| Summary: | 碩士 === 國立陽明大學 === 生理學研究所 === 92 === Endothelin-1 (ET-1) was originally suggested to be a potent vasoconstrictive peptide, and further investigations demonstrated that ET-1 may play an important role in the pathology of cardiovascular diseases. Clinical studies revealed that in addition to hyperglycemia, impaired glucose tolerance, and hyperendothelinemia, dyslipidemia is a common characteristic in patients with type 2 diabetes. I performed experiments to test the hypothesis that ET-1 may directly or indirectly interfere with lipid metabolism through an unknown signaling. Adipocytes isolated from the epidydimal fat pads of male Sprague Dawley rats were used to study the lipolytic effect of isoproterenol (10-6 M~10-10 M) and antilipolytic effect of insulin (10-9 M~10-12 M). The influence of ET-1 alone or in combination with isoproterenol or insulin on lipolysis was also investigated. Treatment of BQ610 (10-6 M) and BQ788 (10-6 M), selective antagonist for ET-1 A receptor and B receptor, respectively, was conducted to analyze what type of ET receptor was involved in the ET-1-mediated lipolytic effect. Additionally, an adenylate cyclase inhibitor was used to observe the role of cAMP in the in the ET-1- mediated lipolytic effect. My data indicated that: (a) ET-1 stimulated lipolysis via ET type A receptor, and the ET-1–induced lipolytic effect did not involve cAMP and adenylate cyclase; (b) the ET-1-induced lipolysis was inhibited by insulin; and (c) ET-1 also suppressed the lipolysis stimulated by isoproterenol. Conclusively, these findings suggested that ET-1 may serve a dual role in the regulation of lipolysis in rat adipocytes.
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