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Endocrinology 1 > Digestion, Absorption, Transport, and Delivery of Lipids > Flashcards

Digestion, Absorption, Transport, and Delivery of Lipids Flashcards

1
Q

Digestion, Absorption, Transport, and Delivery of Lipids - What?

A

The digestion and absorption of dietary (exogenous) lipids involves emulsification using bile salts and breakdown - by hydrolytic enzymes - of these lipids and absorption of the digested products into the intestinal mucosal cells for packaging and transport to the necessary tissues

Transport of BOTH the digested lipid products as well as endogenous lipids through the body via the bloodstream REQUIRES various types of lipoprotein vesicles

Delivery of lipids from the lipoproteins to the various tissues for cellular use

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2
Q

Digestion, Absorption, Transport, and Delivery of Lipids - Why?

A

Digestion/Absorption
The problem: lipids are insoluble in water, but hydrolytic enzymes are water-soluble enzymes

The solution: emulsify the lipid droplets and membranes using bile salts, which ahve amphipathic properties; this process increases the surface area of these lipid droplets to allow access to the digestive enzymes, which work at the interface of the droplet/aqueous surroundings

Transport/Delivery

The problem: again, lipids are insoluble in water, but the bloodstream and cell cytoplasm are primarily water

The solution: package the lipids (but exogenous and endogenous) into various types of micelles - called lipoprotein particles - which have a hydrophilic surface and a hydrophobic center containing the various types of lipids (chylomicrons, VLDL, LDL, and HDL)

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3
Q

Digestion, Absorption, Transport, and Delivery of Lipids - Where?

A

Digestion: initial processing begins in the stomach, but most hydrolysis takes place in the small intestine

Absorption: digested products are absorbed into the intestinal mucosal cells (aka enterocytes)

Packaging and transport: the intestinal mucosal cells package the dietary lipid products into lipoprotein particle called chylomicrons; endogenous lipids are transported via other lipoprotein particles (VLDL, LDL, and HDL): VLDLs are produced in the liver & secreted directly to the bloodstream; LDLs are produced in the bloodstream as VLDLs become ‘modified’ as they circulate; HDLs are produced in the liver and intestine and secreted directly to the bloodstream

Delivery: lipids are delivered to various organs/peripheral tissues (excluding the brain)

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4
Q

Digestion, Absorption, Transport, and Delivery of Lipids - How?

A

First: Digestion and Absorption

Second: Transport

Third: Delivery to tissues

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5
Q

Where does the processing of dietary lipids begin?

A

Stomach

Primarily TAGs with short- or medium-chain length (<12C) are main target of gastric lipases

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6
Q

Where does emulsification of dietary lipids occur? How does this occur?

A

Small Intestine

Bile is secreted by the liver or gallbladder (containing bile salts), which emulsifies the large lipid droplets into much smaller lipid droplets for access by the hydrolytic enzymes that are water-soluble

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7
Q

What enzymes cause degradation of dietary lipids? What are they? What are their products?

A

Pancreatic enzymes

Pancreas secretes lipid hydrolytic enzymes into small intestine to digest: TAG, cholesterol esters, and phospholipids

Pancreatic Lipase - removes FAs from C1 and C3 (glycerol ‘end’ carbons)

Colipase - binds to the lipase for anchoring at the interface

Phospholipase A2 - removes FA from C2 of phospholipids

Products:

2-monoacylglycerols (from TAG breakdown)

lysophospholipids (from phospholipid breakdown)

free fatty acids (from both TAG and phospholipid breakdown)

free cholesterol (not esterified)

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8
Q

What cells absorb the lipids? What are they encased in? What does that contain?

A

Intestinal mucosal cells (enterocytes) - absorb the lipids of the mixed micelles

Mixed micelles - cholic acid and other bile salts (help emulsify dietary lipids); products of digestion; cholesterol; lipid-soluble vitamins (from diet; absorbed, but not digested)

FAs <12C do not require mixed micelles for absorption by intestinal mucosal cells

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9
Q

What kind of processing occurs after lipid digestion? Transport?

A

In mucosal cells

Cholate (other bile salts and bile acids) - sent back to liver (recycled)

TAGs, phospholipids, and cholesterol esters (the complex lipids) are resynthesized in ER

FAs <12C - bound to serum albumin; released to portal circulation for return to liver

Packaging for export:

Newly synthesized TAGs, cholesterol esters, etc - very hydrophobic, insoluble

Packaged in lipoprotein particles called chylomicrons (water-soluble form of lipid droplets) - for transport to necessary tissues

Chylomicrons are released by exocytosis from mucosal cells

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10
Q

What do transport lipoproteins do? What are the classes of transport lipoproteins?

A

Both exogenous and endogenous lipids are transported

transport lipids in the blood:

Classes:

Chylomicrons

VLDL: very low density lipoproteins

IDL: intermediate-dense lipoproteins (VLDL remnants)

LDL: low density lipoproteins

HDL: high density lipoproteins

Lipoprotein (a) [lp(a)] - nearly identical to LDL particle

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11
Q

What are the general features of transport lipoproteins?

A

Surface layers = amphipathic monolayer consisting of: phospholipids, cholesterol, apolipoproteins (aka apoproteins)

Interior = hydrophobic, containing: TAG, cholesterl (cholesteryl) esters

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12
Q

Explain cholesterol ester synthesis and why it is important.

A

FA attached (ester bond) to -OH group of cholesterol

LDL - uses ACAT (acyl CoA:cholesterol acyltransferase): attaches a fatty acid (from FA-CoA derivative) to cholesterol, which is then stored in lipoprotein particle

HDL - uses LCAT (lecithin:cholesterol acyltransferase): lecithen = phosphatidylcholine; cholesterol taken up by HDL are immediately esterified by transferring the FA from C2 of PC to cholesterol

Importance: cholesterol now completely hydrophobic and in interior of lipoprotein for safe packaging/transport

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13
Q

What are the characteristics of major classes of human plasma lipoproteins?

A

From chylomicrons & remnants -> VLDL -> IDL -> LDL -> HDL :

density increases

particle diameter decreases

Major lipids:

chylomicrons & remnants = dietary TAGs

VLDL = endogenous TAGs, cholesterol esters, cholesterol

IDL = cholesterol esters, cholesterol, TAGs

LDL = cholesetrol esters, cholesterol, TAGs

HDL = cholesterol esters, cholesterol

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14
Q

What are the major apolipoproteins?

A

apo B-100: LDL, VLDL, IDL - synthesized in liver; Ligand for LDL receptor

apo C-II: VLDL, HDL, chylomicrons; activator of extrahepatic lipoprotein lipase

apo E: VLDL, IDL, HDL, chylomicrons, chylomicron remnants; Ligand for chylomicron remnant receptor in liver and VLDL receptor (may play a role in Alzheimer’s Disease)

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15
Q

Summarize Chylomicrons - Key apoproteins? Synthesized? Transports? Transports from? Delivers to? Result?

A

Key Apoproteins: C-II; E

Synthesized: intestinal mucosal cells

Transports: DIETARY TAG, C, CE, PL, lipid soluble vitamins

Transports from: intestine

Delivers to: Tissues - the FAs from the TAGs via lipoprotein lipase (with apo C-II)

Result: ~90% of TAGs are removed

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16
Q

Summarize VLDL - Key apoproteins? Synthesized? Transports? Transports from? Delivers to? Result?

A

Key Apoproteins: B-100; C-II; E

Synthesized: liver

Transports: ENDOGENOUS TAG, C, CE, PL

Transports from: liver

Delivers to: Tissues - the FAs from the TAGs via lipoprotein lipase (with apo C-II)

Result: most of the TAGs are removed - VLDL remnants are IDLs

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17
Q

Summarize IDL - Key apoproteins? Synthesized? Transports? Transports from? Delivers to? Result?

A

Key Apoproteins: B-100; E

Synthesized: in plasma- remnants of VLDLs after TAG removal

Transports: C and CE

Transports from: Liver (as VLDL) and plasma

Delivers to: Endocytosed by liver or become LDLs if stay in plasma

Result: contain mostly CE in interior

18
Q

Summarize LDL - Key apoproteins? Synthesized? Transports? Transports from? Delivers to? Result?

A

Key Apoproteins: B-100 only

Synthesized: in plasma - from VLDL -> IDL -> LDL

Transports: C and CE; primary function of LDLs is to provide C to the peripheral tissues (or may return it to the liver)

Transports from: liver (as VLDL) and plasma

Delivers to: endocytosed by ALL TISSUES (except brain) via LDL receptors for B-100 (ligand)

Result: LDL = ‘bad’ cholesterol because all tissues can take up these particles for acquiring cholesterol

19
Q

Summarize HDL - Key apoproteins? Synthesized? Transports? Transports from? Delivers to? Result?

A

Key Apoproteins: A-I; D

Synthesized: Liver (precursor) and intestine

Transports: C and CE (‘scavenger’ of C from membranes of cells or other lipoprotein particles)

Transports from: tissues; plasma

Delivers to: LIVER (note: only means of excreting C is as bile salts via the liver)

Result: HDL = ‘good’ cholesterol because scavenges cholesterol from tissues for return to live rand possible excretion from body

20
Q

Summarize lipoprotein (a) - Synthesized? Key apoproteins? Result?

A

Synthesized: liver

Apoproteins: like LDL, but contains both apo B-100 and apo(a) [resembles plasminogen; interferes with plaque dissolution]

Result: increases plaque formation (inhibits blood clot dissolution); responsible for ~25% of heart attacks for people under 60

21
Q

What is the pathway of lipid transport of dietary lipids (metabolism of chylomicrons)?

A

Exogenous dietary lipids

22
Q

What is the pathway of lipid transport for endogenous lipids (metabolism of VLDL and LDL)?

A
23
Q

Describe triacylgycerol delivery to tissues.

A

Extracellular lipoprotein lipase - cleaves off free FAs from TAG in chylomicrons and VLDL

  • an extracellular enzyme anchored by heparin sulfate to capillary walls of most tissues (but mainly adipose, cardiac, and skeletal muscle tissues)

Fatty acids - taken up by tissues (i.e. adipose tissue); glycerol is returned to liver

24
Q

Describe the regulation of TAG metabolism by Lipoprotein Lipase (LPL) - Location//Acts on? Function? Regulation?

A

Location//Acts on: Capillary//Chylomicrons, or VLDL, TAG core

Function: converts (cleaves) TAG to fatty acids to be absorbed by tissues

Regulation: Apoprotein C-II

25
Q

Describe the regulation of TAG metabolism by Hormone Sensitive Lipase (HSL) - Location//Acts on? Function? Regulation?

A

Location//Acts on: Adipose tissue//stored fat

Function: mobilizes TAG to release FAs in circulation

Regulation: Glucagon (+); Epinephrine (+); Insulin (-)

26
Q

Describe the regulation of TAG metabolism by Pancreatic Lipase - Location//Acts on? Function? Regulation?

A

Location//Acts on: intestines, excreted by pancreas//dietary fat

Function: digests dietary TAG to monoacylglycerol + free FAs

Regulation: co-lipase (+

27
Q

Describe endocytosis of lipid particles

A

LDLs (all tissues except brain); chylomicron remnants (liver only); IDLs (liver only); HDLs (liver only)

the ENTIRE lipoprotein particle is taken up by a cell

28
Q

Using LDL as an example, describe the process of endocytosis of lipoproteins

A

LDL Receptor-mediated endocytosis (i.e. clarthrin-dependent)

LDL primary function: provide cholesterol to peripheral tissues [or return it to liver]

LDL receptors (bind ApoB-100) - clustered in pits on membranes

Clathrin - protein on intracellular side of pit

Once LDL vesicle inside - loses clathrin coat and fuses with similar vesicles to form larger vesicles called endosomes

Contents of LDL degraded and released into cell

29
Q

Describe the effects of endocytosed cholesterol on cellular cholesterol homeostasis

A

HMG-CoA reductase: high [cholesterol] - inhibits

de novo cholesterol synthesis - decreases

New LDL receptor protein synthesis - reduced (limits further entry of LDL cholesterol into cells)

30
Q

Diagram the Cellular Uptake and Degradation of LDL via endocytosis

A
31
Q

Clinical Problems associated with lipid digestion, absorption, and transport - Lipid Malabsorption

A

Increased lipids (even lipid-soluble vitamins) in the feces

Cause: disturbances in lipid digestion/absorption (i.e. cystic fibrosis, shortened bowel)

32
Q

Clinical Problems associated with lipid digestion, absorption, and transport - Heart Disease

A

recall lipoprotein (a) - inhibits blood clot dissolution

33
Q

Clinical Problems associated with lipid digestion, absorption, and transport - Hypercholesterolemias

A

High plasma levels of cholesterol

20% of population has defective regulation of cholesterol synthesis

Defect in cholesterol uptake into cells:

  • most often due to defective LDL receptor [could also be due to a ligand defect (apo B-100), but more rare cause]
  • solution: inhibition of cholesterol synthesis

Drugs like the statins (simvastatin, lovastatin, and mevastatin): structural analogs of HMG-CoA - thus competitive inhibitors of HMG-CoA reductase

34
Q

Hypercholesterolemias - Familial Hypercholesterolemia

A

Genetic cause = defective LDL receptor synthesis

IDL not taken back up to liver, LDL stuck in blood

Diet: lower cholesterol, fat

Drugs: inhibit cholesterol synthesis (statins)

Resin: increase excretion

35
Q

Hypercholesterolemias - High cholesterol diet

A

Increase in dietary cholesterol -> cholesterol repression of LDL receptor synthesis -> LDL reuptake taken back into liver, LDLs stuck in tissues

Diet: lower fat/cholesterol - increase unsaturated w-3 fats; - antioxidants

increase fiber (resin)

36
Q

Describe dyslipidemia

A

Definition: elevated TAGs (in chylomicrons/VLDLs) and low high-density lipoproteins (HDL) levels

37
Q

Describe dyslipidemia and how it relates to Diabetes

A

lipoprotein lipase activity (LPL) is low in adipose tissue (particularly) and in muscle [note: lipoprotein lipase activity is stimulated by insulin - particularly in adipose tissue by causing increased secreted of LPL to the extracellular surface]

Result: hypertriacylglycerolemia, which is increased plasma amounts of chylomicrons and VLDLs (carrying exogenous and endogenous TAGs, respectively)

38
Q

Describe dyslipidemia and how it relates to metabolic syndrome

A

Metabolic syndrome: (aka abdominal obesity)

  • associated with a cluster of metabolic abnormalities
  • including: glucose intolerance, insulin resistance, hyperinsulinemia, dyslipidemia, and hypertension
  • dyslipidemia associated with metabolic syndrome is by far the most common lipid disorder in the US
39
Q

Diagram the intertissue relationships in type 2 diabetes - leading to hypertriacylglycerolemia

A
40
Q
A

Endocrinology 1 (17 decks)

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