Serum apelin and resistin levels in patients with impaired fasting glucose, impaired glucose tolerance, type 2 diabetes, and metabolic syndrome.

INTRODUCTION: The aim of this study was to investigate serum apelin and resistin levels in patients with impaired fasting glucose, impaired glucose tolerance, type 2 diabetes and metabolic syndrome. MATERIAL AND METHODS: The study comprised 18 patients with type 2 diabetes mellitus (T2DM) (nine females, nine males), 18 patients with impaired fasting glucose (IFG) (nine females, nine males), 18 patients with impaired glucose tolerance (IGT) (nine females, nine males), 18 patients with metabolic syndrome (MeS) (nine females, nine males), and 16 healthy individuals (eight females, eight males); serum adiponectin, apelin, resistin levels, fasting and postprandial blood glucose, insulin resistance markers, and lipid parameters were measured. RESULTS: In the study, serum apelin levels were determined to be significantly lower in IGT, MeS, and T2DM groups compared with the control group (p = 0.002, p = 0.006, and p < 0.001, respectively). Serum resistin levels were determined to be significantly higher in IGT and T2DM groups compared with the control group (p < 0.001 and p < 0.001, respectively). CONCLUSIONS: Apelin and resistin are thought to affect glucose metabolism and insulin resistance. Apelin is an important indicator in individuals with IGT in the prediabetic period and may play a role in preventing diabetic complications and treatment of T2DM.

Nesfatin-1 and ghrelin levels in serum and saliva of epileptic patients: hormonal changes can have a major effect on seizure disorders.

Nesfatin-1 and ghrelin are the two recently discovered peptide hormones involved in the control of appetite. Besides its main appetite-control function, ghrelin also has anticonvulsant effects, while nesfatin-1 causes depolarization in the paraventricular nucleus (PVN). The aims of this study, therefore, were to investigate: (i) whether there are differences in the concentrations of nesfatin-1 and ghrelin in saliva and serum samples between eplilepsy patients and normal controls and (ii) whether salivary glands produce nesfatin-1. The study included a total of 73 subjects: 8 patients who were newly diagnosed with primary generalized seizures and had recently started antiepileptic drug therapy; 21 who had primary generalized seizures and were continuing with established antiepileptic drug therapy; 24 who had partial seizures (simple: n = 12 or complex: n = 12) and were continuing with established antiepileptic drug therapy; and 20 controls. Salivary gland tissue samples were analyzed for nesfatin-1 expression by immunochemistry and ELISA. Saliva and serum ghrelin levels were measured by ELISA and RIA, and nesfatin-1 levels by ELISA. Nesfatin-1 immunoreactivity was detected in the striated and interlobular parts of the salivary glands and the ducts. The nesfatin-1 level in the brain was around 12 times higher than in the salivary gland. Before antiepileptic treatment, both saliva and serum nesfatin-1 levels were around 160-fold higher in patients who are newly diagnosed with primary generalized epilepsy (PGE) than in controls; these levels decreased with treatment but remained about 10 times higher than the control values. Saliva and serum nesfatin-1 levels from patients with PGE and partial epilepsies who were continuing antiepileptic drugs were also 10-fold higher than control values. Serum and saliva ghrelin levels were significantly (twofold) lower in epileptic patients before treatment than in controls; they recovered somewhat with treatment but remained below the control values. These results suggest that the low ghrelin and especially the dramatically elevated nesfatin-1 levels might contribute to the pathophyisology of epilepsy. Therefore, serum and saliva ghrelin and especially the remarkably increased nesfatin-1 might be candidate biomarkers for the diagnosis of epilepsy and for monitoring the response to anti-epileptic treatment.

Ghrelin, paraoxonase and arylesterase levels in depressive patients before and after citalopram treatment.

OBJECTIVES: The purpose of this study was to examine alterations in lipid profiles and in the serum concentrations of acylated and desacylated ghrelin, paraoxonase and arylesterase in psychiatric patients before and after treatment with 40 mg citalopram daily for 3 months. DESIGN AND METHODS: Samples were collected from 22 healthy controls and 24 psychiatric patients before and after citalopram treatment. Blood levels of acylated and desacylated ghrelin were measured by radioimmunoassay. Paraoxonase and arylesterase activities were determined spectrophotometrically. Lipid parameters were measured on the OLYMPUS-AU400. RESULTS: It was found that the levels of acylated, desacylated ghrelin, paraoxonase arylesterase, total cholesterol and triglyceride were lower in depressive patients before citalopram treatment than in the control group. Those parameters were not restored after citalopram treatment except for the arylesterase level. CONCLUSION: Decreased PON1 and ghrelin levels as well as fluctuations in lipid profiles may be involved in the etiology of depressive disorders.