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Youri E C Taes

Publications and source records attributed to Youri E C Taes.

13 recordsLinked to original sources

Biological and clinical aspects of the vitamin D binding protein (Gc-globulin) and its polymorphism.

The vitamin D binding protein (DBP) is the major plasma carrier protein of vitamin D and its metabolites. Unlike other hydrophobic hormone-binding systems, it circulates in a considerably higher titer compared to its ligands. Apart from its specific sterol binding capacity, DBP exerts several other important biological functions such as actin scavenging, fatty acid transport, macrophage activation and chemotaxis. The DBP-gene is a member of a multigene cluster that includes albumin, alpha-fetoprotein, and alpha-albumin/afamin. All four genes are expressed predominantly in the liver with overlapping developmental profiles. DBP is a highly polymorphic serum protein with three common alleles (Gc1F, Gc1S and Gc2) and more than 120 rare variants. The presence of unique alleles is a useful tool for anthropological studies to discriminate and to reveal ancestral links between populations. Many studies have discussed the link between DBP-phenotypes and susceptibility or resistance to osteoporosis, Graves' disease, Hashimoto's thyroiditis, diabetes, COPD, AIDS, multiple sclerosis, sarcoidosis and rheumatic fever. This article reviews the general characteristics, functions and clinical aspects of DBP.

Disease↗

Vitamin D binding protein, bone status and body composition in community-dwelling elderly men.

The vitamin D binding protein (DBP) is the major carrier protein for vitamin D metabolites in plasma. Polymorphisms in DBP have been described to be associated with an increased bone fracture risk and diabetes. The present study investigates the influence of both phenotypic and (TAAA)(n)-Alu repeat DBP-polymorphism and DBP-concentration on bone mineral density, body composition, bone turnover- and metabolic markers in a cohort of ambulatory elderly men. We included 211 men (>70 years) in this study. Bone mineral density (BMD) was determined by dual energy X-ray absorptiometry. Bone turnover was assessed by measurement of serum osteocalcin, serum and urinary C-terminal telopeptides of type I collagen and urinary deoxypyridinoline, together with 25(OH)-vitamin D and 1,25(OH)(2)-vitamin D concentrations. DBP-phenotypes were determined electrophoretically and the (TAAA)(n)-Alu repeat polymorphism was determined by polymerase chain reaction. Body composition was estimated using bioelectrical impedance analysis, together with handgrip and arm strength, fasting serum glucose and leptin concentrations. No differences in BMD or bone turnover markers among DBP-phenotypes or (TAAA)(n)-genotypes were observed in this study. Serum 25(OH)-vitamin D was comparable among DBP-variants and did not relate to DBP-concentrations, whereas 1,25(OH)(2)-vitamin D was different among DBP-phenotypes and was correlated positively with DBP-concentrations. DBP-concentrations related positively to body mass index, fat mass, leptin and glucose concentration. The correlation with leptin remained significant after correction for fat mass. Fasting glucose concentrations were different among DBP-phenotypes, whereas no difference was observed between (TAAA)(n)-genotypes. In conclusion, serum 1,25(OH)(2)-vitamin D concentrations are codetermined by DBP-phenotypes and DBP-concentrations. No major effect of DBP-polymorphism was demonstrated on BMD, bone turnover markers or body composition.

Absorptiometry, Photon↗

Serum vitamin C concentration is influenced by haptoglobin polymorphism and iron status in Chinese.

BACKGROUND: Vitamin C is a powerful antioxidant (free radical scavenger). Apart from the diet, other factors regulating its catabolism may affect its serum concentration. Haptoglobin (Hp) is a plasma protein participating in iron metabolism. It shows a genetic polymorphism which shows marked geographical differences. We investigated the relationship between vitamin C, iron status and haptoglobin polymorphism in Chinese men and women. METHODS: Iron status markers were compared according to Hp phenotypes determined by chemiluminescence detection in 110 healthy Chinese subjects. The concentration of haptoglobin was determined using an immunoturbidimetric method. Serum vitamin C was tested by a 2,4-dinitrophenylhydrazine based method. RESULTS: In Chinese, the haptoglobin phenotype distribution was 10.0% Hp 1-1, 33.6% Hp 2-1, and 56.4% Hp 2-2. In the study group, serum vitamin C concentration was associated with haptoglobin type, showing lowest values in serum from Hp 2-2 subjects in males (p=0.028, ANOVA). In contrast to Hp phenotype, Hp concentration did not affect vitamin C concentration. Hp 2-2 shows higher haptoglobin (p=0.002 (ANOVA)) than individuals with the other types. Furthermore, vitamin C was influenced by (log)ferritin levels. In Chinese, vitamin C is influenced by haptoglobin polymorphism and iron status. CONCLUSION: The present findings support the role of non-nutritional factors in vitamin C status.

Ascorbic Acid↗

Creatine supplementation does not decrease total plasma homocysteine in chronic hemodialysis patients.

BACKGROUND: Hyperhomocysteinemia is present in the majority of chronic hemodialysis patients. Treatment with folic acid, vitamin B12, and vitamin B6 cannot fully normalize plasma homocysteine concentrations (tHcy). Previously we have demonstrated the tHcy-lowering effect of creatine supplementation in an animal model of uremia (Kidney Int 64:1331-1337, 2003). The present study investigates the effects of creatine supplementation on tHcy in a vitamin-repleted chronic hemodialysis population. METHODS: Forty-five hemodialysis patients receiving folic acid and vitamin B6 and B12 were included. Patients were treated with creatine (2 g/day) or placebo during 2 treatment periods of 4 weeks, separated by a washout of 4 weeks. Plasma tHcy, creatine, Kt/V(urea), folic acid, vitamin B12, and routine biochemistry were determined, as well as the prognostic inflammatory and nutritional index. RESULTS: All patients had elevated tHcy concentrations (21.2 +/- 5.6 micromol/L). Creatine treatment resulted in increased plasma and red blood cell creatine levels, documenting uptake of creatine. Creatine did not affect tHcy concentrations. There was no relationship between plasma creatine concentrations and tHcy concentrations. No changes in body weight, routine biochemistry, nutritional status, folic acid, or vitamin B12 were observed during the study. CONCLUSION: Creatine supplementation at a rate of 2 g/day does not further decrease tHcy concentrations in chronic dialysis patients already treated with high dose folic acid, vitamin B6, and B12 supplementation.

Aged↗

Effect of dietary creatine on skeletal muscle myosin heavy chain isoform expression in an animal model of uremia.

BACKGROUND: Chronic renal failure is accompanied with muscle dysfunction and myopathy, characterized by muscle weakness and increased fatigue. Myosin heavy chain (MHC) is the principal structural protein that controls the intrinsic contractile properties of striated muscle. Creatine is widely used as an ergogenic nutritional supplement in sportsmen. This study investigates the effect of creatine supplementation on MHC expression in the setting of uremic myopathy. METHODS: Male Wistar rats were either sham operated or subtotally nephrectomized and received a control diet or creatine (2% w/w)-supplemented diet. After 4 weeks of treatment, serum creatinine, creatine, urea and creatinine clearances were determined. MHC isoforms were determined electrophoretically in the extensor digitorum longus and soleus muscles. RESULTS: Creatinine clearances were lower in nephrectomized animals, but similar in creatine-supplemented and control diet animals. Nephrectomized animals had significantly higher MHC IIb and lower MHC IIx isoform expression in the extensor digitorum longus muscle compared to sham-operated animals. In the soleus muscle, MHC IIb expression was increased in nephrectomized animals. Creatine supplementation reversed the MHC transitions observed in uremia in the soleus muscle, but not in the extensor digitorum longus muscle. CONCLUSION: We observed altered expression of MHC isoforms in uremia. In uremic animals, fast MHC IIb isoforms were increased, whereas MHC I and IIx isoforms predominate in control animals. Dietary creatine supplementation reversed the altered MHC expression during uremia in slow-twitch, but not in fast-twitch muscles.

Administration, Oral↗

Prohepcidin accumulates in renal insufficiency.

BACKGROUND: The understanding of iron metabolism has increased substantially during the last decade. Several new transporters and iron regulating molecules have been described. Hepcidin, a small hepatic peptide has recently been proposed as a central mediator of dietary iron absorption. We have investigated the relationship between prohepcidin, the prohormone of hepcidin, and renal function and iron status. METHODS: Forty six patients, referred for 51Cr-EDTA clearance were included in this study. Renal function was assessed by determination of serum creatinine, creatinine clearance, serum cystatin C and serum beta-trace protein. Iron status was evaluated by determination of serum iron, transferrin, transferrin saturation and serum ferritin. All determinations were performed using commercial reagents (Roche Diagnostics, Dade Behring). Serum prohepcidin was determined using an ELISA kit. RESULTS: Serum prohepcidin was found to correlate with 51Cr-EDTA clearance (r = -0.44; p = 0.005), creatinine clearance, serum creatinine, beta-trace protein and cystatin C. No significant relationship was observed between serum prohepcidin concentrations and red cell count, hemoglobin concentration or hematocrit. No significant correlation was found in this population between prohepcidin concentrations and iron status. CONCLUSION: Increased serum prohepcidin concentrations were observed with declining kidney function. We observed no relationship between red cell indices or iron status and serum prohepcidin concentrations.

Aged↗

Creatine supplementation decreases homocysteine in an animal model of uremia.

BACKGROUND: Hyperhomocysteinemia is prevalent in more than 85% of patients with end-stage renal disease (ESRD) and is thought to contribute to the excess cardiovascular mortality and morbidity. Creatine is synthesized by methylation of guanidinoacetate with formation of S-adenosylhomocysteine and subsequently, homocysteine (Hcy). Creatine supplementation down-regulates its endogenous synthesis and, thus, may reduce Hcy production. The present study investigates the effect of creatine supplementation on Hcy concentrations in an animal model of uremia. METHODS: Male Wistar rats were either sham-operated and received a control diet (N = 8) or a 2% creatine-supplemented diet (N = 8), or underwent subtotal nephrectomy and received a control diet (N = 10) or a 2%-supplemented creatine diet (N = 10). After 2 weeks of treatment, total plasma Hcy, creatine, creatinine, folate, and vitamin B12 were determined, as well as hepatic folate and vitamin B12 concentrations. RESULTS: Plasma creatinine concentrations were higher in nephrectomized animals, but similar in creatine-supplemented and control diet-fed animals. Plasma Hcy was higher in nephrectomized animals but lower in creatine-supplemented nephrectomized animals compared to nephrectomized control diet-fed animals (12.1 +/- 2.4 micromol/L vs. 15.4 +/- 1.7 micromol/L; P < 0.01). Total plasma Hcy inversely correlated with plasma creatine concentrations (r =-0.39; P = 0.02). Plasma folate was higher in supplemented animals and hepatic tetrahydrofolate (THF) was higher in nephrectomized supplemented animals. Plasma vitamin B12 was similar in all groups, whereas hepatic vitamin B12 was higher in nephrectomized animals. CONCLUSION: Creatine supplementation can effectively lower plasma Hcy concentrations in an animal model of uremia and should be further investigated as a potential treatment for hyperhomocysteinemia in patients with ESRD.

Animals↗

Creatine supplementation does not affect kidney function in an animal model with pre-existing renal failure.

BACKGROUND: Creatine is widely used as an ergogenic substance among athletes. Safety of prolonged creatine intake has been questioned, based upon case reports and animal data. We investigated the effect of prolonged creatine ingestion on renal function in animals with normal kidney function or pre-existing kidney failure, respectively. METHODS: Male Wistar rats were randomly allocated to four experimental groups: (i) sham-operated, control diet; (ii) sham-operated, creatine-supplemented diet (2% w/w (0.9+/-0.2 g creatine/kg body weight/day)); (iii) two-thirds nephrectomized, control diet; and (iv) two-thirds nephrectomized, creatine supplemented diet. Glomerular filtration rate was determined using inulin and creatinine clearance, together with albumin excretion, urea clearance, muscle and serum creatine and serum cystatin C concentrations. RESULTS: In contrast to previous reports, no detrimental effects of creatine supplementation on the renal function indices were observed in two-thirds nephrectomized or sham-operated animals. No differences were observed in inulin (0.28+/-0.08 vs 0.25+/-0.08 ml/min/100 g; P=NS) or creatinine clearance rates. Serum cystatin C concentration, urinary protein excretion, and albumin and urea clearance were comparable between creatine-supplemented and control-diet fed animals in both sham-operated and two-thirds nephrectomized animals. Serum creatine and intramuscular total creatine concentrations were higher in creatine-supplemented groups (P<0.05). CONCLUSIONS: Creatine supplementation at a dosage of 2% w/w for 4 weeks does not impair kidney function in animals with pre-existing renal failure or in control animals.

Albuminuria↗