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. Author manuscript; available in PMC: 2023 Dec 1.
Published in final edited form as: Pain. 2022 Apr 28;163(12):e1207–e1216. doi: 10.1097/j.pain.0000000000002667

Figure 2. A ketogenic diet contributes to methylglyoxal scavenging.

Figure 2.

(A) Quantification of blood MG-H1 levels 48 hours post-injection in chow- and ketogenic diet-fed mice (n=4–5). Chow-fed mice exhibit significantly elevated circulating MGO 48 hours post-injection, whereas ketogenic diet-fed mice show no such increase. (B) Quantification of blood β-hydroxybutyrate (β-HB) levels in chow- and ketogenic diet-fed mice 48 hours after MGO injection (n=4–5). Chow-fed mice show normal blood ketone levels, while mice fed a ketogenic diet exhibit elevated β-HB, indicative of nutritional ketosis. (C) Negative correlation between circulating MGO and β-HB 48 hours after MGO injection in mice fed a chow or ketogenic diet (n=14; p < 7.28e−5, ρ = −0.86). (D) Quantification of Glyoxalase 1 enzyme activity from various tissues in chow and ketogenic diet-fed mice. Both spinal cord and footpad skin from ketogenic diet fed mice show a strong trend toward increased glyoxalase 1 activity compared to those from chow fed mice (n=4). (A-B and D) Two-way ANOVA and Tukey’s post hoc test; * p < 0.05 compared to chow-fed saline-injected, *p < 0.05 between two conditions. (C) Spearman’s Rank Correlation.