice”) (10, 11).”
BackgroundInfluentialSelf-citationAutophagy in the eye: Development, degeneration, and aging
Boya, P., Esteban‐Martínez, L., Serrano‐Puebla, A., Gómez‐Sintes, R., & Villarejo‐Zori, B. (2016) · Progress in Retinal and Eye Research · doi:10.1016/j.preteyeres.2016.08.001 · Cited by 236
Advanced Glycation End Products (AGEs) May Be a Striking Link Between Modern Diet and Health
Gill, V., Kumar, V., Singh, K., Kumar, A., & Kim, J.-J. (2019) · Biomolecules · doi:10.3390/biom9120888 · Cited by 232
“Eyes Opsin Macular degeneration of the retina [66,67]”
BackgroundThe role of declining adaptive homeostasis in ageing
Pomatto, L. C. D., & Davies, K. J. A. (2017) · The Journal of Physiology · doi:10.1113/jp275072 · Cited by 231
“In turn, decreased glycation slows the formation of toxic metabolites that can cause proteotoxicity (Uchiki et al. 2012).”
BackgroundMechanistic targeting of advanced glycation end-products in age-related diseases
Rowan, S., Bejarano, E., & Taylor, A. (2018) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2018.08.036 · Cited by 219
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Prevention of Protein Glycation by Natural Compounds
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“Glycation of enzymes of the ubiquitin-proteasome system and of the lysosomal proteolytic system has been shown to inhibit their action [16].”
BackgroundHow does the macula protect itself from oxidative stress?
Handa, J. T. (2012) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2012.03.006 · Cited by 154
“Consistent with these data, systemic increases in AGEs and advanced AMD-related lesions is also observed in C57BL6 mice that consumed higher glycemic index diets (Uchiki et al., 2011) Handa Page 13”
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Kellow, N. J., & Coughlan, M. T. (2015) · Nutrition Reviews · doi:10.1093/nutrit/nuv030 · Cited by 160
Aldini, G., Vistoli, G., Štefek, M., Chondrogianni, N., Grune, T., Sereikaitė, J., Sadowska‐Bartosz, I., & Bartosz, G. (2013) · Free Radical Research · doi:10.3109/10715762.2013.792926 · Cited by 154
“A functional interaction between both lysosomal and UPS-mediated degradation was also shown in both live cell and cell-free systems by Taylor and colleagues [364].”
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“The ubiquitin–proteasome system (UPS) plays essential roles in degrading misfolded or glycated proteins, thus preventing the accumulation of AGEs and reducing their harmful consequences (Goldberg 2003; Taylor 2012; Uchiki et al. 2012).”
BackgroundNowak, J. Z. (2013) · Pharmacological Reports · doi:10.1016/s1734-1140(13)71005-3 · Cited by 145
G lycation in P arkinson's disease and Alzheimer's disease
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“In addition, ubiquitin is itself a target for MGO glycation, and this might hamper the conjugation of ubiquitin to its target proteins.(54) Failure of the UPS may account for an increase in the levels of aSyn, promoting a vicious cycle because accumulation of aSyn further impairs proteasome function,(82,83) consequent…”
BackgroundNutritional modulation of cataract
Weikel, K., Garber, C., Baburins, A., & Taylor, A. (2013) · Nutrition Reviews · doi:10.1111/nure.12077 · Cited by 128
Self-citationThe Potential of Carnosine in Brain-Related Disorders: A Comprehensive Review of Current Evidence
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Review of nutrient actions on age-related macular degeneration
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How Can Diet Affect the Accumulation of Advanced Glycation End-Products in the Human Body?
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The Role of Microbiota in Retinal Disease
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Self-citationAdvanced Glycation End Products, Inflammation, and Chronic Metabolic Diseases: Links in a Chain?
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Recent findings on the physiological function of DJ-1: Beyond Parkinson's disease
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“High glycemic index (GI) diets and their resultant hyperglycemic effect have been shown to enhance AGE formation in healthy individuals [109].”
BackgroundKidney, heart and brain: three organs targeted by ageing and glycation
Frimat, M., Daroux, M., Litke, R., Nevière, R., Tessier, F. J., & Boulanger, E. (2017) · Clinical Science · doi:10.1042/cs20160823 · Cited by 88
Nutritional modulation of age-related macular degeneration
Weikel, K., Chiu, C., & Taylor, A. (2012) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2012.03.005 · Cited by 89
“Importantly, using controlled laboratory studies, the data have been corroborated and pathophysiologic mechanisms to explain the relationships between glycemic index and AMD have been proposed (Uchiki et al., 2012; Weikel et al., 2012) (See review by Shang in this issue).”
MethodResultInfluentialSelf-citationThe microbiome and ophthalmic disease
Baim, A. D., Movahedan, A., Farooq, A. V., & Skondra, D. (2018) · Experimental Biology and Medicine · doi:10.1177/1535370218813616 · Cited by 87
Diabetes, a Contemporary Risk for Parkinson’s Disease: Epidemiological and Cellular Evidences
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Ocular Microbiota and Intraocular Inflammation
Li, J. J., Yi, S., & Wei, L. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.609765 · Cited by 96
“developed hallmarks of AMD, such as retinal pigment epithelium (RPE) hypopigmentation and atrophy, lipofuscin accumulation, and photoreceptor degeneration, whereas mice fed the lower-glycemia diet did no (83, 84).”
BackgroundMitochondrial Dysfunction: Cause or Consequence of Vascular Calcification?
Phadwal, K., Vrahnas, C., Ganley, I. G., & MacRae, V. E. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.611922 · Cited by 86
Dietary advanced glycation end products (dAGEs): An insight between modern diet and health
Tian, Z., Chen, S., Shi, Y., Wang, P., Wu, Y., & Li, G. (2023) · Food Chemistry · doi:10.1016/j.foodchem.2023.135735 · Cited by 90
p62 provides dual cytoprotection against oxidative stress in the retinal pigment epithelium.
Wang, L., Cano, M., & Handa, J. T. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2014.03.016 · Cited by 82
“RPE homeostasis is therefore, dependent upon the ef fi cient removal of harmful protein aggregates via the proteasomal and autophagic protein clearance systems, both of which gradually decline with aging [10 – 13].”
Self-citationUnderstanding the Role of Protein Glycation in the Amyloid Aggregation Process
Sirangelo, I., & Iannuzzi, C. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22126609 · Cited by 84
Autophagy in Age-Related Macular Degeneration: A Regulatory Mechanism of Oxidative Stress
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Klettner, A., Kauppinen, A., Błasiak, J., Roider, J., Salminen, A., & Kaarniranta, K. (2013) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2013.04.013 · Cited by 83
“…such as malondialdehyde, 4-hydroxynonenal and advanced glycation endproducts can reduce the degradation of phagocytosed photoreceptor outer segments and increase cellular stress in RPE cells (Finnemann et al., 2002; Kaarniranta et al., 2005; Kaemmerer et al., 2007; Uchiki et al., 2012).”
Background5-HT systems: emergent targets for memory formation and memory alterations
Meneses, A. (2013) · Reviews in the Neurosciences · doi:10.1515/revneuro-2013-0026 · Cited by 79
Bhattacharya, S., Chaum, E., Johnson, D. A., & Johnson, L. R. (2012) · Investigative Ophthalmology & Visual Science · doi:10.1167/iovs.12-10495 · Cited by 73
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“This data is consistent with findings that animals fed high-GI diets show an accumulation of AGEs and increased retinal lesions and AMD-like phenotypes (Rowan et al., 2017; Uchiki et al., 2012; Weikel et al., 2012b).”
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Metadata
- Authors
- Uchiki, T., Weikel, K. A., Jiao, W., Shang, F., Caceres, A., Pawlak, D., Handa, J. T., Brownlee, M., Nagaraj, R., & Taylor, A.
- Affiliations
- Tufts University (US)
- Boston Children's Hospital (US)
- Johns Hopkins University (US)
- Albert Einstein College of Medicine (US)
- Case Western Reserve University (US)
- Corresponding author
- Taylor, Allen
- Venue
- Aging Cell
- Publisher
- Wiley
- Published
- 2011-11-15
- Volume
- 11
- Issue
- 1
- Pages
- 1-13
- ISSN
- 1474-9718 (ISSN-L)
- 1474-9726
- PMC
- PMC3257376
- OpenAlex
- W1501698769
- Semantic Scholar
- 5999b747d91388b28b15967143fbd004a9a7d1f0
- Cited by
- 200
- References
- 106
- Citations by year
- 2026: 6 · 2025: 9 · 2024: 10 · 2023: 13 · 2022: 8 · 2021: 21 · 2020: 14 · 2019: 14 · 2018: 18 · 2017: 15 · 2016: 11 · 2015: 16 · 2014: 12 · 2013: 13 · 2012: 18
- FWCI
- 8.41
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Aging Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Agriculture (1950‐510000‐060‐01A)
- National Institutes of Health
- U.S. Public Health Service (R01-13250, R01 21212)
- National Eye Institute (R01EY021212, R01EY014005, R01 EY21212, R01 EY13250, R01EY013250, R01EY019904)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- glycemic index, advanced glycation end products, glycation stress, age-related macular degeneration, retinal lesions, ubiquitin-proteasome system, lysosomal proteolysis, autophagy, ubiquitin conjugation, aging, age-related diseases, glycemic load
- MeSH terms
- Aging, Animals, Autophagy, Cell-Free System, Diet, Disease Models, Animal, Glucose, Humans, Lysosomes, Macular Degeneration, Mice, Inbred C57BL, Retina, Severity of Illness Index, Glycation End Products, Advanced, Ubiquitin, Glycemic Index, Ubiquitin-Conjugating Enzymes, Proteasome Endopeptidase Complex, Mice
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