Polyunsaturated fatty acids in plasma lipids of diabetic children during and after diabetic ketoacidosis

Décsi, Támas; Szabó, Éva; Kozári, A.; Erhardt, Éva; Marosvölgyi, Tamás; Soltész, Gyula

doi:10.1080/08035250510028254

Cited by 12 publications

(5 citation statements)

References 17 publications

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“…Insulin deficiency causes increased lipolysis, ketogenesis and metabolic acidosis. The downregulated non-esterified acids show in Figure 3 are in agreement with previously reported observations ( 27 ). The increased lipolysis results in formation of ketone bodies ( 28 , 29 ).…”

Section: Discussionsupporting

confidence: 93%

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Metabolic trajectories of diabetic ketoacidosis onset described by breath analysis

Awchi,

Singh,

Brenner

et al. 2024

Front. Endocrinol.

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PurposeThis feasibility study aimed to investigate the use of exhaled breath analysis to capture and quantify relative changes of metabolites during resolution of acute diabetic ketoacidosis under insulin and rehydration therapy.MethodsBreath analysis was conducted on 30 patients of which 5 with DKA. They inflated Nalophan bags, and their metabolic content was subsequently interrogated by secondary electrospray ionization high-resolution mass spectrometry (SESI-HRMS).ResultsSESI-HRMS analysis showed that acetone, pyruvate, and acetoacetate, which are well known to be altered in DKA, were readily detectable in breath of participants with DKA. In addition, a total of 665 mass spectral features were found to significantly correlate with base excess and prompt metabolic trajectories toward an in-control state as they progress toward homeostasis.ConclusionThis study provides proof-of-principle for using exhaled breath analysis in a real ICU setting for DKA monitoring. This non-invasive new technology provides new insights and a more comprehensive overview of the effect of insulin and rehydration during DKA treatment.

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Section: Discussionsupporting

confidence: 93%

“…A portion of the metabolome covered by this breath analysis technique plays a significant role in DKA. For example, butanoate metabolism ( 24 ), tricarboxylic acid (TCA) cycle ( 25 ), amino acid metabolism ( 26 ) and fatty acid metabolism ( 27 ). Insulin deficiency causes increased lipolysis, ketogenesis and metabolic acidosis.…”

Section: Discussionmentioning

confidence: 99%

Metabolic trajectories of diabetic ketoacidosis onset described by breath analysis

Awchi,

Singh,

Brenner

et al. 2024

Front. Endocrinol.

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“…Specific candidates for induction and stimulation of autophagy include: insulin deficiency/resistance (Barrett et al, 1982; Evans et al, 2005; Hoffman et al, 2010; Yu et al, 2008); deficiency of insulin growth factor-1 (IGF-1) and insulin growth factor-1 receptor (IGF-1R) (Bains et al, 2011; Cinaz et al, 1996; Hoffman et al, 2010); hyperglucagonemia (Schworer and Mortimore, 1979); and hyperglycemia (Liu et al, 2010). Based on the expression of 8OHG and NT (Greenacre and Ischiropoulos, 2001; Hoffman et al, 2011; Nunomura et al, 2006) other candidates for perturbation of autophagy include: alteration of protein synthesis and degradation (Ding et al, 2007) due to the oxidative stress of RNA (Castellani et al, 2008; Hoffman et al, 2011), protein damage, altered lipid metabolism (Decsi et al, 2005; Kim et al, 2007; Singh et al, 2009); increased production of ketones and aldehydes (Finn and Dice, 2005; Hill et al, 2008; Wood et al, 2006) and lipid peroxidation (Hoffman et al, 2011; Kostolanska et al, 2009; Lee et al, 2002; Muller et al, 2011). …”

Section: Discussionmentioning

confidence: 99%

Autophagy in the brains of young patients with poorly controlled T1DM and fatal diabetic ketoacidosis

Hoffman

Shacka

Andjelkovic

2012

Experimental and Molecular Pathology

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Semi-quantitative neuroradiologic studies, quantitative neuron density studies and immunocytochemistry markers of oxidative stress and neuroinflammation indicate neuronal injury and deficits in young patients with chronic poorly controlled type 1 diabetes mellitus (T1DM). Present data suggest that pathogenesis of the neuronal deficits in young patients, who die as the result of diabetic ketoacidosis (DKA) and brain edema (BE), does not involve apoptosis, a prominent form of regulated cell death in many disease states. To further address this we studied mediators of macroautophagy, endoplasmic reticulum (ER) stress and apoptosis. In all areas studied we demonstrated increased levels of macroautophagy-associated proteins including light chain-3 (LC3) and autophagy related protein-4 (Atg4), as well as increased levels of the ER-associated glucose-regulated protein78/binding immunoglobulin protein (GRP78/BiP) in T1DM. In contrast, cleaved caspase-3 was rarely detected in any T1DM brain regions. These results suggest that chronic metabolic instability and oxidative stress may cause alterations in the autophagy-lysosomal pathway but not apoptosis, and macroautophagy-associated molecules may serve as useful candidates for further study in the pathogenesis of early neuronal deficits in T1DM.

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“…These changes in cardiac fatty acids may contribute to cardiac side effects of glucocorticoids. A recent analysis of plasma of diabetic children during and after diabetic ketoacidosis revealed that GLA levels were lower during ketoacidosis but were brought to normal levels following successful treatment [53]. The earlier studies have shown that treatment with GLA improves the nerve conduction velocity in diabetic patients and animals.…”

Section: Insulin Resistance and Diabetesmentioning

confidence: 99%

Gamma Linolenic Acid: An Antiinflammatory Omega-6 Fatty Acid

Kapoor¹,

Huang²

2006

CPB

284

160

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Inflammation plays an important role in health and disease. Most of the chronic diseases of modern society, including cancer, diabetes, heart disease, arthritis, Alzheimer's disease, etc. have inflammatory component. At the same time, the link between diet and disease is also being recognized. Amongst dietary constituents, fat has gained most recognition in affecting health. Saturated and trans fatty acids have been implicated in obesity, heart disease, diabetes and cancer while polyunsaturated fatty acids (PUFAs) generally have a positive effect on health. The PUFAs of omega-3 and omega-6 series play a significant role in health and disease by generating potent modulatory molecules for inflammatory responses, including eicosanoids (prostaglandins, and leukotrienes), and cytokines (interleukins) and affecting the gene expression of various bioactive molecules. Gamma linolenic acid (GLA, all cis 6, 9, 12-Octadecatrienoic acid, C18:3, n-6), is produced in the body from linoleic acid (all cis 6,9-octadecadienoic acid), an essential fatty acid of omega-6 series by the enzyme delta-6-desaturase. Preformed GLA is present in trace amounts in green leafy vegetables and in nuts. The most significant source of GLA for infants is breast milk. GLA is further metabolized to dihomogamma linlenic acid (DGLA) which undergoes oxidative metabolism by cyclooxygenases and lipoxygenases to produce anti-inflammatory eicosanoids (prostaglandins of series 1 and leukotrienes of series 3). GLA and its metabolites also affect expression of various genes where by regulating the levels of gene products including matrix proteins. These gene products play a significant role in immune functions and also in cell death (apoptosis). The present review will emphasize the role of GLA in modulating inflammatory response, and hence its potential applications as an anti-inflammatory nutrient or adjuvant.

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Polyunsaturated fatty acids in plasma lipids of diabetic children during and after diabetic ketoacidosis

Cited by 12 publications

References 17 publications

Metabolic trajectories of diabetic ketoacidosis onset described by breath analysis

Metabolic trajectories of diabetic ketoacidosis onset described by breath analysis

Autophagy in the brains of young patients with poorly controlled T1DM and fatal diabetic ketoacidosis

Gamma Linolenic Acid: An Antiinflammatory Omega-6 Fatty Acid

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