Effects of vitamin B12 deficiency on lipid metabolism of the rat liver and nervous system

1978 ◽  
Vol 39 (3) ◽  
pp. 501-513 ◽  
Author(s):  
C. Fehling ◽  
Margaretha JÄgerstad ◽  
B. Åkesson ◽  
J. Axelsson ◽  
A. Brun
Keyword(s):  
Fatty Acids ◽  
Nervous System ◽  
Fatty Acid ◽  
Motor Nerve ◽  
Vitamin B12 Deficiency ◽  
Neurological Dysfunction ◽  
Vitamin B ◽  
Deficient Diet ◽  
Neurological Signs ◽  
The Central Nervous System

1. Rats bred from vitamin B12-depleted dams were fed on a vitamin B12-deficient diet for 12–15 months and developed a severe vitamin B12 deficiency, as judged from methylmalonic acid excretion and tissue vitamin B12 levels at slaughter. Control rats were supplemented with vitamin B12 in the drinking-water.2. Neurological signs were recorded after 7 months but the motor nerve conduction velocities remained normal. Neuropathological examination revealed mild changes in the peripheral nerves but no changes in the central nervous system.3. The amounts of total lipids and phospholipids were normal, but in all examined tissues the proportions of pentadecanoate (C15 fatty acid) and heptadecanoate (C17 fatty acid) were considerably increased in vitamin B12 deficiency.4. 3H2O was incorporated to the same extent into the fatty acids of nervous tissue from vitamin B12-deficient and control rats after 48 h. Less 3H was found in the liver fatty acids of the vitamin B12-deficient rats.5. Neurological dysfunction can be demonstrated in the vitamin B12-deficient rat; the relation of the biochemical and neuropathological changes to the neurological signs needs further study.

The Golgi Material of the Neurones of the Central Nervous System of Sheep Infected with Louping-Ill

1947 ◽  
Vol s3-88 (1) ◽  
pp. 55-63
Author(s):  
R. A. R. GRESSON ◽  
I. ZLOTNIK
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Purkinje Cells ◽  
Medulla Oblongata ◽  
Motor Nerve ◽  
Pyramidal Cells ◽  
Cell Processes ◽  
The Central Nervous System ◽  
Louping Ill

1. The Golgi material of the pyramidal cells of the cerebral cortex, the Purkinje cells of the cerebellum, and the multipolar cells of the medulla oblongata and ventral horns of the spinal cord of the sheep is present as filaments and as irregularly shaped bodies. In some of the cells, particularly in the lamb (Sheep V), the Golgi material has the appearance of a network. As it is frequently present as separate bodies it is suggested that it may always consist of discrete Golgi elements which are sometimes situated in close proximity or in contact with one another. Filamentous Golgi elements are present in the basal part of the cell processes. 2. An examination of neurones from the corresponding regions of the central nervous system of sheep infected experimentally with louping-ill showed that the Golgi material undergoes changes consequent upon the invasion of the cells by the virus. The Golgi material undergoes hypertrophy, and at the same time there is a reduction in the number of filamentous Golgi elements and a reduction in the amount of Golgi substance present in the cell processes. These changes are followed by fragmentation. All the neurones of a particular region are not affected equally at the same time. The Golgi material of the Purkinje cells tends to form groups in the cytoplasm prior to fragmentation. In the multipolar cells of the medulla oblongata the hypertrophy of the Golgi material is not as great as in the other regions of the central nervous system. The Golgi material of the motor nerve-cells of the ventral horns of the spinal cord undergoes considerable hypertrophy which is followed by a grouping of the Golgi elements and fragmentation.

scholarly journals Superficial siderosis of the central nervous system is a rare and possibly underdiagnosed disorder

2017 ◽  
Vol 75 (2) ◽  
pp. 92-95 ◽  
Author(s):  
Yara Dadalti Fragoso ◽  
Tarso Adoni ◽  
Joseph Bruno Bidin Brooks ◽  
Sidney Gomes ◽  
Marcus Vinicius Magno Goncalves ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Disease Onset ◽  
Clinical Findings ◽  
Neurological Dysfunction ◽  
Superficial Siderosis ◽  
Blood Products ◽  
The Central Nervous System ◽  
Magnetic Resonance Imaging Mri ◽  
Intermittent Bleeding

ABSTRACT Superficial siderosis (SS) of the central nervous system (CNS) is a rare and possibly underdiagnosed disorder resulting from chronic or intermittent bleeding into the subarachnoid space, leading to deposition of blood products in the subpial layers of the meninges. Magnetic resonance imaging (MRI) shows a characteristic curvilinear pattern of hypointensity on its blood-sensitive sequences. Methods Series of cases collected from Brazilian centers. Results We studied 13 cases of patients presenting with progressive histories of neurological dysfunction caused by SS-CNS. The most frequent clinical findings in these patients were progressive gait ataxia, hearing loss, hyperreflexia and cognitive dysfunction. The diagnoses of SS-CNS were made seven months to 30 years after the disease onset. Conclusion SS-CNS is a rare disease that may remain undiagnosed for long periods. Awareness of this condition is essential for the clinician.

Acute reversible toxic encephalopathy during capecitabine and oxaliplatin treatment

2017 ◽  
Vol 25 (2) ◽  
pp. 497-501 ◽  
Author(s):  
João Godinho ◽  
Mafalda Casa-Nova ◽  
Teresa Mesquita ◽  
Maria João Baptista ◽  
Francisco Araújo ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Clinical Findings ◽  
Neurological Dysfunction ◽  
Toxic Encephalopathy ◽  
Central Nervous System Toxicity ◽  
Cerebellar Dysfunction ◽  
Oxaliplatin Treatment ◽  
Tumor Involvement ◽  
The Central Nervous System

Introduction Capecitabine is a fluoropyrimidine commonly used in the treatment of colorectal cancer which may cause central nervous system toxicity, namely cerebellar dysfunction. Case report We describe a 77-year-old man undergoing adjuvant treatment of colon cancer with capecitabine and oxaliplatin who presented with acute cerebellar ataxia and encephalopathy that progressed to coma. Diagnosis of toxic encephalopathy was made after the exclusion of alternative causes of neurological dysfunction and complete resolution of clinical findings with permanent discontinuation of chemotherapy. Discussion When patients with cancer develop symptoms and signs of central nervous dysfunction, metabolic and infectious causes plus tumor involvement of central nervous system must be sought. However, chemotherapy may also cause toxicity to the central nervous system. Capecitabine is no exception, although cerebellar dysfunction is rarely reported. Conclusion Although rare, capecitabine-induced encephalopathy may be severe and physicians should be aware of this possible side effect.

scholarly journals Determining the Bioenergetic Capacity for Fatty Acid Oxidation in the Mammalian Nervous System

2020 ◽  
Vol 40 (10) ◽  
Author(s):  
Cory J. White ◽  
Jieun Lee ◽  
Joseph Choi ◽  
Tiffany Chu ◽  
Susanna Scafidi ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Nervous System ◽  
Fatty Acid ◽  
Conditional Knockout ◽  
Mammalian Brain ◽  
Metabolic State ◽  
Peripheral Tissues ◽  
Mitochondrial Fatty Acid ◽  
The Brain ◽  
Long Chain

ABSTRACT The metabolic state of the brain can greatly impact neurologic function. Evidence of this includes the therapeutic benefit of a ketogenic diet in neurologic diseases, including epilepsy. However, brain lipid bioenergetics remain largely uncharacterized. The existence, capacity, and relevance of mitochondrial fatty acid β-oxidation (FAO) in the brain are highly controversial, with few genetic tools available to evaluate the question. We have provided evidence for the capacity of brain FAO using a pan-brain-specific conditional knockout (KO) mouse incapable of FAO due to the loss of carnitine palmitoyltransferase 2, the product of an obligate gene for FAO (CPT2B−/−). Loss of central nervous system (CNS) FAO did not result in gross neuroanatomical changes or systemic differences in metabolism. Loss of CPT2 in the brain did not result in robustly impaired behavior. We demonstrate by unbiased and targeted metabolomics that the mammalian brain oxidizes a substantial quantity of long-chain fatty acids in vitro and in vivo. Loss of CNS FAO results in robust accumulation of long-chain acylcarnitines in the brain, suggesting that the mammalian brain mobilizes fatty acids for their oxidation, irrespective of diet or metabolic state. Together, these data demonstrate that the mammalian brain oxidizes fatty acids under normal circumstances with little influence from or on peripheral tissues.

Effect of a Vitamin B-12-Deficient Diet on Lipid and Fatty Acid Composition of Spinal Cord Myelin in the Fruit Bat

1983 ◽  
Vol 113 (3) ◽  
pp. 531-537 ◽  
Author(s):  
Justin van der Westhuyzen ◽  
Richard C. Cantrill ◽  
Francisco Fernandes-Costa ◽  
Jack Metz
Keyword(s):  
Spinal Cord ◽  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Acid Composition ◽  
Vitamin B ◽  
Deficient Diet ◽  
Fruit Bat ◽  
Vitamin B 12

Suspected myelinolysis following rapid correction of hyponatremia in a dog

1999 ◽  
Vol 35 (6) ◽  
pp. 493-497 ◽  
Author(s):  
RK Churcher ◽  
AD Watson ◽  
A Eaton
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurological Dysfunction ◽  
Laboratory Findings ◽  
Neurological Signs ◽  
Therapeutic Guidelines ◽  
Chronic Hyponatremia ◽  
Iatrogenic Damage ◽  
Gastrointestinal Parasitism ◽  
Rapid Correction

A dog developed signs of neurological dysfunction five days after rapid correction of severe electrolyte derangements, including hyponatremia, caused by gastrointestinal parasitism (i.e., trichuriasis). History, laboratory findings, and onset of neurological signs following correction of hyponatremia led to a diagnosis of myelinolysis. Myelinolysis is a noninflammatory, demyelinating brain disease caused by sudden, upward osmotic shifts in central nervous system plasma, often a result of rapid correction of chronic hyponatremia. The pathogenesis is complex, but recovery is possible. Iatrogenic damage due to myelinolysis can be avoided by adherence to therapeutic guidelines for correction of chronic hyponatremia.

scholarly journals Levels of polyunsaturated fatty acids in lymphocytes of rats fed on diets varying in polyunsaturated fatty acid content

1980 ◽  
Vol 43 (2) ◽  
pp. 367-373 ◽  
Author(s):  
W. M. Tsagn ◽  
J. Belin ◽  
A. D. Smith
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Polyunsaturated Fatty Acid ◽  
Fatty Acid Content ◽  
Inverse Correlation ◽  
Normal Diet ◽  
Deficient Diet ◽  
Polyunsaturated Fatty Acid Content ◽  
Weanling Rats ◽  
Total Fatty Acids

1. When weanling rats were fed on a diet containing 0.1 g/kg of the diet as polyunsaturated fatty acid, it was found that after 2 weeks the level of linoleate in the lymphocyte total lipids was 56 mg/ g total fatty acids, as compared with a level of 138 mg/ g in rats on a normal diet (P < 0.005). Similar levels were obtained from rats which had been fed for up to 16 weeks on the deficient diet, but in a group killed after 28 weeks on the diet the level was found to be only 20 mg/ g total fatty acids. The arachidonate level was found to be approximately 220 mg/ g total fatty acids, regardless of whether the rats were fed on a diet deficient in linoleate for up to 16 weeks or on a normal diet. In the group of rats killed after 28 weeks on the linoleate deficient diet, however, the arachidonate level was only 60 mg/ g total fatty acids.2. Percentage values for total fatty acids are given for plasma, adipose tissue, and lymphocytes for rats on normal and experimental diets.3. Scatter diagrams of the levels of linoleate v. arachidonate in the lymphocyte total fatty acids showed no correlation between the levels of the two acids (r 0.05), but similar plots of linoleate and oleate levels showed an inverse correlation (r – 0.68).

scholarly journals The experimental production of vitamin B12 deficiency in the baboon (Papio cynocephalus). A 2-year study

1974 ◽  
Vol 32 (2) ◽  
pp. 219-228 ◽  
Author(s):  
R. C Siddons
Keyword(s):  
Methylmalonic Acid ◽  
Daily Intake ◽  
Serum Vitamin ◽  
Vitamin B12 Deficiency ◽  
Vegetarian Diet ◽  
Vitamin B ◽  
Papio Cynocephalus ◽  
Experimental Production ◽  
Deficient Diet ◽  
Liver Vitamin

1. The development of vitamin B12 deficiency, as indicated by the serum and liver vitamin B12 levels and the excretion of methylmalonic acid, was studied over a 2-year period in baboons (Papio cynocephalus) given a diet deficient in vitamin B12. The effects of partial hepatectomy and the inclusion of either ampicillin or sodium propionate in the diet on the rate of development of the deficiency were also studied.2. The baboons had previously been fed on a mainly vegetarian diet. Their serum vitamin B12 levels were less than 100 ng/l and the mean liver vitamin B12 concentration was 0·56 μ/g. Similar serum and liver vitamin B12 levels were found in baboons given a purified diet supplemented with 1 μg vitamin B12/d, and marked increases in the serum and liver vitamin B12 levels occurred when the daily intake was increased to 2 μg.3. The serum vitamin B12 levels decreased to less than 20 ng/l in all baboons given a vitamin B12-deficient diet.4. The liver vitamin B12 concentration also decreased in all baboons given a deficient diet. At 9 months the lowest levels (0·20 μ/g) were found in partially hepatectomized baboons but subsequently baboons given the diet containing ampicillin had the lowest levels (0·11 μ/g).5. The excretion of methylmalonic acid after a valine load was found to be inversely related to the liver vitamin B12 concentration. In the early part of the study, partially hepatectomized baboons excreted the highest amount but subsequently baboons given a diet containing ampicillin excreted the highest amount.6. Increased formiminoglutamic acid excretion after a histidine load was observed in two baboons given a vitamin B12-deficient diet and in both baboons the liver folic acid concentration was low.7. No haematological or neurological symptoms of the vitamin B12 deficiency were observed.

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