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A Journal on Pediatrics, Neonatology, Adolescent Medicine,
Child and Adolescent Psychiatry
Indexed/Abstracted in: CAB, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
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Minerva Pediatrica 2010 December;62(6):551-7
Carnitine status and lactate increase in patients with type I juvenile diabetes
Evangeliou A. 1, Gourgiotis D. 2, Karagianni C. 2, Markouri M. 2, Anogianaki N. 4, Mamoulakis D. 1, Maropoulos G. 2, Tsakalidis C. 1, Frentzayias A. 3, Nicolaidou P. 3
1 4th Pediatric Clinic of the Aristotle University of Thessaloniki, Papageorgiou Hospital, Thessaloniki, Greece
2 2nd Department of Pediatrics, University of Athens, Athens, Greece
3 3rd Department of Pediatrics, University of Athens, Attikon Hospital, Athens, Greece
4 Bio-Statistics Laboratory, University of Crete Heraklion, Crete, Greece
AIM: In 32 juvenile patients suffering from insulin dependent diabetes we observed a carnitine imbalance (increase in acylcarnitine and reduction of free carnitine), which was higher in patients with the highest levels of glycosylated hemoglobin. Parallel to that, in patients with the most prominent carnitine imbalance, there was the highest increase in the postprandial lactic acid level and the highest increase in the lactate/pyruvate ratio, without relating to ketosis. In addition, we observed a decrease in free carnitine related to the length of time after appearance of diabetes.
METHODS: This was a prospective study of a cohort of 32 children and young adolescents with insulin dependent diabetes mellitus. All patients were on insulin treatment. Plasma concentrations of total, free and acyl-Carnitine were evaluated in 12 hours fasting blood samples and before the morning administration of insulin. Blood glucose, cholesterol, triglycerides, and lactate, pyruvate, beta-hydroxybutyrate and free fatty acid levels were measured.
RESULTS: The postprandial highest increase of the lactate and lactate/pyruvate ratio observed in patients with the highest degree of carnitine imbalance, namely with poorliest regulated diabetes, raises the question of a coincidental mitochondrial dysfunction. On the ground of our own data, such a claim cannot be substantiated for our patients. In contrast we suggest that the role of other factors like increased gluconeogenesis, degree of ketosis need to be sought.
CONCLUSION: In order to clarify the role of carnitine in the pathophysiology of disease we need also data from other tissues. Carnitine in the peripheral blood reflects only the 1% of the total body carnitine ; furthermore, patients with diabetes exhibit changes in carnitine status not only in the peripheral blood but also in other body tissues, mainly in muscles.