Establishment of Atherosclerosis Mouse Model with Diabetes Mellitus by Deficiency of Leptin and ApoE
Chen Ting-tin, Hu HongLian
Abstract
Chen Ting-tin, Hu HongLian
Abstract
Objective To mate the mice with obesity type Ⅱ diabetes mellitus by Leptin gene deficiency with the mice with high cholesterolemia and artery atherosclerosis mice by ApoE gene knockout, to produce the mice with combined high triglyceridemia, high cholesterolemia and much more serious artery atherosclerosis than only ApoE gene knockout mice. Methods By crossbred, backcross and intercross of the 2 lines of knockout mice, the genotyping was determined by mice tail gene PCR and plasma lipid test, meanwhile, from the large pathological sample, comparing the artey atherosclerosis from the longitudinal aorta. Results Use this breeding,both Leptin and ApoE gene knockout mice were produced. The adult mice showed extremely combined high lipidemia. The plasma triglyceride and cholesterol of this double gene knockout mice is 2.6 folds and 8.6 folds higher than normal mice. The atherosclerosis lesion in the aorta is much more prominent than ApoE knockout mice only. Conclusion Leptin/ApoE double knockout mice with hereditary combined high triglyceridemia, high cholesterolemia and much more prominent arterial atherosclerosis have been developed.
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Objective To mate the mice with obesity type Ⅱ diabetes mellitus by Leptin gene deficiency with the mice with high cholesterolemia and artery atherosclerosis mice by ApoE gene knockout, to produce the mice with combined high triglyceridemia, high cholesterolemia and much more serious artery atherosclerosis than only ApoE gene knockout mice. Methods By crossbred, backcross and intercross of the 2 lines of knockout mice, the genotyping was determined by mice tail gene PCR and plasma lipid test, meanwhile, from the large pathological sample, comparing the artey atherosclerosis from the longitudinal aorta. Results Use this breeding,both Leptin and ApoE gene knockout mice were produced. The adult mice showed extremely combined high lipidemia. The plasma triglyceride and cholesterol of this double gene knockout mice is 2.6 folds and 8.6 folds higher than normal mice. The atherosclerosis lesion in the aorta is much more prominent than ApoE knockout mice only. Conclusion Leptin/ApoE double knockout mice with hereditary combined high triglyceridemia, high cholesterolemia and much more prominent arterial atherosclerosis have been developed.
Key concepts: Apolipoprotein E, Knockout mouse, Internal medicine, Endocrinology, Leptin, Diabetes mellitus, Cholesterol, Biology