University of kufa
Center for Development of teaching
and training of university
Lipid metabolism and Transport
Preparation
The Lecturer: Abeer Ghassan mahdi
College of dentistry
Email: abeerg.alzubaidi@uokufa.edu.iq
2014 A.D.
1435A.H
Lecture content
1. Transporting lipids
2. Classes of lipoproteins particles
3. Apoproteins
4. Getting lipids off lipoproteins
5. Hyperlipoproteinaemias
The aim of this lecture: : To give the student concept lipid metabolism and
transport .
After the end of this lecture should be the student able to:
1- Recognize how lipids are transported around the body in the blood
—
stream.
2-Demonstrate how tissue get their lipid from lipoprotein.
3-Discuss the clinical problems associated with lipid transport .
— 4- lists the causes of Hyperlipoproteinaemias.
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Transporting lipids:
1-Need to coat small collections of lipid molecules with polar molecules.
-Coated with proteins.
-Lipoproteins.
Protein Phospholipids
Polar molecules
triacylglycerol
Hydrophobic molecules
— Fig (1)
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—
—
Classes of lipoprotein particle
1-Chylomicrons
2-Very low density lipoproteins (VLDL)
3-Low density lipoproteins (LDL)
4-High density lipoproteins (HDL
Apoproteins
1-Each class of lipoprotein particle has its own set of specific apoproteins
2-Have hydrophilic and hydrophobic regions
3-Enabling them to coat lipid particles
4-Functional roles
-Activation of enzymes
-Recognition of cell surface receptors
Chylomicrons
1-Formed by enterocytes lining the intestine
2-Combine triacylglycerols from food with specific apoproteins
3-Vary in size – up to 750nm
4-Less dense than water
5-Carry lipids from diet to tissues (Especially adipose tissue)
6-Only present in blood after a meal
Very low density lipoproteins
1-Formed in liver for storage of energy
2-Rich in triacylglycerols
3-Combine triacylglycerols synthesised in liver with specific apoproteins
(30-80nm, Density similar to water)
4-Carry lipid from liver to tissues (Mainly adipose tissue)
Low density lipoproteins
1-Formed in liver
2-Cholesterol rich
3-Combine cholesterol synthesised in liver with a specific apoproteins
(18-25nm, Slightly more dense than water)
4-Carry cholesterol to tissues from liver
High density lipoproteins
1-Formed in tissues
2-Cholesterol from tissues combined with specific apoproteins
(5-12nm ,Significantly more dense than water)
3-Carry excess cholesterol back from tissues to liver.
Getting lipids off lipoproteins
1-Cells must bind circulating particles
2-And release the lipids
3-Different mechanisms for triacylglycerols and cholesterol.
Getting triacylglycerols from chylomicrons and VLDL
1-Endothelial cells of capillaries have lipoprotein lipase on outside of
membranes
2-Binds chylomicrons and VLDL
3-Cleaves triacylglycerols into: Glycerol – remains in circulation .Fatty
acids – enter tissues for metabolism.
4-Leave VLDL remnants (Usually removed by liver or converted to other
types of lipoprotein particles).
Getting cholesterol from LDL
1-Cells have LDL receptors :
-Complex proteins binds LDL at N-terminal domain.
- Receptor/LDL complex taken into cell by endocytosis .
-Cholesterol ester released, and cleaved into cholesterol and fatty acid.
2-LDL receptor synthesis controlled by cholesterol concentration in cell:
-Uptake stimulated by need.
Loading HDL
1-Some HDL synthesised as ‘shells’ in liver (Nascent HDL)
2-Other comes from VLDL remnants
3-Both types sequester cholesterol from capillaries
4-Mature into HDL particles
5-Carry cholesterol back to liver and other cells
Disposal of Cholesterol
1-Some converted to hormones
2-Some excreted by conversion to bile acids
-More polar molecules
-Important for digestion of fats in gut
Scavenger receptors
1-Macrophages pick up LDL damaged by oxidation via ‘scavenger
receptors’
2-Cytoplasm becomes loaded with lipid (Form ‘foam cells’).
3-Accumulate in intima of blood vessels(‘fatty streak’).
4-Eventually form Atheroma
Fig (2)
Hyperlipoproteinaemias
1-Raised levels of one or more lipoprotein classes
-Variety of causes (Over-production, Under-removal).
- Defective (Enzymes, Receptors, Apoproteins).
2-Complex classification depending on which lipid values are increased.
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Reference
Martin A C. Clinical chemistry and metabolic medicine.2006.
Marks’ Essentials of Medical Biochemistry, Chapter 30, Chapter 31, Chapter
20.
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‫جامعة الكوفة‬
‫مركز تطوير التدريس والتدريب الجامعي‬
‫((التمثيل الغذائي للدهون ونقلها ))‬
‫إعداد‬
‫المحاضرة عبير غسان مهدي‬
‫كلية طب األسنان‬
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‫نقل—الدهون—‬
‫أنواع—البروتينات—الدهنية—‬
‫—االبوبروتين—‬
‫الحصول—عل—الهون—من—البروتينات—الدهنية—‬
‫فرط—الدهون—‬
‫الهدف من المحاضرة‪—:‬اكتساب—الطالب—مفهوم——التمثيل—الغذائي—للدهون—ونقلها—‪— .‬‬
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‫بعد االنتهاء من هذه المحاضرة يجب أن يكون الطالب قادرا ً على—‪— :‬‬
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‫أن—يشرح—كيف—يتم—حصول—األنسجة—الدهنية—عل—الدهون—من—البروتينات—الدهنية—‬
‫أن—يناقش—المشاكل—السريرية—المرتبطة—بقل—الدهون—‬
‫أن—يعدد—أسباب—فرط—الدهون— —‬
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‫ترتبط—جزئيات—الدهن—مع—جزئية—بروتين—اثناء—انتقالها—في—مجرى—الدم—لتكون—البروتينات—الدهنية—والتي——هي—‬
‫أربعة—أنواع—(الكايلومايكرون—‪,‬الدهون—القليلة—الكثافة—جدا—‪,‬الدهون—القليلة—الكثافة—‪,‬الدهون—الحميدة—)—تستخدم—‬
‫الدهون—في—تخليق—الهرمونات—وبعضها—يحول—إلى—األحماض—الصفراوية—‪—.‬زيادة—نسبة—الدهون—تؤدي—إلى—‬
‫بعض—اإلمراض—الخطرة—منها—(اللويحة—الصفراء—‪—,‬وتصلب—الشرايين—‪,‬وورم—الوتر—وغيرها—)‪— .‬‬
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‫المصادر‪— —:‬‬
‫‪-0‬مارتن—‪—.C‬الكيمياء—السريرية—واأليض—‪— .‬‬
‫‪ -4‬أساسيات—عالمات—'الكيمياء—الحيوية—الطبية‪—،‬الفصل—‪—،41‬الفصل—‪—،40‬الفصل—‪— .41‬‬