Редактирование: AHSG

Alpha-2-HS-glycoprotein precursor (Alpha-2-Z-globulin) (Ba-alpha-2-glycoprotein) (Fetuin-A) [Contains: Alpha-2-HS-glycoprotein chain A; Alpha-2-HS-glycoprotein chain B] [FETUA] [PRO2743]

==Publications==

{{medline-entry
|title=Fetuin-A serum levels are not correlated to kidney function in long-lived subjects.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/22425942
|abstract=Serum Fetuin A has been identified as an inhibitor of ectopic calcification. It is reduced in subjects with chronic kidney disease (CKD) and it has been proposed as a potential link between CKD and the higher prevalence of arterial calcification observed in these patients. During aging both the stiffening of arterial wall due to calcification and a decline in kidney function are frequent. The aim of the study is to investigate if Fetuin A serum levels are associated with aging and with [[AHSG]] T256S polymorphism. Moreover, we aim at investigate whether serum Fetuin A is correlated to kidney function in this setting of senescence. 256 health long-lived subjects (age 92 [81-100]) were recruited for the study. Serum Fetuin A was evaluated by ELISA, Cystatin C by immune-nephelometry. [[AHSG]] T256S was determinated by PCR-RFLP. Serum Fetuin A shows a significant correlation with age (r=0.20; P=0.0048). [[AHSG]] TS and SS genotypes are associated to lower levels of serum protein (0.27 [0.19-0.29] g/L vs 0.42 [0.32-0.49] g/L; P<0.027 and 0.34 [0.25-0.41] g/L vs 0.42 [0.32-0.49] g/L; P<0.001, respectively). No significant correlation between Fetuin A and Cystatin C was observed. Serum Fetuin A increases with age in elder individuals and subjects with the TS or SS [[AHSG]] polymorphism have lower levels of the circulating protein. No correlation with kidney function decline was observed. Other mechanisms should be investigated to explain the increase of Fetuin A with age.
|mesh-terms=* Aged, 80 and over
* Aging
* Calcinosis
* Cystatin C
* Female
* Gene Expression
* Humans
* Kidney
* Kidney Failure, Chronic
* Kidney Function Tests
* Male
* Polymerase Chain Reaction
* Polymorphism, Restriction Fragment Length
* Polymorphism, Single Nucleotide
* alpha-2-HS-Glycoprotein

|full-text-url=https://sci-hub.do/10.1016/j.clinbiochem.2012.02.024
}}
{{medline-entry
|title=Genetic variation in alpha 2HS-glycoprotein is related to calcaneal broadband ultrasound attenuation in older women.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/9632839
|abstract=Calcaneal broadband ultrasound attenuation (BUA) is an independent predictor of hip and vertebral fractures. BUA is under genetic control, but the specific genes contributing to BUA are not well defined. We examined the relationship between genetic variation in alpha2HS-glycoprotein ([[AHSG]]), an abundant noncollagenous protein of bone matrix, and calcaneal BUA. Genetic polymorphism in [[AHSG]] was determined in 222 Caucasian women (age 66-92) enrolled in the Pittsburgh Study of Osteoporotic Fractures clinical center by isoelectric focusing of serum samples. Calcaneal BUA and bone mineral density (BMD) were measured on the same foot with a Walker Sonix UBA 575( ) and single X-ray absorptiometry. Hip and spine BMD were determined with a Hologic QDR-1000 densitometer using dual-energy X-ray absorptiometry. [[AHSG]] polymorphism was not significantly related to hip, lumbar spine, or calcaneal BMD. Compared with the homozygous [[AHSG]]*2 women, calcaneal BUA was 13% lower in heterozygous (P < 0.05) and 16% lower in homozygous [[AHSG]]*1 women (P < 0.05). This relationship persisted after controlling for age, weight, height, walks for exercise, and calcaneal BMD. Current and self-reported height were also lowest in homozygous [[AHSG]]*1 women, intermediate in heterozygous women, and highest among homozygous [[AHSG]]*2 subjects. These results suggest that the [[AHSG]] polymorphism may contribute to the genetic influence on calcaneal BUA and stature.
|mesh-terms=* Aged
* Aged, 80 and over
* Aging
* Alleles
* Blood Proteins
* Body Mass Index
* Body Weight
* Bone Density
* Calcaneus
* Female
* Gene Frequency
* Genetic Variation
* Humans
* Phenotype
* Random Allocation
* Ultrasonography
* alpha-2-HS-Glycoprotein

|full-text-url=https://sci-hub.do/10.1007/s002239900481
}}