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Войти в исследования Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2001
Influence of type 2 diabetes on the inflammatory response in rats.
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Cuman R K, Bersani-Amado C A, Fortes Z B
Аннотация
OBJECTIVES AND DESIGN: To verify whether the inflammatory responses in animals with type 2 diabetes are altered to an extent similar to that in type 1 diabetes.
MATERIALS: Male newborn (2 days old) Wistar rats were made diabetic by streptozotocin (160 mg/kg, i.p.) and used 8-10 weeks later (10 rats/group).
METHODS: The inflammatory responses were evaluated using paw edema (induced by local injection of carrageenan or dextran), pleurisy (by pleural injection of carrageenan), increases in vascular permeability (induced by intradermal injection of histamine, serotonin and bradykinin) and leukocyte counts in peripheral blood and pleural exudate.
RESULTS: Diabetic animals showed reduced inflammatory responses to carrageenan but not to dextran. The increase in vascular permeability induced by serotonin and bradykinin was reduced whereas that to histamine was not altered in diabetic compared to control rats. Although the pleural exudate was reduced, leukocyte counts were similar in diabetic and control rats. Insulin (2 IU, 4 h before), though effective in reducing blood sugar levels, did not restore the altered responses in diabetic rats. In contrast to that in rats with type 1 diabetes, in rats with type 2 diabetes, removal of the adrenal glands restored the reduced inflammatory responses.
CONCLUSIONS: Insulin resistance in type 2 diabetic rats led to reduced inflammatory responses, which were partially corrected by adrenalectomy.
MATERIALS: Male newborn (2 days old) Wistar rats were made diabetic by streptozotocin (160 mg/kg, i.p.) and used 8-10 weeks later (10 rats/group).
METHODS: The inflammatory responses were evaluated using paw edema (induced by local injection of carrageenan or dextran), pleurisy (by pleural injection of carrageenan), increases in vascular permeability (induced by intradermal injection of histamine, serotonin and bradykinin) and leukocyte counts in peripheral blood and pleural exudate.
RESULTS: Diabetic animals showed reduced inflammatory responses to carrageenan but not to dextran. The increase in vascular permeability induced by serotonin and bradykinin was reduced whereas that to histamine was not altered in diabetic compared to control rats. Although the pleural exudate was reduced, leukocyte counts were similar in diabetic and control rats. Insulin (2 IU, 4 h before), though effective in reducing blood sugar levels, did not restore the altered responses in diabetic rats. In contrast to that in rats with type 1 diabetes, in rats with type 2 diabetes, removal of the adrenal glands restored the reduced inflammatory responses.
CONCLUSIONS: Insulin resistance in type 2 diabetic rats led to reduced inflammatory responses, which were partially corrected by adrenalectomy.