ABSTRACT
Background: Acromegaly is associated with increased morbidity and mortality relatedto cardiovascular diseases. Leptin [LEP] and Leptin Receptor [LEPR] gene polymorphismscan increase cardiovascular risks. The aim of this study was to investigateassociation between the frequencies of LEP and LEPR gene polymorphisms and subclinicalatherosclerosis in acromegalic patients
Methods: Forty-four acromegalic patients and 30 controls were admitted to study.The polymorphisms were identified by using polymerase chain reaction from peripheralblood samples. The levels of systolic and diastolic blood pressure, BMI, fastingplasma glucose, fasting insulin, IGF-I, GH, IGFBP3, leptin, triglyceride, carotid IntimaMedia Thickness [cIMT] and HDL and LDL cholesterol concentrations were evaluated
Results: There was statistically significant difference between the LEPR genotypes ofacromegalic patients [GG 11.4%, GA 52.3%, and AA 36.4%] and controls [GG 33.3%,GA 50%, and AA 16.7%] although their LEP genotype distribution was similar. In addition,the prevalence of the LEPR gene G and A alleles was significantly different betweenpatients and controls. No significant difference was found among the G[-2548]A leptin genotypes of groups in terms of the clinical parameters. cIMT significantly increasedhomozygote LEPR GG genotype group compared to AA subjects in patients.But the other parameters were not different between LEPR genotypes groups of patientsand controls
Conclusion: It can be said that the LEPR gene polymorphism may affect cIMT in patients.The reason is that LEPR GG genotype carriers may have more risk than othergenotypes in the development of subclinical atherosclerosis in acromegaly
ABSTRACT
BACKGROUND: Systemic inflammation in psoriasis causes insulin resistance and cardiovascular diseases. Adipokines are adipose-tissue-derived factors that are involved in metabolic processes. It is thought that these adipokines are associated with the development of psoriasis. OBJECTIVE: The purpose of this study was to determine the changes in adipokine levels, insulin resistance, hypertension, and dyslipidemia over a 12-week period. METHODS: The study comprised 35 psoriasis patients and 50 controls. Blood samples were obtained twice from the patients, one sample at the start and one at the end of a 12-week follow-up period. The following parameters were assessed in both groups: serum fasting glucose, fasting insulin, homeostasis model assessment-estimated insulin resistance (HOMA-IR) index, serum lipids, adiponectin, leptin, resistin, chemerin, omentin, vaspin, visfatin, retinol-binding protein 4, and high-sensitivity C-reactive protein (hs-CRP) levels; blood pressure; body mass index; and the psoriasis area severity index (PASI) scores. RESULTS: The patients showed an improvement in the PASI score and a significant decrease in serum hs-CRP, omentin, and chemerin values. Moreover, at the start of the follow-up, the psoriasis patients had significantly lower levels of adiponectin and visfatin and significantly higher levels of vaspin and resistin than those of the control group. Visfatin levels correlated negatively with low-density lipoprotein (LDL) and cholesterol, while vaspin and omentin levels correlated positively with diastolic blood pressure. Decreased adiponectin levels correlated negatively with diastolic blood pressure and LDL. CONCLUSION: Plasma levels of adipokines might be useful for evaluating the disease activity of psoriasis and its comorbidities.