Mujde Akturk

Atherogenic lipoprotein phenotype and LDL size and subclasses in women with gestational diabetes

Aims  Women with gestational diabetes are more likely to develop Type 2 diabetes and cardiovascular disease after pregnancy; however, the exact nature of the lipid alterations present is not clear. In Mediterranean women with gestational diabetes, we measured low‐density lipoprotein (LDL) size and all seven subclasses, as well as the ‘atherogenic–lipoprotein phenotype’[ALP, e.g. concomitant presence of elevated triglycerides, reduced high‐density lipoprotein (HDL)‐cholesterol and increased small, dense LDL].

Adiponectin levels and cardiovascular risk factors in hypothyroidism and hyperthyroidism.

Objective  Adiponectin, an adipose tissue‐derived hormone, has been reported to have anti‐inflammatory and anti‐atherogenic effects. The physiological effect of adiponectin on the metabolic changes and its relation with cardiovascular risk factors in thyroid dysfunction states is still not clear. The aim of the study was to evaluate plasma adiponectin level and its relation to cardiovascular risk factors in patients with thyroid dysfunction.

Visfatin concentration is decreased in women with gestational diabetes mellitus in the third trimester.

Our aim is to investigate visfatin concentration and its relationship to glycated hemoglobin (HbA1c), insulin resistance, lipid parameters, and neonatal birth weight in women with gestational diabetes mellitus (GDM). In our study group, there were 47 women with GDM and 31 women with normal glucose tolerance (NGT) between 33–39 weeks of gestation. Plasma visfatin levels were significantly decreased in pregnant women with GDM compared to those with NGT (p=0.001). Homeostasis model assessment-insulin resistance (HOMA-IR) levels were higher in the GDM group than in the NGT group (p=0.006). In all subjects, plasma visfatin levels were negatively correlated with HOMA-IR, post-prandial blood glucose, triglycerides, and VLDL cholesterol (p<0.05). We did not observe any statistically significant correlation between the plasma visfatin levels and the selected parameters in the GDM group, but in the NGT group plasma visfatin levels were negatively correlated with HOMA-IR (r=-0.36, p=0.04). There was no correlation between visfatin concentrations and fetal birth weight in either group (p>0.05). By regression analysis, having GDM was found to be the only significant determinant (t=3.5, p=0.001) of visfatin concentration (R=0.39, r2=0.15). We conclude that women with GDM have significantly decreased visfatin concentrations in the third trimester. Future studies are required to establish the exact role of visfatin in the pathogenesis of GDM.

Reduced Serum Acylated Ghrelin Levels in Patients with Hyperthyroidism

Background and Objective: Recent studies have revealed that circulating ghrelin levels seem to play a role in energy homeostasis. The effect of hyperthyroidism on ghrelin levels is not fully known. Methods: Serum levels of ghrelin and its relationship with insulin resistance were evaluated in 48 patients with hyperthyroidism and 43 euthyroid healthy controls. Thyroid hormones, insulin, glucose, ghrelin levels and lipid parameters were measured in all subjects. Insulin sensitivity was determined using the homeostasis model assessment. Results: Serum ghrelin levels were significantly decreased in hyperthyroid patients than in controls (32.5 ± 23.3 vs. 54.1 ± 35.5 pg/ml, p < 0.001). Circulating ghrelin levels significantly correlated with age (r = –0.26, p = 0.01), fasting glucose (r = –0.21, p = 0.01), free triiodothyronine (r = –0.18, p = 0.04), free thyroxine (r = –0.23, p = 0.02) and thyroid stimulating hormone (r = 0.21, p = 0.04), but not with blood pressure, body mass index, lipid parameters, insulin and homeostasis model assessment (p > 0.05). Multiple regression analysis revealed glucose level to be the most important predictor of circulating ghrelin level. Conclusion: These results indicate that hyperthyroidism has effect on serum ghrelin levels. Further studies are needed for the exact mechanism.

Relationship between serum osteoprotegerin, glycemic control, renal function and markers of atherosclerosis in type 2 diabetes

Abstract We aimed to investigate the relationship between serum osteoprotegerin (OPG) level and glycemic control, lipids, renal function, microalbuminuria, insulin resistance and markers of atherosclerosis including C-reactive protein (CRP), fibrinogen and erythrocyte sedimentation rate (ESR) in patients with type 2 diabetes mellitus (DM). A total of 166 patients (99 women and 67 men) with type 2 DM were recruited in the study. Serum OPG level was higher in poorly controlled diabetic patients (HbA1c ≥ 7%) than in well-controlled diabetic patients (HbA1c < 7%) [4.0 (3.6–5.0) and 3.5 (2.9–4.4) pmol/L, p = 0.02]. There was no difference between the patients with and without microalbuminuria with respect to OPG levels (p > 0.05). LogOPG was correlated with age (r = 0.47, p = 0.0001). After adjustment for age, sex and BMI, logOPG correlated positively with fasting blood glucose (FBG) (r = 0.28, p = 0.001), prandial blood glucose (PBG) (r = 0.22, p = 0.009), glycated hemoglobin (HbA1c) (r = 0.26, p = 0.002), logHOMA-IR (r = 0.30, p = 0.006), fibrinogen (r = 0.17, p = 0.04), mean albumin excretion rate (MAER) (r = 0.20, p = 0.01) and negatively with creatinine clearance (r = − 0.20, p = 0.01). Regression analysis revealed that logOPG was independently associated with age (p = 0.0001), HbA1c (p = 0.01) and MAER (p = 0.02) (r2 = 0.25). In conclusion; we found that serum OPG levels are increased in poorly controlled type 2 DM and associated with age, glycemic control and microalbuminuria.

Association of polymorphisms in the IL-18 and IL-12 genes with susceptibility to Type 1 diabetes in Turkish patients

Background: Recent studies have indicated that polymorphisms of the interleukin-18 (IL-18) and interleukin-12 (IL-12) genes are associated with the development of Type 1 diabetes mellitus (T1 DM) in some populations, but not all. Aim: The present study was designed to examine the roles of polymorphisms in the IL-18 promoter and IL-12p40 with respect to susceptibility to T1 DM in Turkish patients. Subjects and Methods: Ninety-one patients with T1 DM and 87 unrelated healthy subjects were included in the study. The IL-18 polymorphisms at positions −607 and −137 were detected by a sequence-specific PCR method. The single nucleotide polymorphism in the IL-12p40 3′ untranslated region (3′-UTR) at position +1188 was analyzed by the PCR-restriction fragment length polymorphism (RFPL) method. Results: The allelic and genotypic frequencies of the IL-18 and IL-12p40 polymorphisms did not differ significantly between subjects with T1DM and the controls (p>0.05). However, diabetic patients with the −137 (CC) genotype showed a younger onset age compared to patients with the −137 (GG) genotype (p=0.02). In addition, patients with the −607 (CC) genotype had higher levels of glycated hemoglobin (HbA1 c) than patients with the −607 (AC) genotype (p=0.004). Furthermore, patients with the IL-12p40 (AC) genotype had higher HbA1c levels than patients with the IL-12p40 (AA) genotype (p=0.01). Conclusions: The results of the present study show that the IL-18 and IL-12p40 polymorphisms may have some effect on the onset age and deterioration of glycemic control in Turkish patients with T1 DM.

A Case With Immunoassay Interferences in the Measurement of Multiple Hormones

CONTEXT Commonly used immunoassays are not free from interference, which can be a confounder in the interpretation of test results. We present a case with extremely high multiple hormone levels due to such interference. CASE DESCRIPTION A 33-year-old woman with no specific symptoms had markedly elevated TSH with normal free T4 and free T3 levels. Repeated measurements revealed discordantly high TSH, ACTH, FSH, PTH, IGF-1, prolactin, β-human chorionic gonadotropin, and calcitonin levels without the associated clinical pictures. The measurements were repeated with the same patient sample on four different analytical platforms using chemiluminescence immunoassays/electrochemiluminescence immunoassays, and the results were divergent on each platform. Serial dilutions of serum samples revealed nonlinearity, suggesting assay interference. All hormonal measurements were in the normal range when heterophile antibody blocking tubes were used. The serum of the patient was then subjected to polyethylene glycol precipitation. The post-polyethylene glycol recovery resulted in hormone levels in the normal range. The patient did not receive any medications and has been under follow-up without any signs and symptoms for 24 months. CONCLUSIONS This report illustrates a rare case of falsely elevated hormone levels due to assay interference caused by heterophile antibodies. We point out the importance of a close collaboration between clinicians and the laboratory to avoid unnecessary clinical investigations as well as inappropriate treatments.

The relationship between adipocyte fatty acid binding protein-4, retinol binding protein-4 levels and early diabetic nephropathy in patients with type 2 diabetes

Adipocyte fatty acid binding protein-4 (A-FABP4) and retinol binding protein-4 (RBP4) have recently been linked to type 2 diabetes mellitus (DM). Serum A-FABP4 and RBP4 levels and their relationships with early diabetic nephropathy were examined in 87 type 2 diabetic patients. The patients with diabetic nephropathy showed high A-FABP4 levels compared to the patients without diabetic nephropathy (p=0.0001). Log A-FABP4 correlated positively with age (p=0.02), log duration of diabetes (p=0.04), log body mass index (BMI) (p=0.0001), log creatinine (p=0.007), log C-reactive protein (CRP) (p=0.01), log albumin excretion rate (AER) (p=0.001), and negatively with MDRD-GFR (p=0.0001). Serum RBP4 levels were similar between the patients with and without diabetic nephropathy. RBP4 correlated positively with triglycerides (p=0.001), log creatinine (p=0.009), and negatively with MDRD-GFR (p=0.04). In regression analysis, log A-FABP4 was associated with age, sex, log BMI, and log AER (r(2)=0.43) and RBP4 was associated with triglycerides and log creatinine (r(2)=0.22). In conclusion, we found high serum A-FABP4 but unchanged RBP4 concentrations and their associations with renal function and early diabetic nephropathy in type 2 DM.

Craniofacial and pharyngeal airway morphology in patients with acromegaly.

Abstract Objective. The aim of this study was to assess differences in craniofacial characteristics, upper spine and pharyngeal airway morphology in patients with acromegaly compared with healthy individuals. Materials and methods. Twenty-one patients with acromegaly were compared with 22 controls by linear and angular measurements on cephalograms. The differences between the mean values of cephalometric parameters were analyzed with Mann-Whitney U-test. Results. With respect to controls, anterior (p < 0.05), middle (p < 0.01) and posterior (p < 0.05) cranial base lengths were increased, sella turcica was enlarged (p < 0.001) and upper spine morphology demonstrated differences in the height of atlas (p < 0.01) and axis (p < 0.05) in patients with acromegaly. Craniofacial changes were predominantly found in the frontal bone (p < 0.01) and the mandible (p < 0.05). As for the airway, patients with acromegaly exhibited diminished dimensions at nasal (p < 0.001), uvular (p < 0.01), mandibular (p < 0.01) pharyngeal levels and at the narrowest point of the pharyngeal airway space (p < 0.001) compared to healthy controls. Soft palate width was significantly higher (p < 0.001) and the hyoid bone was more vertically positioned (p < 0.01) in patients with acromegaly. Conclusions. Current results point to the importance of the reduced airway dimensions and that dentists and/or orthodontists should be aware of the cranial or dental abnormalities in patients with acromegaly.

Effects of rosiglitazone treatment on the pentose phosphate pathway and glutathione-dependent enzymes in liver and kidney of rats fed a high-fat diet

BACKGROUND Animals fed high-fat diets have been shown to develop hyperglycemia, insulin resistance, hyperlipidemia, and moderate obesity, which resemble the human metabolic syndrome. Obesity, the metabolic syndrome, and some thiazolidinediones, which act as insulin sensitizers, may increase oxidative stress, and/or influence the levels of cellular reducing equivalents and homeostasis. OBJECTIVE This study investigated the effects of a high-fat diet, rosiglitazone, or a high-fat diet plus rosiglitazone on metabolic syndrome parameters and crucial liver and kidney enzyme activities in rats. METHODS Male Wistar rats were assigned to 4 groups (n = 6 per group): (1) the fat (F) group was fed a rodent diet comprising 45 kcal% fat, (2) the rosiglitazone (R) group was fed a standard rat chow comprising 4.97 kcal% fat plus rosiglitazone (3 mg/kg.d), (3) the fat + rosiglitazone (FR) group was fed a rodent diet comprising 45 kcal% fat (as lard, product D12451) plus rosiglitazone (3 mg/kg.d), and (4) the control (C) group was fed a standard rat chow comprising 4.97 kcal% fat. Animals were housed for 4 weeks, at which time the liver and kidney were isolated for spectrophotometric determination of enzyme activities. Body weight was measured before treatment (baseline) and then weekly throughout the study. Adiposity was measured at the end of the 4 weeks. RESULTS The activities of glucose-6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6-PGD), glutathione reductase (GR), and glutathione-S-transferase (GST) were significantly reduced in the livers of groups F, R, and FR compared with group C (all P < 0.05). Kidney G6PD, 6-PGD, and GR were found to be significantly lower in group R compared with the other groups (all P < 0.05). Kidney GST was similar in all groups. Plasma glucose, triglyceride, and insulin concentrations were significantly higher than in group F versus the other groups (all P < 0.05). Adiposity was increased in groups F and FR compared with groups C and R (all P < 0.05). Serum cholesterol concentrations were similar in all groups. CONCLUSIONS In this study, high-fat diet in rats decreased the enzyme activities responsible for pentose phosphate pathway and glutathione-dependent metabolism in liver but not in kidney. Similarly, these enzyme activities were inhibited with rosiglitazone treatment alone in both organs.