Plasma HDL cholesterol in epileptics with elevated triglyceride and cholesterol

Luoma, P. V.; Myllylä, Vilho V.; Sotaniemi, Eero A.; Hokkanen, Tuula

doi:10.1111/j.1600-0404.1979.tb02951.x

Cited by 15 publications

(3 citation statements)

References 13 publications

(8 reference statements)

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“…The results in our study findings are similar to those other investigations done by P Kumar et al, Pelkonen et al, Nikkila et al, and Luoma et al, also reported same findings i.e. an increase in TG, LDL-C and HDL-C levels in epileptic patients on long-term treatment with Phenytoin [5][6][7][8].…”

Section: Discussionsupporting

confidence: 92%

Evaluation of Effect of Antiepileptic Drugs on Serum Lipid Profile among Young Adults with Epilepsy in a Tertiary Care Hospital in Pondicherry

Manimekala¹

2014

JCDR

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Introduction: Several studies have reported that commonly used antiepileptic drugs like phenytoin, and carbamazepine increase serum High Density Lipoproteins Cholesterol (HDL-C) levels, while some others documented no such effect. Further, some researchers also observed that valproic acid and other newer antiepileptic drugs like lamotrigine and levetiracetam has no influence on serum lipid profile. The present study was planned to assess and compare serum lipid profile of young adult patients on commonly used antiepileptic drugs (phenytoin, oxcarbazepine and valproic acid) and newer antiepileptic drug (levetiracetam) attending Neurology OPD of a tertiary care hospital in Puducherry, India compared to normal subjects. Materials and Methods:A prospective hospital based crosssectional study was conducted in Tertiary care hospital. Epileptic patients attending Department of Neurology and taking antiepileptic drugs for last six months or more and on regular follow up; approximately 60 patients on commonly used antiepileptic drugs (20 on phenytoin, 20 on oxcarbazepine, 20 on valproic Acid) and 20 patients on newer antiepileptic drug (levetiracetam) was included in the study. Age and sex matching 80 controls were taken. Statistical analysis:Descriptive statistics explained using mean ± SD. Inferential statistics was used depending on the nature of variables. We used one-way-ANOVA and followed by independent t-test for comparison with control group and statistically significant was considered at p-value <0.05.

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Section: Discussionsupporting

confidence: 92%

Evaluation of Effect of Antiepileptic Drugs on Serum Lipid Profile among Young Adults with Epilepsy in a Tertiary Care Hospital in Pondicherry

Manimekala¹

2014

JCDR

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“…Hence, previous studies have shown that patients with epilepsy had increased carotid artery intimamedia thickness and increased vascular risk factors (Tan et al, 2009). This coincides with (Luoma et al, 1979) who reported that epileptic patients showed elevated plasma HDL cholesterol levels.…”

Section: Discussionsupporting

confidence: 77%

Untitled

2020

IBSPR

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The aim of this study was to determine the efficacy of sub-anesthetic doses of ketamine on plasma oxidative stress in pilocarpine-induced epilepsy in mice. Mice received either 0.9% saline (control group), or pilocarpine (100 mg/kg every 20 minutes), or ketamine (10 mg/kg every 30 minutes), or ketamine that was administrated after status epilepticus (SE) at the same doses. Blood samples were collected for the determination of oxidative stress parameters and antioxidant enzymes. Data showed that pilocarpineinduced drastic oxidative stress characterized by high lipid oxidation (+202%, p<0.01), the increase of nitric oxide (+255%, p=0.01) and decrease in antioxidant enzyme activities catalase (-36%, p<0.01), peroxidase (-170%, p<0.01) and superoxide dismutase (-35%, p=0.01). Significant reduction of the non-enzymatic antioxidant uric acid (+232%, p=0.03) was realized. Pilocarpine also increased glucose (+213%, p<0.01). Ketamine had the reverse effect and counteracted almost all pilocarpine-induced deleterious impacts around control levels. In conclusion, post-treatment with ketamine exerts a decrease in oxidative damage associated with a decrease in lipid peroxidation and an increase in antioxidant defenses of plasma in mice model of epilepsy.

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“…Clinical studies demonstrated a link between the use of CAR-activating drugs and the occurrence of metabolic disruptions in patients. Long-term use of phenobarbital (PB), a CAR activator, as an antiepileptic drug, induced a change in plasma lipid profiles of patients (3)(4)(5) and chronic treatment with other CAR activators like valproic acid or tamoxifen were associated with the occurrence of hepatic disorders (6,7).…”

Section: Introductionmentioning

confidence: 99%

Activation of the Constitutive Androstane Receptor induces hepatic lipogenesis and regulates Pnpla3 gene expression in a LXR-independent way

Marmugi

Lukowicz

Lasserre

et al. 2016

Toxicology and Applied Pharmacology

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The Constitutive Androstane Receptor (CAR, NR1I3) has been newly described as a regulator of energy metabolism. A relevant number of studies using animal models of obesity suggest that CAR activation could be beneficial on the metabolic balance. However, this remains controversial and the underlying mechanisms are still unknown. This work aimed to investigate the effect of CAR activation on hepatic energy metabolism during physiological conditions, i.e. in mouse models not subjected to metabolic/nutritional stress. Gene expression profiling in the liver of CAR knockout and control mice on chow diet and treated with a CAR agonist highlighted CAR-mediated up-regulations of lipogenic genes, concomitant with neutral lipid accumulation. A strong CAR-mediated up-regulation of the patatin-like phospholipase domain-containing protein 3 (Pnpla3) was demonstrated. Pnpla3 is a gene whose polymorphism is associated with the pathogenesis of nonalcoholic fatty liver disease (NAFLD) development. This observation was confirmed in human hepatocytes treated with the antiepileptic drug and CAR activator, phenobarbital and in immortalized human hepatocytes treated with CITCO. Studying the molecular mechanisms controlling Pnpla3 gene expression, we demonstrated that CAR does not act by a direct regulation of Pnpla3 transcription or via the Liver X Receptor but may rather involve the transcription factor Carbohydrate Responsive Element-binding protein. These data provide new insights into the regulation by CAR of glycolytic and lipogenic genes and on pathogenesis of steatosis. This also raises the question concerning the impact of drugs and environmental contaminants in lipid-associated metabolic diseases.

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Plasma HDL cholesterol in epileptics with elevated triglyceride and cholesterol

Cited by 15 publications

References 13 publications

Evaluation of Effect of Antiepileptic Drugs on Serum Lipid Profile among Young Adults with Epilepsy in a Tertiary Care Hospital in Pondicherry

Evaluation of Effect of Antiepileptic Drugs on Serum Lipid Profile among Young Adults with Epilepsy in a Tertiary Care Hospital in Pondicherry

Untitled

Activation of the Constitutive Androstane Receptor induces hepatic lipogenesis and regulates Pnpla3 gene expression in a LXR-independent way

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