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Physiology > Lipid Metabolism > Flashcards

Lipid Metabolism Flashcards

1
Q

Types of lipids

A
  • triglycerides (main one)
  • phosopholipids
  • cholesterol
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2
Q

Fatty acids

A

Basic moiety of all lipids

- long chain hydrocarbon organic acids

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3
Q

Lipid functions

A

Triglycerides are used primarily for energy production (similar to CHO)

  • composition: 3 fatty acids and 1 glycerol
  • cholesterol and phospholipids used to make cell membranes
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4
Q

Lipoproteins

A

Carrier service for lipids in the plasma

  • transport lipids to and from liver
  • transport lipids to other tissues for use/storage
  • made of cholesterol, triglycerides, phospholipids, and protein
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5
Q

Types of lipoproteins

A
  • chylomicrons: carry digested fat from intestines to lymphatics (most relevant)
  • low density lipoproteins: contains higher cholesterol
  • very low density lipoproteins: high triglycerides/moderate cholesterol
  • high density lipoproteins: contains lower cholesterol
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6
Q

Bile formation

A

Bile is made by hepatocytes at rate of 1/2 - 1 liter/day
- stored in gallbladder
Functions
- fat digestion
- excretion of wastes, including cholesterol and bilirubin

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7
Q

Bile composition

A

Bile salts make up 50% of composition
- bile salts made from cholesterol –> cholic acid or chenodeoxycholic acid –> conjugation with taurine or glycine –> conjugated bile acids

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8
Q

Role of bile salts

A

Bile released from gallbladder when fat reaches duodenum

  • contraction stimulated by cholecystokinin
  • bile salts emulsify fat globules and then form micelles that allow further digestion/absorption of fats
  • bile salts are left behind in GIT lumen and recycled back to liver for repeat use
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9
Q

Cholecystokinin via blood stream causes

A
  • gallbladder contraction

- relaxation of sphincter of Oddi

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10
Q

Where is bile stored?

A

Gallbladder

- concentrated up to 15 times

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11
Q

What does secretin in the bloodstream do?

A

Stimulates liver ductal secretion

- Na and HCO3 added via secretin hormone to prevent bile from being too acidic

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12
Q

Step 1 of lipid digestion

A

Bile salts break down fat globules (mostly TG) into smaller sizes (emulsification) so lipase enzymes can act on them

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13
Q

Step 2 of lipid digestion

A

Bile salts form micelles

  • micelles allow water soluble enzymes to act further on fat for digestion
  • shuttle broken down fats (free fatty acids) to the intestinal brush border and release them into the intestinal cells
  • free fatty acids shuttled to smooth ER of cell and new TG are packaged into chylomicrons –> released from base of cell into thoracic duct OR FFA are absorbed directly into blood from GIT
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14
Q

What is the biggest component of a chylomicron?

A

Triglycerides

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15
Q

Chylomicrons

A

Type of lipoprotein, mostly triglycerides

  • increase in serum after a meal, causing turbidiy or whitish color, while they carry TG in the bloodstream
  • are cleared within 30 minutes in normal animals
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16
Q

Primary hypertriglyceridemia in dogs

A 
Breed predisposition
- schnauzers
- shetland sheepdogs
Diagnosis
- elevated FASTING triglycerides
Consequences
- pancreatitis
- poor glucose regulation in diabetics
- ocular problems
17
Q

Fate of triglycerides in the blood: option 1

A

Taken up by liver
- TG split into free FA –> oxidation of FA to supply ATP for body functions OR synthesis of cholesterol, phospholipids, and most lipoproteins

18
Q

_____ of cholesterol made in liver is converted to bile salts

A

80%

- remainder is transported in lipoproteins in the blood to needy tissues

19
Q

Phospholipids made in liver

A

Transported by lipoproteins

  • cell membrane formation
  • intracellular structure formation/reactions
  • second messenger systems
20
Q

Fate of TG in the blood: option 2

A

Used by other tissues for energy or storage

  • especially adipose, heart, and muscle
  • taken up via lipoprotein lipase (LPL) found in walls of capillaries
  • chylomicron –> LPL –> TG and phospholipids –> free FA + glycerol (lipolysis)
  • left over chylomicron is cholesterol rich and gets cleared by liver
21
Q

Free FA is used for

A
  • energy via beta oxidation, Kreb’s cycle, and oxidative phosphorylation
  • storage of fat
  • production of new TG or other lipids
22
Q

Lipolysis

A

TG hydrolyzed to FA + glycerol

  • glycerol enters cells –> glycolysis
  • FA goes to needy tissues –> further processing
23
Q

Lipolysis step 2

A

Fatty acids shuttled to mitochondria

  • FA moved to mitochondria for degradation and oxidation
  • amino acid carnitine acts as an enzyme to assist in this movement
24
Q

Lipolysis step 3

A

Beta oxidation of fatty acids yields acetyl CoA

- yields 4 H+

25
Q

Lipolysis step 4

A

Acetyl CoA enters TCA cycle

- products (per acetyl CoA): 2 CO2, 8 H+, 1 ATP

26
Q

Lipolysis step 5

A

Oxidative phosphorylation of >100 H+ atoms from previous steps
- yields more than >100 ATP

27
Q

When would the body make more fatty acids?

A
  • if body can’t use carbs (diabetes)
  • in starvation
  • to store excess carbs and protein
28
Q

Synthesis of fatty acids from excess carbs and protein

A

Necessary if CHO or protein are in excess and no more glycogen can be formed

  • storage of fat provides a log of energy back up
  • fat is more energy dense than carbs
  • 1st step is conversion of glucose or AA to acetyl CoA
29
Q

Synthesis of fat from proteins and CHO occurs in the ____

A

Liver

30
Q

Lipid storage

A

Adipose tissue’s major function is storage of TG until needed by liver or other tissues

  • adipocytes are 80-90% stored fat
  • TG stored inside cell in liquid form
  • lipases are activated once this stored fat is needed by the rest of the body
31
Q

Tapping into lipid stores

A

When cells need energy, hormone sensitive lipase can signal release of stored fat from adipose
- stored fat –> hormone sensitive lipase –> free FA in blood –> binds albumin –> tissue in need

32
Q

Free FA concentration is significantly increased in absence of ____

A

Carbs or inability to use carbs

- ex: diabetes mellitus

33
Q

What happens if lipid concentrations are too elevated?

A

Liver degrades excess fatty acids into keto-acids (ketones)

  • FA –> acetyl CoA –> ketones –> cells –> acetyl CoA –> TCA cycle
  • FA –> acetyl CoA –> ketones –> ketoacidosis (in a state of no carb metabolism)
34
Q

Diabetic ketoacidosis

A

Accumulation of ketones is common in sick or poorly controlled diabetics

  • due to insufficient insulin or insulin resistance
  • causes illness, acidosis, vomiting/diarrhea, lethargy, inappetence
35
Q

Hormonal control over lipid metabolism

A

Insulin-decreased CHO utilization and fat storage, increased fat mobilization (free FA) for energy
- thyroxine-rapid mobilization of fat to release free FA

36
Q

What activates hormone sensitive lipase and releases free FA for energy

A
  • epinephrine
  • glucocorticoids
  • growth hormone
37
Q

What signals satiety to the hypothalamus?

A

Leptin

  • produced by full adipocytes
  • released into bloodstream —> hypothalamus
  • decreases fat storage
  • decreases appetite
38
Q

Fat soluble vitamins

A
  • A: stored as retinol, needed for retinal development, epithelial health, reproduction
  • D: increases calcium and phosphorous absorption from GIT and bone
  • E: antioxidant
  • K: necessary cofactor for activates (carboxylates) clotting factors 2, 7, 9, and 10

Physiology (33 decks)

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