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Regulation of the insulin antagonistic protein tyrosine phosphatase 1B by dietary Se studied in growing rats.
J Nutr Biochem 2009; 20(4):235-47JN

Abstract

Protein tyrosine phosphatase 1B (PTP1B) is a key enzyme in the counterregulation of insulin signaling, and its physiological modulation depends on H2O2 and glutathione (GSH). Se via GSH peroxidases (GPxs) and its specific metabolism is involved in the removal of H2O2 and in the regulation of GSH metabolism. Recent results from animal trials and epidemiological studies with humans have shown that a high GPx1 activity or a permanent surplus of Se may promote the development of obesity and diabetes. Our nutrition physiological study with 7 x 7 growing rats was carried out to examine if PTP1B is modulated by Se supplements and, thus, may represent one trigger mediating these undesirable metabolic effects of Se. One group of rats was fed an Se-deficient diet for 8 weeks. The diets of the other six groups contained Se as selenite or selenate according to the recommendations (0.20 mg/kg diet) and at two supranutritional levels (1.00 and 2.00 mg/kg diet). All Se-supplemented animals featured a significantly higher body weight (6-14%) compared to their Se-deficient companions. Expression and activity of GPx1 in the liver of Se supplemented animals was 10- and 70-fold higher compared to Se deficiency. The detailed study of PTP1B regulation using an enzymatic assay and Western Blot analysis with an antibody against protein glutathionylation revealed that PTP1B was significantly up-regulated by both a maximization of GPx1 activity and by increasing dietary Se supply, reducing its inhibition via glutathionylation. Selenate effected a stronger PTP activation compared to selenite. In conclusion, our results suggest that the modulation of PTP1B activity may represent one plausible mechanism by which a long-term intake of Se supplements exceeding the requirements can promote the development of obesity and diabetes and needs further intensive investigation.

Authors+Show Affiliations

Department of Animal Nutrition and Nutritional Physiology, Interdisciplinary Research Centre, Justus Liebig University Giessen, Giessen D-35392, Germany. andreas.s.mueller@agrar.uni-giessen.deNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18602818

Citation

Mueller, Andreas S., et al. "Regulation of the Insulin Antagonistic Protein Tyrosine Phosphatase 1B By Dietary Se Studied in Growing Rats." The Journal of Nutritional Biochemistry, vol. 20, no. 4, 2009, pp. 235-47.
Mueller AS, Bosse AC, Most E, et al. Regulation of the insulin antagonistic protein tyrosine phosphatase 1B by dietary Se studied in growing rats. J Nutr Biochem. 2009;20(4):235-47.
Mueller, A. S., Bosse, A. C., Most, E., Klomann, S. D., Schneider, S., & Pallauf, J. (2009). Regulation of the insulin antagonistic protein tyrosine phosphatase 1B by dietary Se studied in growing rats. The Journal of Nutritional Biochemistry, 20(4), pp. 235-47. doi:10.1016/j.jnutbio.2008.02.007.
Mueller AS, et al. Regulation of the Insulin Antagonistic Protein Tyrosine Phosphatase 1B By Dietary Se Studied in Growing Rats. J Nutr Biochem. 2009;20(4):235-47. PubMed PMID: 18602818.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulation of the insulin antagonistic protein tyrosine phosphatase 1B by dietary Se studied in growing rats. AU - Mueller,Andreas S, AU - Bosse,Astrid C, AU - Most,Erika, AU - Klomann,Sandra D, AU - Schneider,Sandra, AU - Pallauf,Josef, Y1 - 2008/07/07/ PY - 2007/08/31/received PY - 2008/02/11/revised PY - 2008/02/15/accepted PY - 2008/7/8/pubmed PY - 2009/7/25/medline PY - 2008/7/8/entrez SP - 235 EP - 47 JF - The Journal of nutritional biochemistry JO - J. Nutr. Biochem. VL - 20 IS - 4 N2 - Protein tyrosine phosphatase 1B (PTP1B) is a key enzyme in the counterregulation of insulin signaling, and its physiological modulation depends on H2O2 and glutathione (GSH). Se via GSH peroxidases (GPxs) and its specific metabolism is involved in the removal of H2O2 and in the regulation of GSH metabolism. Recent results from animal trials and epidemiological studies with humans have shown that a high GPx1 activity or a permanent surplus of Se may promote the development of obesity and diabetes. Our nutrition physiological study with 7 x 7 growing rats was carried out to examine if PTP1B is modulated by Se supplements and, thus, may represent one trigger mediating these undesirable metabolic effects of Se. One group of rats was fed an Se-deficient diet for 8 weeks. The diets of the other six groups contained Se as selenite or selenate according to the recommendations (0.20 mg/kg diet) and at two supranutritional levels (1.00 and 2.00 mg/kg diet). All Se-supplemented animals featured a significantly higher body weight (6-14%) compared to their Se-deficient companions. Expression and activity of GPx1 in the liver of Se supplemented animals was 10- and 70-fold higher compared to Se deficiency. The detailed study of PTP1B regulation using an enzymatic assay and Western Blot analysis with an antibody against protein glutathionylation revealed that PTP1B was significantly up-regulated by both a maximization of GPx1 activity and by increasing dietary Se supply, reducing its inhibition via glutathionylation. Selenate effected a stronger PTP activation compared to selenite. In conclusion, our results suggest that the modulation of PTP1B activity may represent one plausible mechanism by which a long-term intake of Se supplements exceeding the requirements can promote the development of obesity and diabetes and needs further intensive investigation. SN - 1873-4847 UR - https://www.unboundmedicine.com/medline/citation/18602818/Regulation_of_the_insulin_antagonistic_protein_tyrosine_phosphatase_1B_by_dietary_Se_studied_in_growing_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0955-2863(08)00067-3 DB - PRIME DP - Unbound Medicine ER -