| 영문 | glycogen | 한글 | 글리코겐, 당원 |
|---|---|---|---|
| 설명 | 동물에서 탄수화물의 저장형태로 주로 간에 대부분이 저장되어 있고 근육에 조금 있다. 포도당으로 분해되어 이용된다. |
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| 영문 | cardiomegaly | 한글 | 심장비대 |
|---|---|---|---|
| 설명 | 심장에 지나치게 부담이 가서 심근이 두꺼워지고 심장이 커진 상태. 선천성 심장 기형, 심장 판막증, 고혈압증 따위의 각종 심장병에 의한 것과 운동선수나 육체노동자에게 나타나는 건강한 것이 있다. 비대(hypertrophy)의 기본 개념은 어떤 원인에 의하여 특정 장기가 세포 수의 변화와 상관없이, 즉 개개 세포의 용적 증가로 인하여 커지는 경우이다. 반면에 세포 수가 증가하여 커지는 경우는 증식(hyperplasia)이라 한다. 심장이 지속적으로 무리한 일을 하였을 경우에 생긴다. 생리적으로 운동 선수나 육체 노동자에게서는 골격근과 더불어 심근이 비대될 수 있다. 그러나 병적으로는 고혈압이나 폐동맥 협착증, 대동맥 협착증 등 심판막 질환이 있을 때 심장이 비대될 수 있다. 고혈압 환자에게는 대동맥의 높은 압력에 대항하여 심장이 비대되며 정상 무게인 350g에 비하여 700~800g까지 무거워질 수 있다. |
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| GFFS | glycogen and fat-free solid |
|---|---|
| GSD | genetically significant dose; Gerstmann-Straussler disease; glutathione synthetase deficiency; glyco... |
| GSD-0 | glycogen storage disease-zero |
| GT1-GT10 | glycogen storage disease, types 1 to 10 |
| MLG | mesiolingual groove; mitochondrial lipid glycogen |
| GSK-3 beta | I)/glycogen synthase kinase-3 beta |
|---|---|
| Gly | Glycogen |
| GP | Glycogen Phosphorylase |
| GSD | Glycogen Storage Disease |
| GSDII | Glycogen Storage Disease type II |
| cardiomegaly | <cardiology, clinical sign> Cardiac hypertrophy. Origin: Gr. Megas = large (18 Nov 1997) |
|---|---|
| brancher glycogen storage disease | Type of glycogen storage disease, due to deficiency of amylo-1,4-1,6-transglucosidase (brancher enzyme). Synonym: brancher deficiency glycogenosis, debrancher deficiency. (05 Mar 2000) |
| glycogen | <biochemistry> Branched polymer of D glucose (mostly _(1-4) linked, but some _(1-6) at branch points). Size range very variable, up to 10exp5 glucose units. Major short term storage polymer of animal cells and is particularly abundant in the liver and to a lesser extent in muscle. In the electron microscope glycogen has a characteristic asterisk or star appearance. (18 Nov 1997) |
| glycogen debranching enzyme system | 1,4-alpha-d-glucan-1,4-alpha-d-glucan 4-alpha-d-glucosyltransferase/dextrin 6 alpha-d-glucanohydrolase. An enzyme system having both 4-alpha-glucanotransferase (ec 2.4.1.25) and amylo-1,6-glucosidase (ec 3.2.1.33) activities. As a transferase it transfers a segment of a 1,4-alpha-d-glucan to a new 4-position in an acceptor, which may be glucose or another 1,4-alpha-d-glucan. As a glucosidase it catalyses the endohydrolysis of 1,6-alpha-d-glucoside linkages at points of branching in chains of 1,4-linked alpha-d-glucose residues. Amylo-1,6-glucosidase activity is deficient in glycogen storage disease type III. (12 Dec 1998) |
| glycogen granule | Glycogen occurring in cells as beta granule's which average about 300 A |
| glycogen phosphorylase | <enzyme> Enzyme that catalyses the sequential removal of glycosyl residues from glycogen to yield one glucose-1-phosphate per reaction. Its activity is controlled by phosphorylation (by phosphorylase kinase). (21 Jun 2000) |
| glycogen storage disease | <hepatology> A group of inherited metabolic disorders involving the enzymes responsible for the synthesis and degradation of glycogen. In some patients, prominent liver involvement is presented. In others, more generalised storage of glycogen occurs, sometimes with prominent cardiac involvement. Synonym: glycogenosis (12 Sep 2002) |
| glycogen storage disease type I | <disease> An autosomal recessive disease in which gene expression of glucose-6-phosphatase is absent, resulting in hypoglycaemia due to lack of glucose production. Accumulation of glycogen in liver and kidney leads to organomegaly, particularly massive hepatomegaly. Increased concentrations of lactic acid and hyperlipidemia appear in the plasma. Clinical gout often appears in early childhood. Inheritance: autosomal recessive. (12 Dec 1998) |
| glycogen storage disease type II | <disease> Glycogenosis due to alpha-1,4-glucosidase (acid maltase) deficiency. It affects muscle, heart, and other organs. (12 Dec 1998) |
| glycogen storage disease type III | <disease> An autosomal recessive metabolic disorder due to deficient expression of amylo-1,6-glucosidase (one part of the glycogen debranching enzyme system). The clinical course of the disease is similar to that of glycogen storage disease type I, but milder. Massive hepatomegaly, which is present in young children, diminishes and occasionally disappears with age. Levels of glycogen with short outer branches are elevated in muscle, liver, and erythrocytes. Six subgroups have been identified, with subgroups type IIIa and type IIIb being the most prevalent. Inheritance: autosomal recessive (12 Dec 1998) |
| glycogen storage disease type IV | <disease> An autosomal recessive metabolic disorder due to a deficiency in expression of branching enzyme (alpha-1,4-glucan-6-alpha-glucosyltransferase), resulting in an accumulation of abnormal glycogen with long outer branches. Clinical features are muscle hypotonia and cirrhosis. Death from liver disease usually occurs before age 2. Inheritance: autosomal recessive (12 Dec 1998) |
| glycogen storage disease type V | <disease> Glycogenosis due to muscle phosphorylase deficiency. Characterised by painful cramps following sustained exercise. Inheritance: autosomal recessive (12 Dec 1998) |
| glycogen storage disease type VI | <disease> A hepatic glycogen storage disease in which there is an apparent deficiency of hepatic phosphorylase activity. However, studies have not been able to distinguish between phosphorylase deficiency and phosphorylase kinase deficiency in patients with hepatic glycogenosis. (12 Dec 1998) |
| glycogen storage disease type VII | <disease> An autosomal recessive muscle glycogen storage disease in which there is deficient expression of muscle phosphofructokinase activity, resulting in increased concentrations of glucose-6-phosphate and fructose-6-phosphate and low concentrations of fructose-1,6-diphosphate in muscle tissue. Glycogen storage in muscle is increased, perhaps due to activation of glycogen synthase by accumulated glucose-6-phosphate. It has been proposed that shunting of glucose-6-phosphate and fructose-6-phosphate into the pentose phosphate pathway may result in increased synthesis of purines and pyrimidines, causing hyperuricaemia and gout. Erythrocytes from patients may show decreased phosphofructokinase activity and 2,3-diphosphoglycerate deficiency. Exercise intolerance is present and severe congenital muscular dystrophy has been reported. Inheritance: autosomal recessive (12 Dec 1998) |
| glycogen storage disease type VIII | <disease> An x-linked recessive hepatic glycogen storage disease resulting from lack of expression of phosphorylase-b-kinase activity. Symptoms are relatively mild; hepatomegaly, increased liver glycogen, and decreased leukocyte phosphorylase are present. Liver shrinkage occurs in response to glucagon. Inheritance: X-linked recessive (12 Dec 1998) |
제품명 |
판매사 |
보험코드 | 성분/함량 | 구분/보험급여 |
|---|
제품명 |
판매사 |
보험코드 | 성분/함량 | 구분/보험급여 |
|---|