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The Effect of Melatonin and Its Receptor Agonist on Insulin Resistance in 3t3-l1 Adipocytes

Author: XuHuanNi
Tutor: YinWeiDong
School: Nanhua University
Course: Pathology and Pathophysiology
Keywords: 3T3-L1 adipocytes cells Free fatty acids Melatonin Melatonin receptor agonist (Neu-P11) Insulin Resistance Adiponectin
CLC: R587.1
Type: Master's thesis
Year: 2010
Downloads: 64
Quote: 0
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Abstract


Objective: Mel of research and its receptor agonist Neu-P11 FFA-induced 3T3-L1 adipocytes insulin resistance associated factor AMPK, P-AMPK, ACC, P-ACC, leptin, adiponectin hormone, adiponectin receptor 1 expression and glucose uptake and triglyceride levels. Methods: The experiment was divided into three parts, the first part of the induction of differentiation of the cells, with the classic \staining fat cell morphology. The second part is the use of the FFA-induced insulin resistance of fat cells, glucose oxidase detection cell glucose uptake capacity. The third part is to detect Mel its receptor agonist NEU-P11 glucose uptake in 3T3-L1 adipocytes cells FFA treatment capabilities and its related proteins leptin, adiponectin and adiponectin receptor 1, AMPK, P- AMPK, ACC, P-ACC expression, and the expression of triglyceride kit detection triglycerides. RESULTS: \Fat cells palmitic acid-induced insulin resistance occurs: 1-300 μM of palmitic acid for 12 hours, the ability of the cellular uptake of glucose significantly reduced intracellular triglyceride content increases adiponectin and adiponectin receptor 1 The decline in the level of expression of leptin, AMPK and phosphorylation of AMPK, ACC and phosphorylation of ACC, Mel/Neu-P11 was added 6 hours before the end of the FFA processing incubated together, the results show that: the ability of the cellular uptake of glucose with increasing insulin concentration a significant increase in triglyceride levels with the the intervention treatment Mel/Neu-P11 reduce to near normal levels, we also found: adiponectin and adiponectin receptor 1 of AMPK and phosphorylation of AMPK, ACC and phosphorylation expression of ACC the level as Mel/Neu-P11 intervention treatment presented upward trend, close to normal levels, leptin did not change significantly for 6 hours, no statistically significant intervention Mel/Neu-P11. Conclusion: 1.Mel/Neu-P11 can increase palmitic acid treatment of fat cells in the insulin-stimulated glucose uptake; 2. Mel/Neu-P11 upregulated palmitic acid treatment of fat cells adiponectin and adiponectin receptor 1 expression, further activation of AMPK, leading to phosphorylation of its downstream protein ACC loss of activity to promote the oxidative metabolism of fatty acids in the cells, lower triglyceride levels in the fat cells, thereby improving insulin resistance.

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CLC: > Medicine, health > Internal Medicine > Endocrine diseases and metabolic diseases > Islet disease > Diabetes
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