Free fatty acids in human cerebrospinal fluid following subarachnoid hemorrhage and their potential role in vasospasm: a preliminary observation

Pilitsis, Julie G.; Coplin, William M.; O’Regan, Michael H.; Wellwood, Jody; Díaz, Fernando G.; Fairfax, Marilynn R.; Michael, Daniel B.; Phillis, John W.

doi:10.3171/jns.2002.97.2.0272

Cited by 48 publications

(32 citation statements)

References 64 publications

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“…This is consistent with increased lipolysis due to hypo-insulinaemia [45], but could also be explained by the increased stress response as higher cortisol levels correlated with higher FFA levels and, in general, an increased stress reaction is accompanied by lipolysis with a subsequent increase in FFA levels [46]. Previous studies reported similar observations, with increased FFA levels in cerebral spinal fluid of patients with aneurysmal SAH or with traumatic brain injury [47,48]. The relationship between FFA and insulin appears to be complex [49].…”

Section: Discussionsupporting

confidence: 73%

Beta-Cell Dysfunction and Insulin Resistance after Subarachnoid Haemorrhage

Kruyt

Musters²,

Biessels

et al. 2011

Neuroendocrinology

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Background: Hyperglycaemia is a common finding and an independent risk factor for increased morbidity and mortality in aneurysmal subarachnoid haemorrhage (SAH). Although in these patients hyperglycaemia is commonly ascribed to insulin resistance, there is little understanding of underlying mechanisms. Aims: To prospectively study temporal disturbances of glucose metabolism after aneurysmal SAH in patients without known abnormalities of glucose metabolism and to explore possible correlations with markers of stress. Methods: In consecutive aneurysmal SAH patients not subjected to insulin therapy, in-hospital and follow-up oral glucose tolerance tests (OGTTs) and assessments of insulin resistance, pancreatic β-cell function, free fatty acids (FFA) and cortisol were performed and compared with reference values. Results: We included 13 patients. In the first 2 weeks of admission, median fasting glucose and FFA levels were elevated while insulin levels were not. OGTTs were indicative of glucose intolerance in all patients at days 3 and 7, while on follow-up 1 patient had glucose intolerance and all patients had normal fasting glucose levels. Pancreatic β-cell function was impaired throughout the first week and insulin resistance from day 4 to 10. Levels of cortisol correlated with higher fasting glucose and increased FFA. FFA in turn correlated with pancreatic β-cell dysfunction. Conclusions: Aneurysmal SAH patients have transient abnormalities of glucose metabolism. During the first week, it appears to result predominantly from transient pancreatic β-cell dysfunction, in combination with insulin resistance.

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Section: Discussionsupporting

confidence: 73%

Beta-Cell Dysfunction and Insulin Resistance after Subarachnoid Haemorrhage

Kruyt

Musters²,

Biessels

et al. 2011

Neuroendocrinology

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“…[25][26][27][28][29] Both negative nitrogen balance and free fatty acid production have been reported to be associated with vasospasm after SAH. 15,30 Our analysis found an additional finding of a strong inverse relationship between prealbumin, a nonspecific marker of protein catabolism, and hsCRP. A more comprehensive measurement of both protein catabolism and lipid peroxidation with assessments of nitrogen balance and free fatty acid production will lead to a better understanding of the impact of hypermetabolism on DCI.…”

Section: Discussionmentioning

confidence: 81%

Relationship Between C-Reactive Protein, Systemic Oxygen Consumption, and Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage

Badjatia

Carpenter

Fernandez

et al. 2011

Stroke

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Background and Purpose-Subarachnoid hemorrhage (SAH) is known to result in elevated systemic oxygen consumption (VO 2 ) and increases in high-sensitivity C-reactive protein (hsCRP), although the relationship among hsCRP, VO 2 , and delayed cerebral ischemia (DCI) after SAH remains unknown. We hypothesized that hsCRP is directly associated with VO 2 and that elevated VO 2 is a predictor of DCI after SAH. Methods-Prospective serial assessments of VO 2 and hsCRP over 4 prespecified time periods during the first 14 days after bleed in consecutive SAH patients admitted to a single academic medical center for a 2-year period. Results-One hundred ten SAH patients met study criteria (mean age, 55Ϯ16 years; 62% women), with a median admission Hunt Hess grade of 3 (interquartile range, 2-4). In multivariate generalized estimating equation model of the first 14 days after bleed, VO 2 was associated with younger age (Pϭ0.01), male gender (Pϭ0.01), and hsCRP levels (Pϭ0.03). Twenty-four (22%) patients had DCI develop, with a median onset on day 7 after bleed (interquartile range, 5-11). The mean VO 2 (291Ϯ65 mL/min versus 226Ϯ55 mL/min; Pϭ0.003) was higher in DCI patients. In a multivariable Cox proportional hazards model, younger age (hazard ratio, 1.2 per 5 years; 95% CI, 1.1-1.3), a higher modified Fisher scale score (hazard ratio, 3.4 per 1-point increase; 95% CI, 1.7-6.9), and higher VO 2 (HR, 1.2 per 50-mL/min increase; 95% CI, 1.1-1.3) were predictive of DCI. Conclusions-Systemic oxygen consumption is associated with hsCRP levels in the first 14 days after SAH and is an independent predictor of DCI. (Stroke. 2011;42:2436-2442.)

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“…However, in studies of Alzheimer (33) and Parkinson (34) diseases, neither free nor acyl-carnitine levels significantly correlate with disease. Free fatty acids were shown to increase in patients with traumatic brain injury (35), stroke (36), and subarachnoid hemorrhage (37), yet a decrease in fatty acid concentrations was demonstrated in multiple sclerosis (38) and Alzheimer disease (39).…”

Section: Discussionmentioning

confidence: 99%

Metabolomic analysis of the cerebrospinal fluid reveals changes in phospholipase expression in the CNS of SIV-infected macaques

Wikoff¹,

Pendyala²,

Siuzdak³

et al. 2008

J. Clin. Invest.

127

113

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HIV infiltrates the CNS soon after an individual has become infected with the virus, and can cause dementia and encephalitis in late-stage disease. Here, a global metabolomics approach was used to find and identify metabolites differentially regulated in the cerebrospinal fluid (CSF) of rhesus macaques with SIV-induced CNS disease, as we hypothesized that this might provide biomarkers of virus-induced CNS damage. The screening platform used a non-targeted, mass-based metabolomics approach beginning with capillary reverse phase chromatography and electrospray ionization with accurate mass determination, followed by novel, nonlinear data alignment and online database screening to identify metabolites. CSF was compared before and after viral infection. Significant changes in the metabolome specific to SIV-induced encephalitis were observed. Metabolites that were increased during infection-induced encephalitis included carnitine, acyl-carnitines, fatty acids, and phospholipid molecules. The elevation in free fatty acids and lysophospholipids correlated with increased expression of specific phospholipases in the brains of animals with encephalitis. One of these, a phospholipase A2 isoenzyme, is capable of releasing a number of the fatty acids identified. It was expressed in different areas of the brain in conjunction with glial activation, rather than linked to regions of SIV infection and inflammation, indicating widespread alterations in infected brains. The identification of specific metabolites as well as mechanisms of their increase illustrates the potential of mass-based metabolomics to address problems in CNS biochemistry and neurovirology, as well as neurodegenerative diseases.

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Free fatty acids in human cerebrospinal fluid following subarachnoid hemorrhage and their potential role in vasospasm: a preliminary observation

Cited by 48 publications

References 64 publications

Beta-Cell Dysfunction and Insulin Resistance after Subarachnoid Haemorrhage

Beta-Cell Dysfunction and Insulin Resistance after Subarachnoid Haemorrhage

Relationship Between C-Reactive Protein, Systemic Oxygen Consumption, and Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage

Metabolomic analysis of the cerebrospinal fluid reveals changes in phospholipase expression in the CNS of SIV-infected macaques

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