ABSTRACT
PURPOSE: The orexigenic peptides, ghrelin, galanin, and orexin-A, have an important role in food intake and energy homeostasis and regulate the higher brain functions including the sleep-wake state. Although the interactions of these neuropeptides affect neuroendocrine systems resulting in obesity, a major risk factor for obstructive sleep apnea syndrome (OSAS), the mechanism has not been fully elucidated. The objective of this study was to evaluate the association of serum ghrelin, galanin, and orexin-A levels with OSAS. METHODS: In this cross-sectional study, patients who underwent one-night polysomnography and conformed to the inclusion criteria were asked to participate. A blood sample was obtained from all participants on the morning of the sleep test to evaluate the serum levels of ghrelin, galanin, and orexin-A using the enzyme-linked immunosorbent assay (ELISA) method. Demographic characteristics, polysomnography data, and serum levels of the participants were recorded and analyzed. Comparison between the OSAS groups was performed by independent sample t-test, Mann-Whitney U test, and Kruskal-Wallis test with post hoc K-W test using SPSS 20.0. RESULTS: Of 272 patients, those in the OSAS group (n=210) were older than patients in the non-OSAS group (n=62), p < 0.003, and had increased BMI, p < 0.006. Patients with, serum ghrelin, galanin, and orexin-A levels were significantly elevated in patients with OSAS (635.9 pg/mL vs. 420.7 pg/mL, 91.0 pg/mL vs. 60.0 pg/mL, 600.3 pg/mL vs. 485.6 pg/mL, respectively) and found to be higher in patients with severe OSAS than mild and moderate cases (p < 0.01). In multinomial logistic regression to predict the OSAS severity, levels of serum ghrelin (OR = 1.016 [1.010-1.021]; p < 0.001), galanin (OR = 1.050 [1.020-1.081]; p < 0.001), and orexin-A (OR = 1.021 [1.012-1.030]; p < 0.001) were significantly associated only with a moderate level of OSAS. CONCLUSION: The orexigenic neuropeptides were found to be an independent determinant of the presence of OSAS and correlate with the severity of OSAS. Increased levels of ghrelin, galanin, and orexin-A were associated with the presence of moderate OSAS.
Subject(s)
Neuropeptides , Sleep Apnea, Obstructive , Cross-Sectional Studies , Galanin , Ghrelin , Humans , OrexinsABSTRACT
BACKGROUND AND OBJECTIVE: The plasminogen (PLG) activation system plays an essential role in severe inflammation based diseases such as periodontitis, destructive membranous periodontal disease (ligneous periodontitis), familial Mediterranean fever (FMF), and amyloidosis. We have aimed to evaluate variations in PLG and the associations between PLG and MEFV genotypes in patients with FMF/ FMF-related secondary amyloidosis and periodontitis. MATERIAL AND METHODS: A total of 247 individuals who were either diagnosed with FMF or systemically healthy were recruited to this human observational study with a cross-sectional design. All individuals were also diagnosed with periodontitis or periodontally healthy. Blood samples were obtained from patients with FMF and systemically healthy controls. Clinical periodontal indicators were recorded. All polymorphisms located in exons 6 and 8 of PLG and mutations located on exons 2 and 10 of the MEFV gene were analyzed by DNA Sanger Sequencing. Genotypes and allele frequencies of PLG and MEFV were detected and tested by the Hardy-Weinberg equilibrium. Serum levels of amyloid A (SAA), high-sensitive C-reactive protein (hs-CRP), PLG, and salivary PLG levels were determined by using enzyme-linked immunosorbent assay (ELISA). RESULTS: Two polymorphisms were identified in PLG: G to A polymorphism on the 14th nucleotide of intron 8 and C to T polymorphism on the 924th nucleotide of the coding region (IVS 8+14 G>A and c.924C>T, respectively). In IVS 8+14 G>A polymorphisms, wild-type genotype: GG, heterozygote genotype: GA and homozygote genotype: AA. In c.924C>T polymorphism, wild-type genotype: CC, heterozygote genotype: CT and homozygote genotype: TT. The frequency of the heterozygous polymorphisms of PLG was significantly increased (17.6%) in FMF patients with periodontitis (p = .027). A large proportion of the test group that was heterozygous for MEFV-R202Q also had heterozygous PLG polymorphisms. Remarkable exacerbation in periodontal parameters was observed in patients with FMF and amyloidosis. SAA and hs-CRP levels were significantly correlated with salivary PLG levels in patients with periodontitis and heterozygous PLG. CONCLUSIONS: The current study describes IVS 8+14 G>A (rs2295368) and c.924C>T (rs1380916375) polymorphisms for the first time in the periodontal literature, which might play an important role in the pathogenesis of periodontitis, FMF, or amyloidosis. The elucidation of PLG polymorphisms is beneficial from a public health perspective by increasing the quality of life in these patients and reducing the mortality and morbidity associated with inflammatory diseases such as periodontal disease, FMF, and FMF-related amyloidosis.