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A variation in the cerebroside sulfotransferase gene is linked to exercise-modified insulin resistance and to type 2 diabetes.

ABSTRACT: AIMS: The glycosphingolipid beta-galactosylceramide-3-O-sulfate (sulfatide) is present in the secretory granules of the insulin producing beta-cells and may act as a molecular chaperone of insulin. The final step in sulfatide synthesis is performed by cerebroside sulfotransferase (CST) (EC 2.8.2.11). The aim of this study was to investigate whether two single nucleotide polymorphisms (SNP), rs2267161 located in an exon or rs42929 located in an intron, in the gene encoding CST are linked to type 2 diabetes (T2D). METHODS: As a population survey, 265 male and female patients suffering from T2D and 291 gender matched controls were examined. RESULTS: A higher proportion of T2D patients were heterozygous at SNP rs2267161 with both T (methionine) and C (valine) alleles present (49.8% versus 41.3%, P = .04). The calculated odd risk for T2D was 1.47 (1.01-2.15, P = .047). Among female controls, the homozygous CC individuals displayed lower insulin resistance measured by HOMA-IR (P = .05) than the C/T or TT persons; this was particularly prevalent in individuals who exercise (P = .03). CONCLUSION: Heterozygosity at SNP rs2267161 in the gene encoding the CST enzyme confers increased risk of T2D. Females with the CC allele showed lower insulin resistance.

SUBMITTER: Roeske-Nielsen A

PROVIDER: S-EPMC2705865 | biostudies-literature | 2009

REPOSITORIES: biostudies-literature

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A variation in the cerebroside sulfotransferase gene is linked to exercise-modified insulin resistance and to type 2 diabetes.

Roeske-Nielsen A A Buschard K K Månson J E JE Rastam L L Lindblad U U

Experimental diabetes research 20090705

<h4>Aims</h4>The glycosphingolipid beta-galactosylceramide-3-O-sulfate (sulfatide) is present in the secretory granules of the insulin producing beta-cells and may act as a molecular chaperone of insulin. The final step in sulfatide synthesis is performed by cerebroside sulfotransferase (CST) (EC 2.8.2.11). The aim of this study was to investigate whether two single nucleotide polymorphisms (SNP), rs2267161 located in an exon or rs42929 located in an intron, in the gene encoding CST are linked t ...[more]

PMID: 19587831

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Project description:Type 2 diabetes and obesity epidemics are in effect in the United States and the two pathologies are linked. In accordance with the growing appreciation that 'exercise is medicine,' it is intuitive to suggest that exercise can play an important role in the prevention and/or treatment of these conditions. However, if exercise is to truly be considered as a viable alternative to conventional healthcare prevention/treatment strategies involving pharmaceuticals, it must be prescribed with similar scrutiny. Indeed, it seems reasonable to posit that the recent initiative calling for 'precision medicine' in the US standard healthcare system should also be applied in the exercise setting. In this narrative review, we consider a number of explanations that have been forwarded regarding the pathological progression to type 2 diabetes both with and without the concurrent influence of overweight/obesity. Our goal is to provide insight regarding exercise strategies that might be useful as 'precision medicine' to prevent/treat this disease. Although the etiology of type 2 diabetes is complex and cause/consequence characteristics of associated dysfunctions have been debated, it is well established that impaired insulin action plays a critical early role. Consequently, an exercise strategy to prevent/treat this disease should be geared toward improving insulin sensitivity both from an acute and chronic standpoint. However, research suggests that a chronic improvement in insulin sensitivity only manifests when weight loss accompanies an exercise intervention. This has resonance because ectopic fat accumulation appears to represent a central component of disease progression regardless of whether obesity is also part of the equation. The cause/consequence characteristics of the relationship between insulin resistance, pathological fat deposition and/or mobilsation, elevated and/or poorly-distributed lipid within myocytes and an impaired capacity to use lipid as fuel remains to be clarified as does the role of muscle mitochondria in the metabolic decline. Until these issues are resolved, a multidimensional exercise strategy (e.g., aerobic exercise at a range of intensities and resistance training for muscular hypertrophy) could provide the best alternative for prevention/treatment.

Dataset Information

A variation in the cerebroside sulfotransferase gene is linked to exercise-modified insulin resistance and to type 2 diabetes.

Publications

A variation in the cerebroside sulfotransferase gene is linked to exercise-modified insulin resistance and to type 2 diabetes.

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