کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2895224 | 1172454 | 2006 | 10 صفحه PDF | دانلود رایگان |

Human growth hormone (GH) excess is linked to increased cardiovascular morbidity and mortality. However, little is known about the effect of GH excess on atherosclerosis. We developed a new mouse model to assess the hypothesis that GH overexpression accelerates atherosclerotic lesion formation. apoE−/− mice were crossed with bovine GH (bGH) transgenic mice to yield apoE−/− mice overexpressing bGH (apoE−/−/bGH). The mice were fed either standard or Western diet. At 22 weeks, atherosclerotic lesion area of thoracic aorta was larger in apoE−/−/bGH mice compared with littermate apoE−/− mice fed either diet (standard: +161 ± 50%, Western: +430 ± 134%). Aortic sinus lesions were more severe in apoE−/−/bGH mice fed standard diet compared with littermate apoE−/− mice. apoE−/−/bGH mice had lower (VLDL + LDL)/HDL ratios compared with littermate apoE−/− mice, while systolic blood pressure was higher in apoE−/−/bGH mice, irrespective of diet. The levels of serum amyloid A and hepatic CRP mRNA were higher in apoE−/−/bGH mice than in littermate apoE−/− mice. In conclusion, this study shows that excess GH augments the development of atherosclerosis in apoE−/− mice. The mechanisms could be direct effects of GH on cellular processes in the vessel wall or the result of concomitant processes such as hypertension or a general inflammatory state.
Journal: Atherosclerosis - Volume 188, Issue 2, October 2006, Pages 331–340