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  Heredity The genetic risk for atherosclerosis is conferred in part through known metabolic risk factors such as hypertension, dyslipidemia, and diabetes mellitus. However, these risk factors alone do not account for the entire contribution to risk of atherosclerotic disease. Aberrations in lipid handling are one of the fundamental mechanisms that have been linked to atherosclerosis particularly in patients presenting with positive family history. Low density lipoprotein receptor gene Familial hypercholesterolemia is a monogenic autosomal codominant trait. FH is characterized by elevated plasma cholesterol bound to LDL due to deficiency in LDLR activity on the cell surfaces. LDLR is located on chromosome 19. Alteration to this gene results to inability to produce immunoprecipitable protein and alter function of the receptors. FH heterozygotes express half of the normal number of functional LDLR on their cell surfaces leading to a twofold elevation in circulating LDL-C concentration ( 300-500 mg/dL) associated with premature atherosclerosis development. The rare Homozygotes express only few or no functional receptors on their cell surfaces. Apolipoprotein B Gene APOB cause the production results to deficiency of lipoprotein transport abolishes transporter activity resulting in elevated cholesterol absorption and LDL synthesis. (www.hindawi.com/journals/srt/2012/362941) Heredity The genetic risk for atherosclerosis is conferred in part through known metabolic risk factors such as hypertension, dyslipidemia, and diabetes mellitus. However, these risk factors alone do not account for the entire contribution to risk of atherosclerotic disease. Aberrations in lipid handling are one of the fundamental mechanisms that have been linked to atherosclerosis particularly in patients presenting with positive family history. Low density lipoprotein receptor gene  Familial hypercholesterolemia is a monogenic autosomal codominant trait. FH is characterized by elevated plasma cholesterol bound to LDL due to deficiency in LDLR activity on the cell surfaces. LDLR is located on chromosome 19. Alteration to this gene results to inability to produce immunoprecipitable protein and alter function of the receptors. FH heterozygotes express half of the normal number of functional LDLR on their cell surfaces leading to a twofold elevation in circulating LDL-C concentration ( 300-500 mg/dL) associated with premature atherosclerosis development. The rare Homozygotes express only few or no functional receptors on their cell surfaces. Apolipoprotein B Gene APOB cause the production results to deficiency of lipoprotein transport abolishes transporter activity resulting in elevated cholesterol absorption and LDL synthesis. (www.hindawi.com/journals/srt/2012/362941) Heredity The genetic risk for atherosclerosis is conferred in part through known metabolic risk factors such as hypertension, dyslipidemia, and diabetes mellitus. However, these risk factors alone do not account for the entire contribution to risk of atherosclerotic disease. Aberrations in lipid handling are one of the fundamental mechanisms that have been linked to atherosclerosis particularly in patients presenting with positive family history. Low density lipoprotein receptor gene Familial hypercholesterolemia is a monogenic autosomal codominant trait. FH is characterized by elevated plasma cholesterol bound to LDL due to deficiency in LDLR activity on the cell surfaces. LDLR is located on chromosome 19. Alteration to this gene results to inability to produce immunoprecipitable protein and alter function of the receptors. FH heterozygotes express half of the normal number of functional LDLR on their cell surfaces leading to a twofold elevation in circulating LDL-C concentration ( 300-500 mg/dL) associated with premature atherosclerosis development. The rare Homozygotes express only few or no functional receptors on their cell surfaces. Apolipoprotein B Gene  APOB cause the production results to deficiency of lipoprotein transport abolishes transporter activity resulting in elevated cholesterol absorption and LDL synthesis. (www.hindawi.com/journals/srt/2012/362941) Heredity The genetic risk for atherosclerosis is conferred in part through known metabolic risk factors such as hypertension, dyslipidemia, and diabetes mellitus. However, these risk factors alone do not account for the entire contribution to risk of atherosclerotic disease. Aberrations in lipid handling are one of the fundamental mechanisms that have been linked to atherosclerosis particularly in patients presenting with positive family history. Low density lipoprotein receptor gene Familial hypercholesterolemia is a monogenic autosomal codominant trait. FH is characterized by elevated plasma cholesterol bound to LDL due to deficiency in LDLR activity on the cell surfaces. LDLR is located on chromosome 19. Alteration to this gene results to inability to produce immunoprecipitable protein and alter function of the receptors. FH heterozygotes express half of the normal number of functional LDLR on their cell surfaces leading to a twofold elevation in circulating LDL-C concentration ( 300-500 mg/dL) associated with premature atherosclerosis development. The rare Homozygotes express only few or no functional receptors on their cell surfaces. Apolipoprotein B Gene APOB cause the production results to deficiency of lipoprotein transport abolishes transporter activity resulting in elevated cholesterol absorption and LDL synthesis. (www.hindawi.com/journals/srt/2012/362941) Heredity The genetic risk for atherosclerosis is conferred in part through known metabolic risk factors such as hypertension, dyslipidemia, and diabetes mellitus. However, these risk factors alone do not account for the entire contribution to risk of atherosclerotic disease.   Aberrations in lipid handling are one of the fundamental mechanisms that have been linked to atherosclerosis particularly in patients presenting with positive family history. Low density lipoprotein receptor gene Familial hypercholesterolemia is a monogenic autosomal codominant trait. FH is characterized by elevated plasma cholesterol bound to LDL due to deficiency in LDLR activity on the cell surfaces. LDLR is located on chromosome 19. Alteration to this gene results to inability to produce immunoprecipitable protein and alter function of the receptors. FH heterozygotes express half of the normal number of functional LDLR on their cell surfaces leading to a twofold elevation in circulating LDL-C concentration ( 300-500 mg/dL) associated with premature atherosclerosis development. The rare Homozygotes express only few or no functional receptors on their cell surfaces. Apolipoprotein B Gene APOB cause the production results to deficiency of lipoprotein transport abolishes transporter activity resulting in elevated cholesterol absorption and LDL synthesis. (www.hindawi.com/journals/srt/2012/362941) Heredity The genetic risk for atherosclerosis is conferred in part through known metabolic risk factors such as hypertension, dyslipidemia, and diabetes mellitus. However, these risk factors alone do not account for the entire contribution to risk of atherosclerotic disease. Aberrations in lipid handling are one of the fundamental mechanisms that have been linked to atherosclerosis particularly in patients presenting with positive family history. Low density lipoprotein receptor gene Familial hypercholesterolemia is a monogenic autosomal codominant trait. FH is characterized by elevated plasma cholesterol bound to LDL due to deficiency in LDLR activity on the cell surfaces. LDLR is located on chromosome 19. Alteration to this gene results to inability to produce immunoprecipitable protein and alter function of the receptors. FH heterozygotes express half of the normal number of functional LDLR on their cell surfaces leading to a twofold elevation in circulating LDL-C concentration ( 300-500 mg/dL) associated with premature

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Jul 23, 2017
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