Abstract
Obese Black women are at increased risk for development of gestational diabetes mellitus and have worse perinatal outcomes than do obese women of other ethnicities. Since hsp72 has been associated with the regulation of obesity-induced insulin resistance, we evaluated associations between glucose ingestion, hsp72 release and insulin production in Black pregnant women. Specifically, the effect of a 50-g glucose challenge test (GCT) on heat shock protein and insulin levels in the circulation 1 h later was evaluated. Hsp27 and hsp60 levels remained unchanged. In contrast, serum levels of hsp72 markedly increased after glucose ingestion (p = 0.0054). Further analysis revealed that this increase was limited to women who were not obese (body mass index <30). Insulin levels pre-GCT were positively correlated with body mass index (p = 0.0189). Median insulin concentrations also increased post GCT in non-obese women but remained almost unchanged in obese women. Post-GCT serum hsp72 concentrations were inversely correlated with post GCT insulin concentrations (p = 0.0111). These observations suggest that glucose intake during gestation in Black women rapidly leads to an elevation in circulating hsp72 only in non-obese Black women. The release of hsp72 may regulate the extent of insulin production in response to a glucose challenge and, thereby, protect the mother and/or fetus from development of hyperglycemia, hyperinsulinemia, and/or immune system alterations.
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References
Association AD (2002) Gestational diabetes mellitus. Diabetes Care 25(Suppl 1):S94–S96
Aranoff SL, Berkowitz K, Shreiner B, Want L (2004) Glucose metabolism and regulation: beyond insulin and glucagon. Diabetes Spectr 17:183–190
Chung J, Nguyen AK, Henstridge DC, Holmes AG, Chan MH, Mesa JL et al (2008) HSP72 protects against obesity-induced insulin resistance. Proc Natl Acad Sci USA 105:1739–1744
Crowther CA, Hillier JE, Moss JR, McPhee AJ, Jeffries WS, Robinson JS et al (2005) Effect of treatment of gestational diabetes mellitus on pregnancy outcomes. N Engl J Med 352:2477–2486
Dokladny K, Ye D, Kennedy JC, Moseley PL, Ma TY (2008) Cellular and molecular mechanisms of heat stress-induced up-regulation of occluding protein expression: regulatory role of heat shock factor-1. Am J Pathol 172:659–670
Esakoff TF, Caughey AB, Block-Kurbisch I, Inturrisi M, Cheng YW (2011) Perinatal outcomes in patients with gestational diabetes mellitus by race/ethnicity. J Maternal Fetal Neonatal Med 24:422–426
Febbraio MA, Mesa JL, Chung J, Steensberg A, Keller C, Nielsen HB et al (2004) Glucose ingestion attenuates the exercise-induced increase in circulating heat shock protein 72 and heat shock protein 60 in humans. Cell Stress Chaperones 9:390–396
Febbraio MA, Ott P, Nielsen HB, Streensberg A, Keller C, Krustrup P et al (2002) Exercise induces hepatosplanchnic release of heat shock protein 72 in humans. J Physiol 544(3):957–962
Kavanagh K, Flynn DM, Jenkins KA, Zhang L, Wagner JD (2011) Restoring hsp70 deficiencies improves glucose tolerance in diabeteic monkeys. Am J Physiol Endocrinol Metab 300:E894–E901
Kim SY, England L, Sappenfield W, Wilson HG, Bish CL, Salihu HM, Sharma AJ (2012) Racial/ethnic differences in the percentage of gestational diabetes mellitus cases attributable to overweight and obesity, Florida, 2004–2007. Prev Chronic Dis 9:E88
Kurucz I, Morva A, Vaag A, Eriksson KF, Huang X, Groop L, Koranyi L (2002) Decreased expression of heat shock protein 72 in skeletal muscle of patients with type 2 diabetes correlates with insulin resistance. Diabetes 51:1102–1109
Makgoba M, Savvidou MD, Steer PJ (2012) An analysis of the interrelationship between maternal age, body mass index and racial origin in the development of gestational diabetes mellitus. BJOG 119:276–282
Marker T, Sell H, Zillessen P, Glode A, Kriebel J, Ouwens DM et al (2012) Heat shock protein 60 as a mediator of adipose tissue inflammation and insulin resistance. Diabetes 61:615–625
McCarty MF (2006) Induction of heat shock proteins may combat insulin resistance. Med Hypotheses 66:527–534
Metzger BE, Buchanan TA, Coustan DR, de Leiva A, Dunger DB, Hadden DR et al (2007) Summary and recommendations of the Fifth International Workshop-Conference on Gestational Diabetes Mellitus. Diabetes Care 30:S251–S260
Negrato CA, Jovanovic L, Tambascia MA, Calderon IMP, Geloneze B, Dias A, Rudge MVC (2009) Mild gestational hyperglycaemia as a risk factor for metabolic syndrome in pregnancy and adverse perinatal outcomes. Diabetes Metab Res Rev 24:324–330
Saito FH, Damasceno DC, Dallaqua B, Linhares IM, Rudge MV, De Mattos Paranhos Calderon I, Witkin SS (2012) Heat shock protein production and immunity and altered fetal development in diabetic pregnant rats. Cell Stress Chaperones 18(1):25–33
Shah A, Stotland NE, Cheng YW, Ramos GA, Caughey AB (2011) The association between body mass index and gestational diabetes mellitus varies by race/ethnicity. Am J Perinatol 28:515–520
Simar D, Jacques A, Caillaud C (2012) Heat shock proteins induction reduces stress kinases activation, potentially improving insulin signaling in monocytes from obese subjects. Cell Stress Chaperones 17:615–621
Wellen KE, Hotamisligil GS (2005) Inflammation, stress, and diabetes. J Clin Invest 115:1111–1119
Xiang AH, Li BH, Black MH, Sacks DA, Buchanan TA, Jacobsen SJ, Lawrence JM (2011) Racial and ethnic disparities in diabetes risk after gestational diabetes mellitus. Diabetologia 54(3016):3021
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Jaffe, S., Doulaveris, G., Orfanelli, T. et al. Induction of the 72 kDa heat shock protein by glucose ingestion in black pregnant women. Cell Stress and Chaperones 18, 527–530 (2013). https://doi.org/10.1007/s12192-013-0401-7
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DOI: https://doi.org/10.1007/s12192-013-0401-7