Determination of free L-carnitine levels in type II diabetic women with and without complications

Poorabbas, A; Fallah, Farnoush; Bagdadchi, J; Mahdavi, Reza; Aliasgarzadeh, Akbar; Asadi, Y; Koushavar, Hossein; Jabbari, Masoumeh

doi:10.1038/sj.ejcn.1602594

Cited by 51 publications

(34 citation statements)

References 23 publications

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“…This assumption is supported by the lack of fasting ketosis in our GDM population and it is in line with previous studies that reported comparable fasting ketonemia in normal pregnancies and well-controlled GDM [22]. Similarly, studies in diabetic patients showed that the FC levels are not decreased in the absence of diabetes-associated complications [23] or ketosis [24]. In contrast to our results, the only previous study dealing with carnitine levels in diabetic pregnancies reported increased FC and decreased AC in pregnancies complicated with GDM compared to normal pregnancies [9].…”

Section: Discussionsupporting

confidence: 77%

Effect of Gestational Diabetes on Circulating Levels of Maternal and Neonatal Carnitine

Agakidou¹,

Diamanti²,

Papoulidis³

et al. 2013

J Diabetes Metab

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Objectives: Free carnitine is reported to decrease in normal pregnancies whereas data on the effect of gestational diabetes mellitus (GDM) on maternal and offspring carnitine status are lacking. This study aimed to assess changes in carnitine status in mothers with GDM and the offspring. Subjects/methods:Prospective case-control study of 54 pairs of mothers -neonates (27 with GDM and 27 with normal pregnancies) and 26 non-pregnant controls. Serum glucose, lipids, and total fatty acids, blood β-hydroxybutyric acid, and whole blood carnitine were assessed in mothers before labor and neonates at birth. Carnitine was assessed in dried blood-spots on Guthrie paper using Tandem Mass Spectrometry.Results: Compared to the controls, both groups of mothers had lower free carnitine and acylcarnitine and higher triglyceride and fatty acid levels. Compared to their respective maternal group, both groups of neonates had significantly higher free carnitine and acylcarnitine and lower triglyceride and fatty acid levels. Free carnitine and acylcarnitine, were comparable between the two maternal groups, whereas they were significantly higher in neonates of GDM mothers versus healthy neonates. Conclusions:Well controlled GDM does not exacerbate changes in free carnitine, acylcarnitine, and fatty acid levels in pregnant women, albeit it is associated with increased carnitine in the newborn indicating enhanced fatty acid oxidation. The potential association of carnitine changes with macrosomia and long-term consequences in the offspring of GDM needs further investigation. increased in neonates born to mothers with uncomplicated pregnancies [6,11], whereas there are no published data on the effect of GDM on the neonatal carnitine levels. The primary aim of this study was to assess the effect of GDM on maternal and offspring's carnitine levels. In addition, we investigated the possible association between circulating carnitine levels and FA changes in the mothers and their neonates. Effect of Gestational Diabetes on Circulating Levels of Maternal and Subjects and MethodsThis is a prospective case-control study. Participants were recruited among pregnant women who attended the antenatal clinic of the 2 nd Department of Obstetrics and Gynecology of the Aristotle University of Thessaloniki, at the Hippokration General Hospital, during a twoyear period. Eligible for the study were all pregnant women with single pregnancies who had an abnormal glucose tolerance test at 26-28 weeks of gestation and no history of pre-gestational diabetes. An

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Section: Discussionsupporting

confidence: 77%

Effect of Gestational Diabetes on Circulating Levels of Maternal and Neonatal Carnitine

Agakidou¹,

Diamanti²,

Papoulidis³

et al. 2013

J Diabetes Metab

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“…Accumulation of long-chain fatty acids and other fatty acid metabolites impair insulin signaling and contribute to the development of insulin resistance in skeletal muscle and heart (18). Some studies reported that subjects with diabetes have reduced plasma free carnitine concentrations compared with healthy subjects, indicating an association between impaired carnitine status and glucose intolerance (18,28,29). All participants in our study had diabetes and experienced significant decreases in HbA 1c after 12 weeks of carnitine-orotate complex treatment compared with no significant change in the placebo group.…”

Section: Discussionmentioning

confidence: 99%

Improvement of Nonalcoholic Fatty Liver Disease With Carnitine-Orotate Complex in Type 2 Diabetes (CORONA): A Randomized Controlled Trial

et al. 2015

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OBJECTIVEWe aimed to evaluate the effects of carnitine-orotate complex in patients with nonalcoholic fatty liver disease (NAFLD) and diabetes. RESEARCH DESIGN AND METHODSEight hospitals in Korea participated in this randomized, controlled, double-blind trial of patients with diabetes and NAFLD. Seventy-eight patients were randomly assigned in a 1:1 ratio to receive carnitine-orotate complex (824 mg, three times daily) or matching placebo. The primary study outcome was decline in alanine aminotransferase (ALT) to the normal range. Secondary study outcomes were change in ALT, radiological hepatic steatosis, parameters for anthropometry, liver function, lipid profiles, and glycemic control. Hepatic steatosis was assessed using Hounsfield units on noncontrast computed tomography (CT) imaging with hepatic attenuation. RESULTSAfter 12 weeks of treatment, compared with placebo group, carnitine-orotate complex-treated participants had a significantly higher rate of normalization of serum ALT level (17.9% vs. 89.7%, P < 0.001). On hepatic CT analysis, participants treated with carnitine-orotate complex showed an increased liver attenuation index (0.74 6 8.05 vs. 6.21 6 8.96, P < 0.008). A significant decrease in HbA 1c was observed in the carnitine-orotate complex group (20.33 6 0.82% [23.6 6 9.0 mmol/mol], P = 0.007), but no significant change was seen in the placebo group. CONCLUSIONSTreatment with carnitine-orotate complex improves serum ALT and may improve hepatic steatosis as assessed by CT in patients with diabetes and NAFLD. Further studies using more advanced magnetic resonance imaging and liver histology as an end point are needed to assess its efficacy in NAFLD.Ectopic fat accumulation in a visceral organ is associated with insulin resistance (1). As an example of such ectopic fat accumulation, nonalcoholic fatty liver disease (NAFLD) is now recognized as the hepatic component of metabolic syndrome and is even reportedly associated with insulin resistance independent of obesity and other metabolic components. Therefore, NAFLD can be a major determinant of insulin

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“…Because CPT1 and CrAT share similar carnitine binding motifs ( 31 ), these data support the notion that carnitine acyltransferases are susceptible to inhibition when local carnitine concentrations fall. This observation is particularly relevant to obesity, diabetes, and other disease conditions associated with carnitine insuffi ciency ( 2,(32)(33)(34)(35)(36)(37)(38)(39)(40). Moreover, results from the current study suggest that the mitochondrial pool of free carnitine is more prone to depletion than other compartments.…”

Section: Discussionmentioning

confidence: 99%

Obesity and lipid stress inhibit carnitine acetyltransferase activity

Seiler

Martin

Noland

et al. 2014

Journal of Lipid Research

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L -Carnitine is a conditionally essential nutrient that serves as a substrate for a family of acyltransferase enzymes that catalyze the interconversion of acyl-CoAs and acylcarnitines. Unlike their acyl-CoA precursors, acylcarnitines can be transported across cellular membranes. Accordingly, carnitine is best known for its obligatory role in shuttling long-chain acyl-CoAs (LCACoAs) from the cytoplasm into the mitochondrial matrix for fatty acid oxidation, a function that is mediated by the outer mitochondrial membrane enzyme, carnitine palmitoyltransferase 1 (CPT1). The long-chain acylcarnitine (LCAC) products of CPT1 are transported across the inner mitochondrial membrane by carnitine acylcarnitine translocase and then converted back to LCACoAs by carnitine palimitoyltransferase 2 (CPT2), also localized to the inner membrane. By contrast, carnitine acetyltransferase (CrAT) resides in the mitochondrial matrix and has strong preference for short-chain acyl-CoA (SCACoA) intermediates of fatty acid, glucose, and amino acid catabolism. Thus, CrAT facilitates traffi cking and effl ux of carbon intermediates from the mitochondrial compartment to other cellular and extracellular sites.Recent animal studies have established important roles for L -carnitine and CrAT in regulating glucose homeostasis and mitochondrial substrate switching ( 1 ). By converting acetyl-CoA to acetylcarnitine, CrAT not only buffers the mitochondrial acetyl-CoA pool but also regenerates free CoA, both of which infl uence the activities of several oxidative enzymes. Carnitine supplementation promotes

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Determination of free L-carnitine levels in type II diabetic women with and without complications

Cited by 51 publications

References 23 publications

Effect of Gestational Diabetes on Circulating Levels of Maternal and Neonatal Carnitine

Effect of Gestational Diabetes on Circulating Levels of Maternal and Neonatal Carnitine

Improvement of Nonalcoholic Fatty Liver Disease With Carnitine-Orotate Complex in Type 2 Diabetes (CORONA): A Randomized Controlled Trial

Obesity and lipid stress inhibit carnitine acetyltransferase activity

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