This document summarizes the metabolism of lipoproteins in the human body. It discusses how lipids are transported in the blood using lipoproteins, which are classified based on their density. The main lipoproteins are chylomicrons, VLDL, LDL, and HDL. Each carries out specific functions to transport lipids between the intestines, liver, and peripheral tissues. The document outlines the synthesis and catabolism of each lipoprotein class and their roles in cholesterol transport. It also discusses inherited disorders that can disrupt lipoprotein metabolism.
Lipoprotein metabolism - (transport of lipids in the Blood)Ashok Katta
This presentation explains metabolism of lipoproteins (Chylomicron, VLDL, LDL, HDL) in very simple way. The presentation contains lots of animation to explain metabolism of individual lipoproteins.
Lipoprotein metabolism - (transport of lipids in the Blood)Ashok Katta
This presentation explains metabolism of lipoproteins (Chylomicron, VLDL, LDL, HDL) in very simple way. The presentation contains lots of animation to explain metabolism of individual lipoproteins.
lipoproteins transfer lipids such as triacylglycerol, cholestryl ester, fat soluble vitamins in the body. there are 5 categories of lipoproteins which includes chylomicrone, VLDL, IDL, LDL and HDL. LDL-cholesterol is called bad cholestrol while HDL-cholesterol is called good cholesterol.
Coronary heart disease due to atherosclerotic process is the major cause of death.Lipids have been implicated for enhanced atherosclerosis. The major lipids involved are triacy glycerol and cholesterol which are transported in the plasma by lipoproteins. So a better understanding of lipid transport and its abnormalities is essential for medical and health professional students.
Lipoprotein introduction, their general characteristics, exogenous and endogenous metabolism focusing on chylomicron and vldl metabolism, ldl metabolism and HDL metabolism , reverse cholesterol transport.
Lipids are insoluble in water, the problem of transportation in the aqueous plasma is solved by associating nonpolar lipids (triacylglycerols and cholesteryl esters) with amphipathic lipids (phospholipids and cholesterol) and proteins to make water-miscible lipoproteins.
Etiopathogenesis and pharmacotherapy of hyperlipidemias
a. the pathophysiology of selected disease states and the rationale for drug therapy;
b. the therapeutic approach to management of these diseases;
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d. the importance of preparation of individualised therapeutic plans based on diagnosis;
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g. summarise the therapeutic approach to management of these diseases including
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h. discuss the controversies in drug therapy;
i. discuss the preparation of individualised therapeutic plans based on diagnosis; and
j. identify the patient-specific parameters relevant in initiating drug therapy, and
monitoring therapy (including alternatives, time-course of clinical and laboratory indices of therapeutic response and adverse effects).
Multiple Choice Questions with Explanatory Answers on Chemistry of Carbohydrates for Medical, Biochemistry and Biology students - Chapter 1 of Multiple Choice Questions in Biochemistry by RC Gupta
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
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Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
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Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
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The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
1. Metabolism of Lipoproteins
R. C. Gupta
Professor and Head
Department of Biochemistry
National Institute of Medical Sciences
Jaipur, India
2. As lipids are hydrophobic, they are not
soluble in the aqueous medium of plasma
For transport in blood, they have to be
made water-soluble
The lipids are solubilized by converting
them into lipoproteins
3.
4. In lipoproteins, more hydrophobic lipids,
e.g. triglycerides and cholesteryl esters,
are present in the interior
These are surrounded by amphipathic
lipids e.g. phospholipids and free
cholesterol
5.
6. The apoproteins present in
lipoproteins are:
• Apo A-I
• Apo A-II
• Apo B-48
• Apo B-100
• Apo C-I
• Apo C-II
• Apo C-III
• Apo D
• Apo E
7.
8. The plasma lipoproteins
are classified into:
Chylomicrons (CM)
Very low density lipoproteins (VLDL)
Low density lipoproteins (LDL)
High density lipoproteins (HDL)
9. Lipoproteins are classified on the basis of
their relative density (specific gravity)
Chylomicrons have the lowest density
High-density lipoproteins have the highest
density
10.
11. CM and VLDL are rich in triglycerides
LDL is rich in cholesterol
HDL is rich in phospholipids and
cholesterol
12.
13. The apoproteins in CM are Apo A-I, A-II,
B-48, C-I, C-II, C-III and E
The apoproteins in VLDL are Apo B-100,
C-I, C-II, C-III and E
The only apoprotein present in LDL is Apo
B-100
14. There are different sub-classes of HDL
e.g. HDL1, HDL2 and HDL3
The apoprotein present in HDL1 is Apo E
HDL2 contains Apo A-I, C-I, C-II, C-III
and E
HDL3 contains Apo A-II and D
15. The common function of all lipoproteins is
to transport lipids in plasma
But each lipoprotein class has a specific
transport function
Functions of lipoproteins
16. Chylomicrons transport dietary triglycerides
from the intestine to peripheral tissues
VLDL transports endogenously synthesized
triglycerides from liver to peripheral tissues
LDL transports cholesterol from liver to
peripheral tissues
HDL transports excess cholesterol from
peripheral tissues to liver
17. Transport of cholesterol from peripheral
tissues to liver is known as reverse
cholesterol transport
This is a mechanism by which HDL
prevents accumulation of cholesterol in
peripheral tissues
18. Chylomicrons (CMs) are synthesized in
the intestinal mucosa
Apoproteins A and B-48 are synthesized
on ribosomes on the rough endoplasmic
reticulum in mucosal cells
These apoproteins enter the lumen of the
endoplasmic reticulum
Metabolism of chylomicrons
19. Apoproteins combine with triglycerides to
form ‘nascent chylomicrons’
Microsomal triglyceride transfer protein
incorporates apoproteins into chylomicrons
The nascent chylomicrons are transported
to Golgi apparatus
They are released from Golgi apparatus
into lacteals as secretory vacuoles
20. After reaching the circulation, nascent
chylomicrons receive apoproteins C and
E from HDL
After acquiring apo C and apo E, nascent
chylomicrons are converted into active
chylomicrons
21. Catabolism of chylomicrons occurs in
extra-hepatic tissues
These tissues possess lipoprotein lipase
which is normally inactive
This enzyme is really present on the
surface of endothelium of capillaries
22. Upon reaching extrahepatic tissues, the
apo C-II and phospholipids present in
chylomicrons activate lipoprotein lipase
Lipoprotein lipase hydrolyses the trigly-
cerides present in the chylomicrons
23. Free fatty acids released from trigly-
cerides are taken up by the tissues
Glycerol released from triglycerides goes
to liver via circulation
The hydrolysis continues until about 90%
of the triglycerides are broken down
24. With the loss of triglycerides, apo A and C
are transferred from chylomicrons to HDL
This converts chylomicrons into 'chylo-
micron remnants'
Chylomicron remnants enter liver cells via
a receptor specific for apo E
Chylomicron remnants are catabolized in
liver
25.
26. Synthesis of VLDL is similar to that of
chylomicrons but the site of synthesis is liver
First, nascent VLDL is synthesized which
contains only apo B-100
It acquires apo C and E in circulation from
HDL, and is converted into VLDL
Metabolism of VLDL
27. VLDL carries the triglycerides of hepatic
origin to extrahepatic tissues
Lipoprotein lipase is activated by apo C-II
and phospholipids present in VLDL
Triglycerides are hydrolysed, and fatty
acids are taken up by the tissues
28. Catabolism of VLDL is also similar to that
of chylomicrons
After hydrolysis of a major portion of
triglycerides, apo C is transferred to HDL
This converts VLDL into VLDL remnants
or IDL (intermediate density lipoproteins)
29. Nearly half of the VLDL remnants are
taken up by liver cells
The uptake is mediated by an apo E-
specific receptor
These VLDL remnants are catabolized
30. The remaining VLDL remnants transfer
their apo E to HDL
This converts VLDL remnants into LDL
31.
32. LDL is synthesized from circulating IDL
The only apoprotein present in LDL is B-100
Apo B-100 is a single long polypeptide chain
which is wrapped around the LDL particle
Only one molecule of apo B-100 is present
in one LDL particle
Metabolism of LDL
34. LDL is rich in cholesterol and carries
cholesterol to different tissues
Cells that require cholesterol take up the
entire LDL
LDL receptors on the cell recognize apo
B-100 and bind LDL
35. The receptor-LDL complex enters the cell
by endocytosis
The lysosomal enzymes hydrolyse apo B-
100 and cholesteryl esters
Apo B-100 is hydrolysed into amino acids
36. Cholesteryl esters are hydrolysed to form
free cholesterol
Free cholesterol is used by the cell
The receptors which have become free
can return to the cell membrane
37. Synthesis of LDL receptors is subject to
regulation
When the cell needs cholesterol,
synthesis of LDL receptor increases
When the cell has sufficient cholesterol,
synthesis of LDL receptors stops
38.
39. HDL is synthesized in liver and intestine
Newly synthesized HDL is known as
'nascent HDL’
Nascent HDL synthesized in liver
contains apo A-I, C-I, C-II, C-III and E
Metabolism of HDL
40. Nascent HDL formed in the intestine
contains only apo A-I
It acquires apo C and E after entering the
circulation
41. Nascent HDL is disc-shaped, and consists of
a phospholipid bilayer and apoproteins
It is capable of picking up cholesterol and
packing it in its interior
An enzyme, lecithin cholesterol acyl
transferase (LCAT) is also present on the
surface of HDL
42. After entering the circulation, HDL comes in
contact with tissue cells
It interacts with a cellular protein, ATP-
Binding Cassette Transporter A1 (ABCA1)
ABCA1 helps in the transfer of cholesterol
into HDL
43. LCAT is activated by apo A-I present in
nascent HDL
LCAT transfers a fatty acid from lecithin to
cholesterol
This converts them into lysolecithin and
cholesteryl ester respectively
Lysolecithin is released into circulation
44. Cholesteryl esters accumulate in the interior
and push the phospholipids outwards
This converts the disc-shaped particle into
spherical and mature HDL3
HDL3 takes up cholesterol from tissues and
from the circulating LDL and VLDL
45. Addition of cholesterol to HDL3 converts it
into HDL2
HDL2 transfers cholesterol to liver, and is
reconverted into HDL3
The HDL2-HDL3 cycle transports cholesterol
from extra-hepatic tissues to liver
46. Cholesteryl ester transfer protein (CETP)
is a protein secreted by tissues into blood
Most of the CETP in plasma is of hepatic
origin
CETP is also known as plasma lipid
transfer protein
It transfers lipids between different
lipoproteins
47. CETP causes exchange of cholesteryl
esters of HDL with triglycerides of LDL
and VLDL
LDL and VLDL would ultimately carry
these cholesteryl esters to the liver
48.
49. Inherited disorders of lipoprotein
metabolism
Disorders of lipoprotein metabolism
result in dyslipoproteinaemia
Dyslipoproteinaemia comprises:
• Hypolipoproteinaemia
• Hyperlipoproteinaemia
50. This is a group of disorders in which the
concentration of one or more lipoproteins
in plasma is decreased
These disorders include: (i) abetalipo-
proteinaemia, (ii) hypobetalipoproteinaemia
and (iii) hypoalphalipoproteinaemia
Hypolipoproteinaemia
51. Abetalipoproteinaemia is a rare auto-
somal recessive disorder
Incorporation of lipids in the lipoproteins
containing apo B is defective
Hence, CMs, VLDL and LDL are absent
or greatly decreased in plasma
Abetalipoproteinaemia
52. Transport of dietary lipids from intestine
to various tissues is impaired
Availability of fatty acids is decreased
Synthesis of cholesterol, glycolipids and
sphingomyelin is decreased
Serum cholesterol and triglycerides are
very low
53. Many patients with abetalipo-
proteinaemia die in childhood
Those who survive develop:
Steatorrhoea
Intestinal malabsorption
Retinitis pigmentosa
Neurological abnormalities
54. This is an autosomal dominant disorder
The defect is decreased synthesis of apo
B
Plasma LDL and cholesterol are low
Clinical abnormalities are mild and
compatible with life
Hypobetalipoproteinaemia
55. This is an autosomal recessive disorder
of a-lipoprotein (HDL) metabolism
It is also known as Tangier disease as it
was first discovered on the Tangier island
Synthesis of apo A is decreased resulting
in a decreased level of HDL
Hypoalphalipoproteinaemia
56. Decreased HDL level impairs transport
of cholesterol
Cholesterol is deposited in liver, spleen,
tonsils, lymph nodes etc
Risk of atherosclerosis is increased
Mild neurological abnormalities are also
common
57. A classification of hyperlipoproteinaemias
of genetic origin was proposed by
Frederickson and his associates in 1967
It was slightly modified by W.H.O. in 1970
Hyperlipoproteinaemia
58. In W.H.O. classification, hyperlipo-
proteinaemia is divided into six
types on the basis of:
Fasting plasma levels of CM, VLDL,
LDL, HDL, cholesterol and trigly-
cerides (after a 14-hour fast)
Appearance of serum after standing
it for 48 hours (serum storage test)
59. Genetic deficiency of lipoprotein lipase
CM present in fasting plasma
LDL and VLDL normal or slightly raised
Triglycerides greatly increased
Cholesterol normal or slightly raised
Hyperlipoproteinaemia, type I
60. Genetic deficiency of LDL receptors
CM absent in fasting plasma
LDL and cholesterol greatly raised
VLDL and triglycerides normal
Hyperlipoproteinaemia, type IIa
61. Variant of type IIa
CM absent in fasting plasma; LDL and
VLDL raised
Cholesterol and triglycerides increased
Hyperlipoproteinaemia, type IIb
62. Due to abnormal apo E
CM and VLDL remnants not removed;
VLDL and LDL raised
Cholesterol and triglycerides increased
On electrophoresis, pre-b and b-lipo-
proteins fuse to form a broad b band
Hyperlipoproteinaemia, type III
63. Cause not known
VLDL and triglycerides increased
LDL and cholesterol normal or slightly
increased
Hyperlipoproteinaemia, type IV
64. Cause is not known; associated with
diabetes and obesity
CM present in fasting plasma
LDL normal; VLDL, triglycerides and
cholesterol increased
Hyperlipoproteinaemia, type V
65.
66. Serum storage test in different
types of hyperlipoproteinaemia
I IIa IIb III IV V