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Transferrin and iron induce insulin resistance of glucose transport in adipocytes.
Metabolism 2006; 55(8):1042-5M

Abstract

Normal serum can increase the rate of lipolysis in isolated adipocytes. Recently, we reported that the lipolytic effect of serum could be partly explained by effects of iron and transferrin. To further investigate these effects on fat cell metabolism, we have investigated effects of serum, iron, and transferrin on glucose transport in isolated rat adipocytes. Adipocytes were isolated by collagenase digestion of rat epididymal fat pads, and glucose transport was measured as uptake of [3H]2-deoxyglucose, measured in the presence of 0 to 25 ng/mL insulin. Insulin stimulated glucose transport approximately 8- to 10-fold, with a half-maximally effective concentration (EC50) of approximately 0.15 ng/mL. This was not affected by 45-minute treatment with normal human serum. However, when adipocytes were incubated with serum for 4 hours, cells became markedly insulin resistant. This was manifested as decrease in maximally stimulated glucose transport and a rightward shift in the dose-response curve. Both FeS04 (3 microg/mL) and transferrin (100 microg/mL) had similar, although less pronounced effects on insulin-stimulated glucose transport. Treatment of adipocytes with palmitic acid (120 micromol/L), representing the concentration of fatty acids released into the media after 4 hours of serum treatment, did not alter the effect of insulin on glucose transport. We conclude that transferrin and iron induce insulin resistance of glucose transport in adipocytes through a mechanism independent of fatty acids. These findings may further explain the association between body iron stores and risk of type 2 diabetes mellitus.

Authors+Show Affiliations

Bassett Research Institute, Bassett Healthcare, Cooperstown, NY 13326, USA. allan.green@bassett.orgNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

16839839

Citation

Green, Allan, et al. "Transferrin and Iron Induce Insulin Resistance of Glucose Transport in Adipocytes." Metabolism: Clinical and Experimental, vol. 55, no. 8, 2006, pp. 1042-5.
Green A, Basile R, Rumberger JM. Transferrin and iron induce insulin resistance of glucose transport in adipocytes. Metab Clin Exp. 2006;55(8):1042-5.
Green, A., Basile, R., & Rumberger, J. M. (2006). Transferrin and iron induce insulin resistance of glucose transport in adipocytes. Metabolism: Clinical and Experimental, 55(8), pp. 1042-5.
Green A, Basile R, Rumberger JM. Transferrin and Iron Induce Insulin Resistance of Glucose Transport in Adipocytes. Metab Clin Exp. 2006;55(8):1042-5. PubMed PMID: 16839839.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Transferrin and iron induce insulin resistance of glucose transport in adipocytes. AU - Green,Allan, AU - Basile,Robin, AU - Rumberger,John M, PY - 2005/12/12/received PY - 2006/03/01/accepted PY - 2006/7/15/pubmed PY - 2006/8/19/medline PY - 2006/7/15/entrez SP - 1042 EP - 5 JF - Metabolism: clinical and experimental JO - Metab. Clin. Exp. VL - 55 IS - 8 N2 - Normal serum can increase the rate of lipolysis in isolated adipocytes. Recently, we reported that the lipolytic effect of serum could be partly explained by effects of iron and transferrin. To further investigate these effects on fat cell metabolism, we have investigated effects of serum, iron, and transferrin on glucose transport in isolated rat adipocytes. Adipocytes were isolated by collagenase digestion of rat epididymal fat pads, and glucose transport was measured as uptake of [3H]2-deoxyglucose, measured in the presence of 0 to 25 ng/mL insulin. Insulin stimulated glucose transport approximately 8- to 10-fold, with a half-maximally effective concentration (EC50) of approximately 0.15 ng/mL. This was not affected by 45-minute treatment with normal human serum. However, when adipocytes were incubated with serum for 4 hours, cells became markedly insulin resistant. This was manifested as decrease in maximally stimulated glucose transport and a rightward shift in the dose-response curve. Both FeS04 (3 microg/mL) and transferrin (100 microg/mL) had similar, although less pronounced effects on insulin-stimulated glucose transport. Treatment of adipocytes with palmitic acid (120 micromol/L), representing the concentration of fatty acids released into the media after 4 hours of serum treatment, did not alter the effect of insulin on glucose transport. We conclude that transferrin and iron induce insulin resistance of glucose transport in adipocytes through a mechanism independent of fatty acids. These findings may further explain the association between body iron stores and risk of type 2 diabetes mellitus. SN - 0026-0495 UR - https://www.unboundmedicine.com/medline/citation/16839839/Transferrin_and_iron_induce_insulin_resistance_of_glucose_transport_in_adipocytes_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0026-0495(06)00118-1 DB - PRIME DP - Unbound Medicine ER -