Analysis of hypoxanthine and lactic acid levels in vitreous humor for the estimation of post-mortem interval (PMI) using LC–MS/MS

Go, Ahra; Shim, Geunae; Park, Ji Won; Hwang, Ji-Hyun; Nam, Mi‐Hyun; Jeong, Hankyung; Chung, Heesun

doi:10.1016/j.forsciint.2019.03.024

Cited by 25 publications

(20 citation statements)

References 26 publications

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“…It requires a simple specimen dilution and the analysis is carried out in a very short time. Moreover, the VH La levels present in literature agree with our results (see Table 4 [4,7,10,16–20]).…”

Section: Discussionsupporting

confidence: 92%

“…This result accomplishes the recent literature investigation; in fact, recently, Go et al. observed correlation La versus PMI by LC‐MS/MS technique and the concentrations of La ranged from 11.6 to 36.4 mM with PMI from 12 to 108 h [4]. Moreover, present data and the correlation of VH La versus PMI positively contribute to answer the Mihailovic question regarding the possibility to estimate the time since death by VH La analysis.…”

Section: Discussionsupporting

confidence: 85%

“…The proposed method confirms its ability to analyze La level in VH with LOQ and LOD comparable with the other used methods, mainly by enzymatic method and absorbance/fluorescence detection [4,13–15].…”

Section: Discussionsupporting

confidence: 58%

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Lactate determination in human vitreous humour by capillary electrophoresis and time of death investigation

et al. 2020

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Forensic inquests, particularly, in assessing time since death currently recognize the importance of the analysis of vitreous humour (VH) biomarkers. Present research, studies, and validates the determination of lactate (La) in VH by CZE with indirect UV detection. The BGE (pH 8.9) consisted of Tris buffer (37 mM) containing 4‐methoxybenzoic acid (4 mM) and alkyl‐trimethyl‐ammonium bromide (1.2 mM). Each VH specimen was diluted with a butyric acid solution (internal standard 0.057 mM) and La and butyrate were separated within 3–5 min (30 kV). The La LOQ and LOD were 4 and 2 mM, respectively. The calibration curve linearity ranged from 4 to 80 mM; intra‐ and interruns precisions were less than 10% for standard as well as for VH specimen, respectively. To investigate postmortem interval (PMI) and VH lactate level correlation, human VH specimens were collected during autopsy (n = 40) and stored at −20°C until assay. La levels ranged from 16 to 42 mM; PMI values ranged from 10 to 141 h. La (mM) and PMI (h) correlation was statistically significant (r2 = 0.527; p < 0.05). In conclusion, the present CZE analysis is efficacious to determine VH La as a biomarker for PMI investigation.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 85%

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Lactate determination in human vitreous humour by capillary electrophoresis and time of death investigation

et al. 2020

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“…The methods were performed as described previously (Shi et al, 2016;Hui et al, 2017;Xin et al, 2018;Go et al, 2019). After thawing, the samples were fully homogenized by vortexing for 2 min.…”

Section: Uplc-orbitrap-ms/ms Analysis For Metabolitesmentioning

confidence: 99%

Exercise‐induced α‐ketoglutaric acid stimulates muscle hypertrophy and fat loss through OXGR1‐dependent adrenal activation

Yuan¹,

Jiang³

et al. 2020

The EMBO Journal

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Beneficial effects of resistance exercise on metabolic health and particularly muscle hypertrophy and fat loss are well established, but the underlying chemical and physiological mechanisms are not fully understood. Here, we identified a myometabolite‐mediated metabolic pathway that is essential for the beneficial metabolic effects of resistance exercise in mice. We showed that substantial accumulation of the tricarboxylic acid cycle intermediate α‐ketoglutaric acid (AKG) is a metabolic signature of resistance exercise performance. Interestingly, human plasma AKG level is also negatively correlated with BMI. Pharmacological elevation of circulating AKG induces muscle hypertrophy, brown adipose tissue (BAT) thermogenesis, and white adipose tissue (WAT) lipolysis in vivo. We further found that AKG stimulates the adrenal release of adrenaline through 2‐oxoglutarate receptor 1 (OXGR1) expressed in adrenal glands. Finally, by using both loss‐of‐function and gain‐of‐function mouse models, we showed that OXGR1 is essential for AKG‐mediated exercise‐induced beneficial metabolic effects. These findings reveal an unappreciated mechanism for the salutary effects of resistance exercise, using AKG as a systemically derived molecule for adrenal stimulation of muscle hypertrophy and fat loss.

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“…The methods were performed as described previously (Go et al, 2019; Hui et al, 2017; Shi et al, 2016; Xin et al, 2018). After thawed, samples were fully homogenized by vortexing for 2 min.…”

Section: Methodsmentioning

confidence: 99%

α-ketoglutaric acid stimulates muscle hypertrophy and fat loss through OXGR1-dependent adrenal activation

Yuan

Jiang

et al. 2019

Preprint

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Running title: α-ketoglutaric acid stimulates lipolysis through OXGR1 31 32 Conflict of interest statement 33The authors have declared that no conflict of interest exists. 34 35 36 37 38 39 40 41 42 43 44 3 Summary: Beneficial effects of resistance exercise on metabolic health and particularly muscle 45hypertrophy and fat loss are well established, but the underlying chemical and physiological 46 mechanisms are not fully understood. Here we identified a myometabolite-mediated metabolic 47 pathway that is essential for the beneficial metabolic effects of resistance exercise in vivo. We showed 48 that substantial accumulation of the tricarboxylic acid cycle intermediate α-ketoglutaric acid (AKG) is 49 a metabolic signature of resistance exercise performance. Interestingly, human plasma AKG level is 50 also negatively correlated with BMI. Pharmacological elevation of circulating AKG induces muscle 51 hypertrophy, brown adipose tissue (BAT) thermogenesis, and white adipose tissue (WAT) lipolysis in 52 vivo. We further found that AKG stimulates the adrenal release of adrenaline through 2-oxoglutarate 53 receptor 1 (OXGR1) expressed in adrenal glands. Finally, by using both loss-of-function and 54 gain-of-function mouse models, we showed that OXGR1 is essential for AKG-mediated 55 exercise-induced beneficial metabolic effects. These findings reveal an unappreciated mechanism for 56 the salutary effects of resistance exercise, using AKG as a systemically-derived molecule for adrenal 57 stimulation of muscle hypertrophy and fat loss. 58 59 Keywords: AKG/lipolysis /obesity/OXGR1/thermogenesis. 60 61 62 63 64 5 provide signatures of endurance exercise performance and cardiovascular disease susceptibility, and 88also identify molecular pathways that may modulate the salutary effects on cardiovascular function. 89However, very few metabolomics data is available for resistance exercise (Berton et al, 2017; Li et al, 90 2012), and the underlying chemical and physiological mechanisms for the stimulatory effects of 91 resistance exercise on fat loss and muscle hypertrophy are not fully understood. Our goal is to identify 92 the essential mediator for the beneficial metabolic effects of resistance exercise and provide potential 93 therapeutic strategies to mimic the health effects of resistance exercise to combat obesity. 94 95Emerging evidence has identified skeletal muscle as secretory organs in regulating energy 96 homeostasis and obesity progression in other tissues (Ibrahim et al, 2017; Rai & Demontis, 2016). 97Exercise can induce systemic metabolic effects either via changes in the mass and metabolic demand 98 of muscle or via the release of muscle-derived cytokines (myokines) and metabolites (myometabolites) 99

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Analysis of hypoxanthine and lactic acid levels in vitreous humor for the estimation of post-mortem interval (PMI) using LC–MS/MS

Cited by 25 publications

References 26 publications

Lactate determination in human vitreous humour by capillary electrophoresis and time of death investigation

Lactate determination in human vitreous humour by capillary electrophoresis and time of death investigation

Exercise‐induced α‐ketoglutaric acid stimulates muscle hypertrophy and fat loss through OXGR1‐dependent adrenal activation

α-ketoglutaric acid stimulates muscle hypertrophy and fat loss through OXGR1-dependent adrenal activation

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