Key result
Hyperinsulinemia plays a role in endothelium dysfunction in obese diabetic OLETF rats, while hyperglycemia/hyperosmolarity-induced eNOS/HO upregulation preserves endothelium function in lean GK rats.
Why the study?
Does insulin or hyperglycemia/hyperosmolarity alter large vessel endothelial function in lean and obese diabetic rat models?
Does insulin or hyperglycemia/hyperosmolarity alter large vessel endothelial function in lean and obese diabetic rat models?
Hyperinsulinemia, rather than hyperglycemia, appears to be a primary driver of endothelial dysfunction in type 2 diabetic rat models.
Hyperinsulinemia may drive endothelial dysfunction in obese diabetic models; leaves open translation to human type 2 diabetes.
We investigated large vessel function in lean Goto-Kakizaki diabetic rats (GK) and Otsuka Long-Evans Tokushima Fatty diabetic rats (OLETF) with possible roles of hyperglycemia/hyperosmolarity and insulin. Both young and old GK showed marked hyperglycemia with normal insulin level and well-preserved endothelium-dependent and endothelium-independent vasodilation in aorta and carotid artery. There were significant elevations in endothelial/inducible nitric oxide synthase (eNOS/iNOS) and inducible/constitutive heme oxygenase (HO-1/HO-2) in GK. The endothelium-dependent vasodilation in GK was inhibited partly by NOS blockade and completely by simultaneous blocking of HO and NOS. In contrast, OLETF showed hyperinsulinemia and mild hyperglycemia but significant endothelium dysfunction beginning at early ages with concomitantly reduced eNOS. Insulin injection corrected hyperglycemia in GK but induced endothelium dysfunction and intima hyperplasia. Hyperglycemia/hyperosmolarity in vitro enhanced vessel eNOS/HO. We suggest that hyperinsulinemia plays a role in endothelium dysfunction in obese diabetic OLETF, while hyperglycemia/hyperosmolarity-induced eNOS/HO upregulation participates in the adaptation of endothelium function in lean diabetic GK.
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Zhong et al. (2011) studied Type 2 Diabetes. Insulin injection / Hyperglycemia/hyperosmolarity in vitro was evaluated on Large vessel function (endothelium-dependent and endothelium-independent vasodilation). Hyperinsulinemia plays a role in endothelium dysfunction in obese diabetic OLETF rats, while hyperglycemia/hyperosmolarity-induced eNOS/HO upregulation preserves endothelium function in lean GK rats.
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