Catecholamine concentration in rat liver after high level transection of the spinal cord

Apostolova, Galina; Angelova, Anna; Vaptzarova, K. I.

doi:10.1016/s0024-3205(99)00191-5

Cited by 2 publications

(2 citation statements)

References 18 publications

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“…34,36 Both the control levels of NA found presently in the organ, as well as the percentage by which they are reduced after denervation are thus in accordance with previous findings. 11,37 The weight of the animals was not affected by liver denervation, also in agreement with earlier studies. 38 Measuring CPT activity in an isolated system presents the advantage of discarding the influence of alterations in malonyl CoA concentration and in the sensitivity to malonyl CoA-induced inhibition 1known to vary with the location of the enzyme (e.g.…”

Section: Discussionsupporting

confidence: 91%

Liver denervation affects hepatocyte mitochondrial fatty acid transport capacity

Carreño

Seelaender

2003

Cell Biochemistry & Function

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The effect of liver denervation on the activity of hepatic carnitine palmitoyltransferase (CPT) system, which catalyses the transfer of long-chain fatty acids into the mitochondria, was studied in rats. Noradrenaline content in phenol-denervated liver (D) was reduced by 87%. CPT I and II activities (measured by radioassay after detergent separation of the enzymes) were decreased (p < 0.001) in D (2.6 +/- 0.1 and 0.68 +/- 0.2 nmol min(-1) mg(-1) protein, respectively) as compared with controls (4.7 +/- 0.3 and 2.5 +/- 0.2 nmol min(-1) mg(-1) protein, for CPT I and II, respectively). A less intense immunoreactive band for denervated liver CPT II was obtained after Western blotting. Concomitantly, long-chain fatty acid incorporation (p < 0.001), evaluated after administration of [14C]-oleate and total fat content (p < 0.001) were increased in D in relation to controls, while incorporation of exogenous [14C]-oleate into secreted VLDL, was decreased (p < 0.01). The effect of sympathetic denervation on CPT activity was different from that evoked by adrenodemedullation, which caused an augmentation of CPT activity (p < 0.01), when compared with the liver of intact rats. The effects of denervation and adrenodemedullation on the other parameters of lipid metabolism studied, were similar. The results strongly suggest a role of liver sympathetic innervation in the regulation of liver lipid metabolism.

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Section: Discussionsupporting

confidence: 91%

Liver denervation affects hepatocyte mitochondrial fatty acid transport capacity

Carreño

Seelaender

2003

Cell Biochemistry & Function

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“…However, humans with SCIs show an indeterminate metabolic phenotype, and the bimodal distribution of metabolizer status is not necessarily or readily discernible. 15,76 Evidence suggests that both systemic biotransformation of drugs and changes in total nutrient blood flow to organs are influenced by SCI. Although the actual mechanisms involved are unknown, the activity of cytokines in modulating the expression or levels of enzyme activity [77][78][79][80][81] and causing changes in regional blood flow or capillary permeability [82][83][84] are well documented, making it possible to infer a role for cytokines and CAMs as regulators of these metabolic and physiologic processes.…”

Section: Biotransformation and Metabolism Of Drugsmentioning

confidence: 99%

Immunoactivation and Altered Intercellular Communication Mediate the Pathophysiology of Spinal Cord Injury

Segal

2005

Pharmacotherapy

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Evidence and inferences from clinical research, clinical observation, and literature review support an etiologic paradigm for the pathophysiology of spinal cord injury (SCI). According to this paradigm, changes in immunoregulation and in the activation of cytokines or intercellular adhesion molecules (ICAMs) contribute to many of the comorbidities, metabolic changes, and pathophysiologic sequelae observed after traumatic SCI. Cytokines and ICAMs are endogenously secreted molecules that serve as intercellular signals and immunoregulators. They modulate the activity of cells and influence the organization and function of tissues or organs. These intercellular signals are posited as molecular links between the damaged, decentralized nervous system of SCI and the acquired autonomic failure, neuroendocrine-immunoregulatory dysfunction, diminished central nervous system (CNS) regenerative capacity, and broad spectrum of pathology, organ failure, and generalized impairment of homeostasis caused by trauma to the spinal cord. These highly bioactive molecules may also mediate or facilitate the intralesional CNS axonal damage and peripheral neurologic deficits sustained at time of acute CNS injury. Ultimately, it should be possible to develop treatments that will block or modulate the local and systemic expression of cytokine or ICAM bioactivity. Such treatments might aid victims of SCI by diminishing overall morbidity or mortality, helping restore sensorimotor function and homeostasis, and enhancing longevity and quality of life.

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Catecholamine concentration in rat liver after high level transection of the spinal cord

Cited by 2 publications

References 18 publications

Liver denervation affects hepatocyte mitochondrial fatty acid transport capacity

Liver denervation affects hepatocyte mitochondrial fatty acid transport capacity

Immunoactivation and Altered Intercellular Communication Mediate the Pathophysiology of Spinal Cord Injury

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