Background: Sex hormone-binding globulin (SHBG) is a protein. The synthesis of SHBG protein is encoded by SHBG gene. Protein polymorphism of SHBG can occur because of a mutation of D327N exon 8 in SHBG gene. D327N mutation causes the addition of glycosylation so that molecular weight of SHBG protein increases. Protein polymorphism of SHBG is suspected to affect the levels of SHBG, testosterone, and insulin in the blood circulation. Objective:To determine the effect of protein polymorphism of SHBG on the levels of SHBG, testosterone, and insulin in healthy adult men. Materials and Methods:Serum samples were collected from 179 healthy adult men. Electrophoresis and western blotting were performed to determine the phenotype of SHBG. All subjects were divided into two groups based on SHBG phenotype; group I (normal SHBG phenotype) n = 159 subjects and group II (variant SHBG phenotype) n = 38 subjects. Result:The levels of serum SHBG, testosterone, and insulin were measured using radioimmunoassay method. The levels of SHBG, total testosterone, and free testosterone between normal SHBG phenotype do not differ with variant SHBG phenotype (p > 0.05), but insulin levels between normal SHBG phenotype compared with variant SHBG phenotype was different (p < 0.05). Conclusion:Protein polymorphisms of SHBG was not found to affect the levels of SHBG, total testosterone, and free testosterone. Protein polymorphism of SHBG was found to affect the insulin levels in the blood serum.
Background: Body mass index (BMI) determined by genetic and environmental factors. One of the genetic factors that determine the BMI is a genetic polymorphism of sex hormone binding globulin (SHBG), whereas the intake of nutrients is one of the environmental factors. The objective: investigate to macronutrient intake of mother in childbearing age with BMI <18.5 kg/m2 and has heterozygous variant D327N SHBG genotype (W/v).Methods: Anthropometric measurement, genotyping of D327N SHBG gen exon 8, and three days repeated food recall and record was done for all subjects. BMI in the group I 16 to <17 kg/m2 and group II 17 to <18.5 kg/m2. For all subjects in both groups has heterozygous variant D327N SHBG genotype (W/v).Results: mother in chieldbearing age with BMI <18.5 kg/m2 and has heterozygous variant SHBG genotype (W/v) is undernutrition. Seventy two percent of the total subjects including type I of chronic energy deficiency (CED), and 28% as type II of CED. Protein, fat and carbohydrate intake and mid-upper arm circumference (MUAC) in the group I was lower than group II (p<0.05), while muscle mass in the group I did not different compare to group II (p>0.097).Conclusions: Mother in childbearing age with BMI <18.5 kg/m2 and has heterozygous variant D327N SHBG genotypes (W/v) shows that the lower of protein, fat and carbohydrate intake then CED status is getting low.
At least 50% of the decline in functional abilities associated with the elderly is caused by neurological conditions, particularly vascular dementia, such as occurs in Binswanger disease. Binswanger disease is a rare condition, characterized by acute strokes with symptoms and signs compatible with lacunar infarction. The disease onset is commonly between 55 and 75 years. The majority of patients with Binswanger disease have chronic hypertension and other putative factors including diabetes mellitus, polycythemia, thrombocytosis, hyperlipidemia, hyperglobulinemia and pseudoxanthoma elasticum, increased fibrinogen levels and the antiphospholipid antibody syndrome. We report the case of a 55 year old man, who suffered from involuntary movements of his right arm, slight hemiparesis on the right side, and also had dementia. He had a history of high blood pressure and laboratory tests showed that he had diabetes mellitus. The brain magnetic resonance imaging showed irregular white matter abnormalities with multiple lacunar infarcts in the basal ganglia and pons. The clinical picture is characterized by acute strokes, followed by involuntary movements and also dementia. Therefore we decided to diagnose it as Binswanger disease. After discharge from hospital, the patient has not returned for follow-up.
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