Gestational diabetes exhibits lack of carnitine deficiency despite relatively low carnitine levels and alterations in ketogenesis.
OBJECTIVE
Previous studies have underlined the importance of the carnitine shuttle system and its dysfunction both in normal pregnancy and in type 1 and 2 diabetes. The objective of this paper was to delineate more systematically the role of the carnitine shuttle system in normal pregnancy and in gestational diabetes.


METHODS
A total of 119 women matched for age comprised three groups: 40 normal adult non-pregnant women (NNP), 46 normal pregnant women with uncomplicated pregnancy (NP) and 33 women with gestational diabetes (GDM). The latter group was further subdivided into those being managed either by diet alone (25 women, GDM-D) or by insulin (8 women,GDM-I). The following biochemical parameters were assayed: fasting plasma total, free and acyl-carnitine, FFA and beta-OH-butyrate, together with several essential anthropometric parameters.


RESULTS
Women with GDM, in contrast to the control groups, displayed the biochemical features characteristic of insulin resistance: higher body weight, higher BMI, higher skinfold and higher HbAlc levels. No differences on any parameters were found between the two GDM subgroups. Both NP and GDM groups had low levels of total carnitine compared to NNP control group, but surprisingly, the GDM group did not exhibit any further decrease of carnitine levels, as would have been expected by the combination of pregnancy and diabetes. Both groups, despite these low carnitine levels, had no clinical symptoms of carnitine deficiency. Furthermore, the GDM group displayed higher levels of FFA and beta-hydroxybutyrate, which were statistically significant compared to the other two control groups.


CONCLUSIONS
The data corroborate the negative effect of normal gestation on the carnitine shuttle system, while they document for the first time that GDM does not further affect the efficiency of the carnitine system. The mild effect of GDMon carnitine status could be explained by the concurrent increased gluconeogenesis, a process which does not affect directly carnitine metabolism.
Pappa
Kalliopi I
KI
Department of Obstetrics and Gynecology, University of Crete School of Medicine, Heraklion, Greece. kpappa@imbb.forth.gr
Anagnou
Nicholas P
NP
Salamalekis
Emmanuel
E
Bikouvarakis
Stylianos
S
Maropoulos
George
G
Anogianaki
Nektaria
N
Evangeliou
Athanasios
A
Koumantakis
Eugene
E
D020155:3-Hydroxybutyric Acid / Q000097:blood; D000328:Adult; D015992:Body Mass Index; D001835:Body Weight; D002331:Carnitine / Q000097:blood / Q000378:metabolism*; D016022:Case-Control Studies; D016640:Diabetes, Gestational / Q000178:diet therapy / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D005215:Fasting / Q000097:blood; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000627:therapeutic use; D007333:Insulin Resistance; D007657:Ketone Bodies / Q000096:biosynthesis*; D011247:Pregnancy; D012885:Skinfold Thickness
D020155:3-Hydroxybutyric Acid; D002331:Carnitine; D005230:Fatty Acids, Nonesterified; D006442:Glycated Hemoglobin; D007328:Insulin; D007657:Ketone Bodies