Serum concentration of inorganic sulfate in mammals: Species differences and circadian rhythm

Krijgsheld, Kr

doi:10.1016/0300-9629(80)90261-3

Cited by 53 publications

(23 citation statements)

References 11 publications

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“…The precision of this method was verified by assaying rat serum samples. Sulfate concentration in normal mouse or rat serum obtained with this method was highly comparable to that published previously in the literature with use of similar or different analytic methods (7,20,36).…”

Section: Animalssupporting

confidence: 82%

Critical role of vitamin D in sulfate homeostasis: regulation of the sodium-sulfate cotransporter by 1,25-dihydroxyvitamin D₃

Bolt¹,

Liu²,

Qiao³

et al. 2004

American Journal of Physiology-Endocrinology and Metabolism

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Critical role of vitamin D in sulfate homeostasis: regulation of the sodium-sulfate cotransporter by 1,25-dihydroxyvitamin D3. Am J Physiol Endocrinol Metab 287: E744 -E749, 2004. First published May 27, 2004 10.1152/ajpendo.00151.2004.-As the fourth most abundant anion in the body, sulfate plays an essential role in numerous physiological processes. One key protein involved in transcellular transport of sulfate is the sodium-sulfate cotransporter NaSi-1, and previous studies suggest that vitamin D modulates sulfate homeostasis by regulating NaSi-1 expression. In the present study, we found that, in mice lacking the vitamin D receptor (VDR), NaSi-1 expression in the kidney was reduced by 72% but intestinal NaSi-1 levels remained unchanged. In connection with these findings, urinary sulfate excretion was increased by 42% whereas serum sulfate concentration was reduced by 50% in VDR knockout mice. Moreover, levels of hepatic glutathione and skeletal sulfated proteoglycans were also reduced by 18 and 45%, respectively, in the mutant mice. Similar results were observed in VDR knockout mice after their blood ionized calcium levels and rachitic bone phenotype were normalized by dietary means, indicating that vitamin D regulation of NaSi-1 expression and sulfate metabolism is independent of its role in calcium metabolism. Treatment of wild-type mice with 1,25-dihydroxyvitamin D3 or vitamin D analog markedly stimulated renal NaSi-1 mRNA expression. These data provide strong in vivo evidence that vitamin D plays a critical role in sulfate homeostasis. However, the observation that serum sulfate and skeletal proteoglycan levels in normocalcemic VDR knockout mice remained low in the absence of rickets and osteomalacia suggests that the contribution of sulfate deficiency to development of rickets and osteomalacia is minimal.vitamin D receptor; sulfate INORGANIC SULFATE is the fourth most abundant anion in mammalian plasma. As such, sulfate is essential for numerous physiological functions. For instance, sulfate is involved in activation and detoxification of a variety of endogenous and exogenous substances such as xenobiotics, steroids, neurotransmitters, and bile acids (30, 31). Sulfate conjugation is essential for biosynthesis of a large number of structural proteins such as sulfated glycosaminoglycans (a major component of the cartilage), cerebroside sulfate (a constituent of the myelin membranes in the brain), and heparin sulfate (required for anticoagulation) (10,12,32). Undersulfation of cartilage proteoglycans has been linked to three types of human inherited osteochondrodysplasia disorders, which are caused by mutations in the diastrophic dysplasia sulfate transporter gene (17,18,39,40). Diastrophic dysplasia sulfate transporter protein transports extracellular sulfate into chondrocytes.In mammals, sulfate homeostasis is largely regulated by the kidney. The majority of filtered sulfate is reabsorbed in the proximal tubules, and only ϳ5-20% of the filtered load is excreted into the urine (5, 29). Transcellular trans...

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Section: Animalssupporting

confidence: 82%

Critical role of vitamin D in sulfate homeostasis: regulation of the sodium-sulfate cotransporter by 1,25-dihydroxyvitamin D₃

Bolt¹,

Liu²,

Qiao³

et al. 2004

American Journal of Physiology-Endocrinology and Metabolism

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“…In general, the major supply of sulfate in humans is provided by metabolism of cysteine and methionine, and consequently intake of a diet deficient in protein might be expected to result in decreased sulfate levels. The serum sulfate level in humans has been shown to increase dramatically 3-8 hours after ingestion of a single large amount of protein (12); in rats, sulfate levels have been shown to drop 30-50% after an overnight fast (11). Feeding rats a diet deficient in protein for 4 days has been shown to reduce sulfate levels by 50% (18).…”

Section: Discussionmentioning

confidence: 99%

“…Using cultures of various animal cell types or tissue explants, we (3-6) and other investigators (7)(8)(9)(10) have found that sulfation of chondroitin is usually lowered when sulfate concentrations in medium are Ͻ0.2 mM. Normal fasting sulfate levels in humans are lower than those in any animals that have been tested (11). In adults, normal fasting sulfate levels have generally been reported to average between 0.25 mM and 0.4 mM (11)(12)(13), with a few individuals reported to have levels as low as 0.1 mM (12), suggesting a potential for chondroitin undersulfation.…”

mentioning

confidence: 96%

“…Normal fasting sulfate levels in humans are lower than those in any animals that have been tested (11). In adults, normal fasting sulfate levels have generally been reported to average between 0.25 mM and 0.4 mM (11)(12)(13), with a few individuals reported to have levels as low as 0.1 mM (12), suggesting a potential for chondroitin undersulfation. Furthermore, it has been suggested that the possible benefit of glucosamine sulfate and chondroitin sulfate in the treatment of OA (14,15) may be attributable to supplementation with sulfate rather than glucosamine or chondroitin.…”

mentioning

confidence: 99%

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Fasting serum sulfate levels before and after development of osteoarthritis in participants of the veterans administration normative aging longitudinal study do not differ from levels in participants in whom osteoarthritis did not develop

Blinn¹,

Dibbs²,

Hronowski³

et al. 2005

Arthritis & Rheumatism

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Objective. To determine whether the development of osteoarthritis (OA) in men over a 33-year period is related to lower sulfate levels in stored serum collected during that time interval.Methods. Stored serum samples from participants in the Veterans Administration Normative Aging Study were assayed for sulfate by ion-exchange chromatography. Samples had been obtained every 3-5 years during part or all of a 33-year portion of the study. Sulfate levels were determined in serum from all participants who underwent knee replacement surgery and had evidence of radiographic hand OA, from some of the participants who had evidence of radiographic hand OA but had not undergone knee replacement surgery, from all participants who underwent knee replacement surgery but had no evidence of radiographic hand OA, and from age-matched participants who had no evidence of OA by history, physical examination, or hand radiography.Results. Serum sulfate levels in participants, with or without radiographic hand OA and/or knee replacements, who were ages 34-72 years at the first examination, ranged from 0.21 mM to 0.51 mM over the course of a maximum of 33 years. Both the overall mean and median sulfate levels rose from 0.32 mM at age 40-50 years to 0.38 mM at age 70-80 years, and the overall mean and median for all ages was 0.36 mM. There were no significant differences in sulfate levels between subjects in any of the 4 groups.Conclusion. There was no evidence of a relationship between these serum sulfate levels and the development of OA. However, all samples were collected after overnight fasting, and no participant was younger than age 34 years at the initiation of the study. It remains to be determined whether differences in the time of ingestion of daily dietary protein providing sulfate are related to the development of OA, or whether sulfate levels measured at an earlier age could be a factor.Proteochondroitin sulfate, primarily aggrecan, plays a major role in the mechanical support of cartilage. In addition to assisting in the positioning and orientation of collagen, it determines salt and water distribution and controls a volume domain of water many times the volume of the proteoglycan itself. This provides a major degree of cushioning, so that water is expressed from the domain under pressure and then can return when the pressure is released. These functions are dependant on the high charge of the sulfate substituents; therefore, any decrease in sulfation might be expected to affect the structure and stability of the cartilage. In addition, undersulfation might increase susceptibility to animal chondroitin-degrading enzymes, because these enzymes degrade much more readily whenever sulfate is absent from the adjacent sugars of chondroitin (1,2). Consequently, undersulfation could produce a functional in-

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“…Normal fasting sulphate concentrations in adult humans are lower than those in any animals that have been tested, 4 generally averaging between 0.25 and 0.4 mmol/l, [4][5][6] with a few people reported to have concentrations as low as 0.1 mmol/l. 5 This has suggested a potential for chondroitin undersulphation.…”

mentioning

confidence: 99%

Sulphate and osteoarthritis: decrease of serum sulphate levels by an additional 3-h fast and a 3-h glucose tolerance test after an overnight fast

Blinn

Biggee

McAlindon

et al. 2006

Annals of the Rheumatic Diseases

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Serum concentration of inorganic sulfate in mammals: Species differences and circadian rhythm

Cited by 53 publications

References 11 publications

Critical role of vitamin D in sulfate homeostasis: regulation of the sodium-sulfate cotransporter by 1,25-dihydroxyvitamin D₃

Critical role of vitamin D in sulfate homeostasis: regulation of the sodium-sulfate cotransporter by 1,25-dihydroxyvitamin D₃

Fasting serum sulfate levels before and after development of osteoarthritis in participants of the veterans administration normative aging longitudinal study do not differ from levels in participants in whom osteoarthritis did not develop

Sulphate and osteoarthritis: decrease of serum sulphate levels by an additional 3-h fast and a 3-h glucose tolerance test after an overnight fast

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