Diabetic ketoacidosis and its treatment increase plasma 3-deoxyglucosone

Hoffman, William H.; Kappler, Francis; Passmore, Gregory G.; Mehta, Renuka

doi:10.1016/s0009-9120(03)00030-4

Cited by 32 publications

(29 citation statements)

References 35 publications

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“…Noteworthy is the evidence that insulin deficiency in T1DM results in variability of metabolic/immunologic insults involving hyperglycemia, dehydration, hyperlipidemia, ketoacidosis (MacGillivray et al, 1982; Durr et al, 1990; Hoffman et al, 2003a,b; Jerath et al, 2005; Edge et al, 2008) and peripheral (Barrett et al, 1982), and cerebral insulin resistance with reduced insulin signaling (Jolivalt et al, 2008) (Hoffman et al, 2010). The latter leading to enhanced activation of the AGE-RAGE system (Liu et al, 2010) and increased oxidative and inflammatory stress (Hoffman et al, 2008) (Sima et al, 2009a,b).…”

Section: Discussionmentioning

confidence: 99%

“…Likewise, evidence for oxidative stress and neuroinflammation are also described in the pathogenesis of diabetic encephalopathy (Mastrocola et al 2005; Hoffman et al 2008; Sima et al 2009 a,b). Additionally, the metabolic crisis of diabetic ketoacidosis (DKA) and its treatment accentuate systemic oxidative stress and a systemic inflammatory response (Jain et al, 1999; Vantyghem et al, 2000; Lee et al, 2002; Dalton et al, 2003; Hoffman et al, 2003 a,b; Jerath et al, 2005; Turk et al, 2006). The systemic insults associated with DKA and its treatment occur in parallel with the progression of subclinical brain edema (BE) and development of clinical BE (Hoffman et al, 1988; Durr et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

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Oxidative damage is present in the fatal brain edema of diabetic ketoacidosis

Hoffman¹,

Siedlak²,

Wang³

et al. 2011

Brain Research

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Oxidative stress is implicated as a pathogenic factor in a spectrum of chronic diseases, notably, neurodegenerative disease. Noteworthy in this regard is that type 1 diabetes mellitus (T1DM) results in oxidative stress, leading to systemic complications of T1DM. We hypothesized that oxidative stress associated with diabetic ketoacidosis (DKA) of T1DM might have measurable brain sequelae. Consistent with this hypothesis are neurohistology and neuroradiologic studies of T1DM that suggest that oxidative insults are involved in the chronic complications of diabetic encephalopathy. To further address the role of oxidative stress in an acute setting, specifically in fatal brain edema (BE) associated with DKA, we studied neuronal localization and levels of oxidative stress markers reported to be increased in other neurodegenerative conditions. We demonstrated increased levels of 8-hydroxyguansine (8OHG), 4-hydroxynonenal (HNE) and hemeoxygenase-1 (HO-1) in the pyramidal neurons of the hippocampus of DKA BE in comparison to controls. However, in the cerebellum, only 8OHG was increased in the Purkinje cells and other cells of the molecular layer. These results indicate a role for oxidative stress in the pathogenesis of T1DM encephalopathy.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Oxidative damage is present in the fatal brain edema of diabetic ketoacidosis

Hoffman¹,

Siedlak²,

Wang³

et al. 2011

Brain Research

Self Cite

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show abstract

“…3-DG present in human plasma was determined after reaction with 2,3-diaminonaphthalene, and the adducts were silylated with 20% BSA (70 • C, 10 min) [101], or with MSTFA (30 min, 65 • C) [102]. 3-DG has been determined along with 3-deoxyfructose in urine and plasma by GC-MS after reduction with NaBH 4 (overnight at 4 • C).…”

Section: Derivatives Of Intermediate Compoundsmentioning

confidence: 99%

Derivatization of carbohydrates for GC and GC–MS analyses

Ruiz‐Matute

Hernández‐Hernández

Rodríguez-Sánchez

et al. 2011

Journal of Chromatography B

367

195

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“…Moreover, the production of Amadori compounds in wines has already been described by Hashiba 1978, and more recently several Maillard-like compounds have been identified in typical and ageing aromas of champagne wines (thiazoles and oxazoles like: 2,4-dimethylthiazole, 4-methylthiazole, 2-acetylthiazole, 2-acetyl-2-thiazoline, or 2,4,5-trimethyloxazole; and furanthiols like furan-2-yl-methanethiol) (Keim, de Revel, Marchand, & Bertrand, 2002;Tominaga, Guimbertau, & Dubourdieu, 2003) Formation of 3DG has been evaluated in model systems (Usui et al, 2007;Fiedler & Kroh, 2007;Golon & Kuhnert, 2013), biological samples (Hoffman, Kappler, Passmore, & Mehta, 2003;Hurtado-Sanchez, Espinosa-Mansilla, Rodrıguez-Caceres, Martın-Tornero & Durán-Merás, 2012), and food products such as: sake (Oka, 1969), soy sauce (Hashiba, 1976;Kim & Lee, 2008), balsamic vinegars (Daglia, Amoroso, Rossi, Mascherpa, & Maga, 2013), carbonated soft drinks (Gensberger, Glomb, & Pischetsrieder, 2013), milk products (Hellwig, Degen, & Henle, 2010), high-fructose corn syrups (Lo et al, 2008;Gensberger, Mittelmaier, Glomb, & Pischetsrieder, 2012;RuizMatute, Vazquez, Hernández-Hernández, Sanza, & Martínez-Castro, 2015), beers (Bravo et al, 2008;Hellwig, Nobis, Witte, & Henle, 2016), commercial honey samples (Weigel, Opitz, & Henle, 2004;Mavric, Wittmann, Barth, & Henle, 2008;Marceau & Yaylayan, 2009;Ruiz-Matute et al, 2015), bee feeds (Ruiz-Matute et al, 2015), coffee substitutes (Ruiz-Matute et al, 2015), baby foods (Kocadağlı & Gökmen, 2014) and wines (in nonsweet wines: 2.2 to 13.5 mg·L -1 ; and in sweet wines: 39 to 133 mg·L -1 ) ( Therefore, dry white and sweet red Port wines were derivatized with orthophenylenediamine and the corresponding 3DG quinoxalines determined by HPLC with photodiode array detector (HPLC-DAD) coupled to tandem mass spectrometry (MS n ). In orde...…”

Section: Introductionmentioning

confidence: 99%