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Increased ghrelin levels in epileptic patients
Seizure (2006) 15, 658
www.elsevier.com/locate/yseiz
LETTER TO THE EDITOR Increased ghrelin levels in epileptic patients Dear Editor, I read with some interest the article by Berilgen et al.1 Although I have great respect for the authors and their respective and collective insight, there are a few issues concerning ghrelin level that this article did not address. First, they reported that total (acyl-modified plus des-acyl ghrelins) was very low in patients with and without epilepsy, whereas the normal total ghrelin concentration of blood samples in human is 100— 150 fmol/ml.2 Possible reason for this observation is that ghrelin is easily digested by many proteases in cells. Thus, to measure ghrelin concentration, it is necessary to use aprotinin when collecting blood samples unless analyzed immediately. It should be also treated with 1/10 volume of 1N HCl before keeping samples in the freezer.2 If they did not inhibit protease digestion of the ghrelin peptide, which should theoretically be the case, then a low level of the ghrelin was detected. Second, the observed results are controversial3 and somewhat perplexed, since antiepileptic drugs (AEDs) that promote weight gain include valproate, carbamazepine and gabapentin.4 We knew that blood ghrelin levels were lower in obese subjects than the age matched lean controls.2 If the treatment caused weight gain, it was therefore hard to explain why ghrelin level increased instead of decrement in the epileptic patients treated with antiepileptic drugs. They also reported ghrelin was still within normal physiological condition. If so, how, then to say ghrelin level linked with epilepsy. There may be other mechanisms where we have not known as yet.
Finally, in such a comparative study the measuring total ghrelin cannot go to right address. Since, octanoylated ghrelin is the bioactive peptide, which is responsible for the physiological response.2 So, they are supposed to use an assay able to discriminate these two forms. Therefore, I can say that the study is purely descriptive and no biochemical mechanism was explored either in the regulation of ghrelin in epilepsy or for the functional consequences of the putative changes described.
References 1. Berilgen MS, Mungen B, Ustundag B, Demir C. Serum ghrelin levels are enhanced in patients with epilepsy. Seizure 2006;15:106—11. 2. Kojima M, Kangawa K. Ghrelin: structure and function. Physiol Rev 2005;85:495—522. 3. Greco R, Latini G, Chiarelli F, Iannetti P, Verrotti A. Leptin, ghrelin, and adiponectin in epileptic patients treated with valproic acid. Neurology 2005;65:1808—9. 4. Ness-Abramof R, Apovian CM. Drug-induced weight gain. Drugs Today (Barc) 2005;41:547—55.
Suleyman Aydin* Department of Biochemistry and Clinical Biochemistry, Firat University, Medical School, Firat Medical Center, 23119 Elazig, Turkey *Tel.: +90 533 493 46 43; fax: +90 424 237 91 38 E-mail address: [email protected]
1059-1311/$ — see front matter # 2006 British Epilepsy Association. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.seizure.2006.07.001
17 March 2006
www.elsevier.com/locate/yseiz
LETTER TO THE EDITOR Increased ghrelin levels in epileptic patients Dear Editor, I read with some interest the article by Berilgen et al.1 Although I have great respect for the authors and their respective and collective insight, there are a few issues concerning ghrelin level that this article did not address. First, they reported that total (acyl-modified plus des-acyl ghrelins) was very low in patients with and without epilepsy, whereas the normal total ghrelin concentration of blood samples in human is 100— 150 fmol/ml.2 Possible reason for this observation is that ghrelin is easily digested by many proteases in cells. Thus, to measure ghrelin concentration, it is necessary to use aprotinin when collecting blood samples unless analyzed immediately. It should be also treated with 1/10 volume of 1N HCl before keeping samples in the freezer.2 If they did not inhibit protease digestion of the ghrelin peptide, which should theoretically be the case, then a low level of the ghrelin was detected. Second, the observed results are controversial3 and somewhat perplexed, since antiepileptic drugs (AEDs) that promote weight gain include valproate, carbamazepine and gabapentin.4 We knew that blood ghrelin levels were lower in obese subjects than the age matched lean controls.2 If the treatment caused weight gain, it was therefore hard to explain why ghrelin level increased instead of decrement in the epileptic patients treated with antiepileptic drugs. They also reported ghrelin was still within normal physiological condition. If so, how, then to say ghrelin level linked with epilepsy. There may be other mechanisms where we have not known as yet.
Finally, in such a comparative study the measuring total ghrelin cannot go to right address. Since, octanoylated ghrelin is the bioactive peptide, which is responsible for the physiological response.2 So, they are supposed to use an assay able to discriminate these two forms. Therefore, I can say that the study is purely descriptive and no biochemical mechanism was explored either in the regulation of ghrelin in epilepsy or for the functional consequences of the putative changes described.
References 1. Berilgen MS, Mungen B, Ustundag B, Demir C. Serum ghrelin levels are enhanced in patients with epilepsy. Seizure 2006;15:106—11. 2. Kojima M, Kangawa K. Ghrelin: structure and function. Physiol Rev 2005;85:495—522. 3. Greco R, Latini G, Chiarelli F, Iannetti P, Verrotti A. Leptin, ghrelin, and adiponectin in epileptic patients treated with valproic acid. Neurology 2005;65:1808—9. 4. Ness-Abramof R, Apovian CM. Drug-induced weight gain. Drugs Today (Barc) 2005;41:547—55.
Suleyman Aydin* Department of Biochemistry and Clinical Biochemistry, Firat University, Medical School, Firat Medical Center, 23119 Elazig, Turkey *Tel.: +90 533 493 46 43; fax: +90 424 237 91 38 E-mail address: [email protected]
1059-1311/$ — see front matter # 2006 British Epilepsy Association. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.seizure.2006.07.001
17 March 2006