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C16 3'-sulfo Galactosylceramide (d18:1/16:0)

Catalog No. T38179   CAS 89771-78-8
Synonyms: C16 3'-sulfo Galactosylceramide (d18:1/16:0)

C16 3'-sulfo Galactosylceramide (d18:1/16:0) is a sulfated glycolipid.C16 3'-sulfo Galactosylceramide (d18:1/16:0) is a relatively abundant sulfide found in porcine brain and plasma that decreases throughout development in mice.C16 3'-sulfo Galactosylceramide is a relatively abundant sulfide found in porcine brain and plasma that decreases throughout development in mice.C16 3'-sulfo Galactosylceramide is a relatively abundant sulfide found in porcine brain and plasma that decreases throughout development in mice. C16 3'-sulfo Galactosylceramide (d18:1/16:0) inhibits retinal ganglion cell growth in vitro.C16 3'-sulfo Galactosylceramide (d18:1/16:0) has been used as an internal standard for quantifying C16 3'-sulfo Galactosylceramide (d18:1/16:0) in rat cerebellum and white matter isolated from patients with multiple sclerosis. reference for sulphides.

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C16 3'-sulfo Galactosylceramide (d18:1/16:0) Chemical Structure
C16 3'-sulfo Galactosylceramide (d18:1/16:0), CAS 89771-78-8
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Biological Description
Chemical Properties
Storage & Solubility Information
Description C16 3'-sulfo Galactosylceramide (d18:1/16:0) is a sulfated glycolipid.C16 3'-sulfo Galactosylceramide (d18:1/16:0) is a relatively abundant sulfide found in porcine brain and plasma that decreases throughout development in mice.C16 3'-sulfo Galactosylceramide is a relatively abundant sulfide found in porcine brain and plasma that decreases throughout development in mice.C16 3'-sulfo Galactosylceramide is a relatively abundant sulfide found in porcine brain and plasma that decreases throughout development in mice. C16 3'-sulfo Galactosylceramide (d18:1/16:0) inhibits retinal ganglion cell growth in vitro.C16 3'-sulfo Galactosylceramide (d18:1/16:0) has been used as an internal standard for quantifying C16 3'-sulfo Galactosylceramide (d18:1/16:0) in rat cerebellum and white matter isolated from patients with multiple sclerosis. reference for sulphides.
In vitro C16:0 sulfatide (20 nmol/ml) inhibits glucose-stimulated insulin secretion by reducing the sensitivity of the K(ATP) channels to ATP. (The half-maximal inhibitory concentration is 10.3 and 36.7 micromol/l in the absence and presence of C16:0 sulfatide, respectively.) [1]
C16:0 sulfatide (20 nmol/ml for 30 min) increased whole-cell K(ATP) currents at intermediate glucose levels and reduced the ability of glucose to induce membrane depolarization, reduced electrical activity, and increased the cytoplasmic free Ca2+ concentration. Recordings of cell capacitance revealed that C16:0 sulfatide increased Ca2+-induced exocytosis by 215%. This correlated with a stimulation of insulin secretion by C16:0 sulfatide in intact rat islets exposed to diazoxide and high K+.[1]
C16:0 sulfatide (20 nmol/l for 24 h) did not modulate glucagon secretion from intact rat islets.[1]
In vivo C16:0 sulfatide (1 µmol/kg,1 mL ; Zucker rats) resulted in significantly elevated glucose-stimulated insulin secretion (60-80% increase, p < 0.05), without significant changes in glucose tolerance. The treatment was associated with an ameliorated first-phase insulin response (3-4-fold, p = 0.009, 0.016) and a 60% increase of pancreatic sulfatide content (p = 0.001), possible by an uptake of C16:0 sulfatide. The fasting hyperinsulinaemia and blood glucose levels were unchanged.[2]
Synonyms C16 3'-sulfo Galactosylceramide (d18:1/16:0)
Molecular Weight 780.1
Formula C40H77NO11S
CAS No. 89771-78-8

Storage

store at low temperature

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

Solubility Information

Chloroform:Methanol (2:1): Soluble

TargetMolReferences and Literature

1. Buschard K, et al. C16:0 sulfatide inhibits insulin secretion in rat beta-cells by reducing the sensitivity of KATP channels to ATP inhibition. Diabetes. 2006 ; 55(10):2826-2834. 2. Blomqvist M, et al. In vivo administration of the C16:0 fatty acid isoform of sulfatide increases pancreatic sulfatide and enhances glucose-stimulated insulin secretion in Zucker fatty (fa/fa) rats. Diabetes Metab Res Rev. 2005 ; 21(2):158-166. 3. Blomqvist M, et al. Selective lack of the C16:0 fatty acid isoform of sulfatide in pancreas of type II diabetic animal models. APMIS. 2003 ; 111(9):867-877. 4. Saxena K, et al. Unusual hydration properties of C16:0 sulfatide bilayer membranes. Biophys J. 2000 ; 79(1):385-393. 5. Buschard K, et al. The C24:0 Sulfatide Isoform as an Important Molecule in Type 1 Diabetes. Front Biosci (Landmark Ed). 2022 ; 27(12):331.

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Keywords

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