Diabetes & Metabolism Journal

Original Articles

Effect of Heat Shock on the Vascular Reactivity and Expression of Heat Shock Protein in an Animal Model of Type 2 Diabetes Mellitus (OLETF rat).: Soon Hee Lee, Sung Woo Ha, Bo Wan Kim; Korean Diabetes J. 2003;27(3):199-212. Published online June 1, 2003

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Abstract PDF: BACKGROUND
Heat shock proteins (HSPs) are highly expressed in cardiovascular tissues, with heat shock possibly modulating the vascular reactivity to vasoactive agents. An abnormal vascular reactivity has been shown in diabetes, and may be closely associated to diabetic vascular complications. The aim of this study was to investigate the effects of heat shock on the vascular reactivity and the expression of HSP70 in the isolated aortae of OLETF rats, a commonly used animal model for type 2 diabetes mellitus, and LETO rats, as age matched controls. METHODS: In 4 ring segments of the thoracic aorta isolated from each rat, the endothelium was denuded in 2 (EC-) and reserved in the other 2 (EC+). To induce heat shock, the aortic rings were exposed to 42 degrees C for 45 minutes. The vascular reactivity responses to various vasoactive agents were measured by organ chamber studies, and by changes in the HSP expression, using Western blotting of the aortic rings in the OLETF rats and controls. RESULTS: The contractile responses to KCl became apparent 4 hours after the end of the heat shock induction. After heat shock, the phenylnephrine-induced contractile responses were similarly increased in the OLETF rats and the controls, but the increase was more significant in the EC(-) than the EC(+) rings, in both the OLETF rats and the controls. The relaxative responses to either acetylcholine (ACh) in the EC(+) aortic rings, or to sodium nitroprusside in the EC(-) rings, were not significantly affected by the heat shock treatment in either the OLETF rats or the controls, although the maximal relaxative response to ACh before the induction of the heat shock was lower in the aortic rings of the OLETF rats than in the controls. The HSP70 levels before the heat shock were higher in the aortic rings of the OLETF rats than in the controls, whereas those after heat shock were higher than those before in both the OLETF rats and the controls. The increase in the expression of HSP70 following the heat shock was higher in rings of the controls than in those of the OLETF rats. The HSP70 levels following the heat shock were increased to a greater extent in the EC(+) than the EC(-) rings of both the OLETF rats and the controls. CONCLUSION: These results suggest that the vascular reactivity to heat shock was decreased to a greater extent in the aortae of OLETF rats than in those of the controls, and that HSP70 seems to play an important role in the vascular response to heat shock through interaction of the endothelium and the smooth muscle.

An Effect of Estrogen Supplementation on the Endothelium Dependent Vasodilation in Postmenopausal Women with Type 2 Diabetes Mellitus.: Jun Kim Yeo, Sang Jun Lee, In Kyu Lee; Korean Diabetes J. 2000;24(1):37-45. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Although estrogen supplementation can reduce cardiovascular events in postmenopausal women, but the mechanism that mediate this beneficial effect is unclear. Thus, we investigated the acute effect of HRT on endothelial dependent vasodilation using high resolution ultrasound in healthy and diabetic postmenopausal women. METHOD: We examined endogenous (flow dependent dilatation affer 5min cuff occlusion) and exogenous (sublingual nitroglycerin) nitric oxide mediated vasodilation in the brachial artery before and after estrogen supplementation (Premarin R 0.625 mg for 1 wk) in 16 postmenopausal women, and in 18 age-matched postmenopausal women with type 2 diabetes mellitus. RESULTS: There were no differences in age, total & LDL cholesterol level, and body mass index between the groups (p>0.05). However, HDL cholesterol level was significantly lower in patient with diabetes than in normal women (1.0+/-0.3 mmol/L in diabetes and 1.4+/-0.2 mmol/L in normal, p<0.05). Basal endothelium dependent vascular reactivity was significantly attenuated in patient with diabetes when compaired with normal subjects (8.0+/-3,9% versus 13.7+/-6.2%, p<0.05). An estrogen supplementation increased endothelium dependent vasodilation not only in patient with diabetes(from 8.0+/-3.9% to 15.1+/-4.0%, p<0.05), but also in normal women (from 13.7+/-6.2% to 20.1+/-4.7%, p<0.05). Moreover the percent increase of vascular reactivity was higher in patient with diabetes(p<0,05), In contrast, the responses to sublingual nitroglycerin were comparable in diabetes (from 21.1+/-6.0% to 22.1+/-4.1%, p>0.05), and in normal women (from 25.8+/-7.8% to 25.2+/-4.5%, p>0.05) before and after estrogen supplementation. CONCLUSION: Endothelial dysfunction was prominent in patient with diabetes and it was significantly attenuated by estrogen. These results suggest that estrogen replacement improves endothelial dependent vasodilation in healthy and diabetic postmenopausal women.

Lipopolysaccharide-Induced Changes in Vascular Reactivity of Diabetic Rat Aorta.: Ye Kyung Seo, Sang Won Chung, Jik Hwa Nam, Byoung Ho Sin, Dong Hee Kim, Jung Guk Kim, Sung Woo Ha, Bo Wan Kim; Korean Diabetes J. 1997;21(3):280-288. Published online January 1, 2001

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Abstract PDF: Backgound: Hemodynamic deteriorations in diabetes mellitus may be mediated by increased contractile response to catecholamines and/or by decreased relaxative response to vasodilators such as acetylcholine(Ach). Decrease in peripheral vascular reactivity to vasoconstrictor was known to be an ominous sign that happens during sepsis or after injection of bacterial lipopolysaccharides(LPS). In this study, we compared the effects of LPS on function of diabetic rat aorta with impaired vascular reactivity with those of control rat aorta. METHODS: Contractile responses to cumulative concentrations(10'M to 3X10'M) of norepinephrine (NE) were measured in aorta isolated ftom the control and 4 to 5-week streptozotocin-induced diabetic rat at 6 hours after LPS treatment to compare with contractile responses of untreated group. We measured relaxative responses to cumulative concentrations(10'M to 10M) of Ach and nitroprusside (NTP) in these aortas contracted submaximally by NE. RESULTS: Diabetic rat aortas showed significantly more impairment in relaxative responses to Ach than control rat aortas before LPS treatment(p0.05 = 0.0l). LPS treatment in those diabetic rat aortas decreased contractile responses to NE by 26.6%(p < 0.01); the changes were sirnilar to those of control (30.9%, p0.01). Relaxative responses to Ach were also significantly decreased by 25.0%(p 0.01) after L.PS treatment; the changes were similar to those of control(34.1%, p0.01). However relaxative responses to NTP were not changed in control and d.iabetic rat aortas by LPS treatment. CONCLUSION: These results suggest that diabetes may induce impairment in endothelium-dependent vascular relaxation and there rnay be no difference of L,P,S-induced effects on hemodynamic deterioration between 4 to 5-week diabetic and control rats.

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