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BIBC 120 > Week 4 Lipids > Flashcards

Week 4 Lipids Flashcards

1
Q

Saturated FA Structure

A
  1. Methyl start (w/n) and carboxyl end (alpha)
    > Stearic acid (C18:0)
    > Oleic Acid (C18:1, w-9)
    > Linoleic Acid (C18:2, W-6; unsaturated at two positions with DB)
  2. Glycerol + 3 FA –> B oxidation (lipogenesis/lysis via lipase) –> TG + 3 H2O with ester bonds
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2
Q

FA Synthesis (Cytosol)

A
  1. Acetyl CoA –> Malonyl CoA (Rate-limiting) –> Palmitate (C16:0) –(elongases/desaturases) –> linoleic acid (C18:2)
    > Human desaturates only work upto a-9 (no W-3/W-6 made, so they are essential)
  2. Proteins involved: ACP (Acyl-carrier), NADPH, ACC and FAS
    > Food intake –> insulin –> ACC on –> fat production
    > Fasting –> AMPK/TRB3 –> ACC off –> fat utilization
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3
Q

FA Degradation

A

Carnitine transports FA into mitochondria –> 2C stripped at a time via B-oxidation –> Ac-CoA –> TCA cycle

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4
Q

Essential FA: Alpha-Linolenic Acid (C18:3; W-3)

A

Alpha-linolenic (AHA) –> Eicosapentaenoic Acid (EPA) –> Docosahexaenoic Acid (DHA, C22:6, W-3)
> EPA: signals in thromboxane and prostaglandins (C20:5, W-3): decrease blood clotting and inflammation; W-6 increase both upon cyclooxygenase + lipooxygenase binding)
> DHA: 60% rods/retina (eye) and 20-25% brain; protects heart/lower arrhythmia risks; lower dementia risk by 50% (low blood DHA –> more brain impairment)

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5
Q

Essential FA: Linoleic Acid (C18:2; W-6)

A

Linoleic Acid –> Arachidonic Acid (C20:4, w-6) –>
1. Thromboxane (COX-1; vasoconstriction, platelet aggregation)
2. Prostaglandins (COX-1 and COX-2; gastric protection, pain and inflammation)
> Aspirin: COX off

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6
Q 
Lipid Digestion (SI):
Overview
A
  1. Difficult to hydrolyze due to long FAC being water insoluble
  2. 95% reabsorbed (Good energy source)
  3. Lecithin (phospholipids): DG (glycerol + 2 FA on top 2 C’s, phosphate and choline)
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7
Q

Lipid Digestion Regulation

A

Large fat enter SI –> cholecystokinin (CCK) –> bild acids/lecithin (Gallbladder): smaller particles –> lipase (pancreas): FA + MG –> reabsorbed in villi via micelles –> TG reform and combine with cholesterol, proteins and phospholipids –> chylomicrons

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8
Q

Lipoprotein: Overview

A

Components: TG + cholesteryl esters, phospholipids, cholesterol and membrane protein

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9
Q

Lipoprotein: Cholesterol

A
  1. Cell membrane; estrogen, testosterone, vitamin D, bile acid precursor
  2. Produced by liver (20%) and rest of body (80%) ANIMALS only
    > Non-essential: body compensates for overproduction of blood cholesterol
    > Diabetic: 1 egg/day –> increase risk of death 2x
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10
Q

Lipoprotein: Chylomicrons, VLDL, LDL, HDL Trends

A
  1. Decreasing triacylglycerol amount and Increasing protein content
  2. Chylomicrons + VLDL have the most TG; LDL most cholesterol (45%)
  3. Chylomicrons (lipase in body cells breakdown; remnants to liver as VLDL) –> VLDL (breakdown in tissues; back to liver; become LDL) –> LDL (taken up by receptor pathways; back to liver; become HDL) –> HDL (came from liver and intestines that bud off lipoproteins and transport cholesterols for disposal)
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11
Q

Lipoprotein: Chylomicrons

A

Transport lipids and cholesterols from SI –> liver and tissues
> When lipoprotein lipase in blood vessels release FA –> muscles burn them and adipose store them

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12
Q

Lipoprotein: VLDL

A

Lots of lipids; major supplier of liver FA to tissues

> When lipids removed –> density increases –> LDL and VLDL remnants

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13
Q

Lipoprotein: LDL

A

VLDL –> LDL as lipids are removed from blood (usually LDLR are in charge, supported by low saturated fat; protects brain function from stroke/dementia)
> Atherosclerosis: blood LDL accumulates –> oxidized from inflammation (CVD biomarker) –> WBC scavengers remove LDL –> artery plaques (trans fat, smoking, HTN)
> Early: foam cells from macrophage and smooth muscle cell uptake, WB Immune cells, artery injury
> Late: plaques and foam cells
> Dementia: thromboembolic occlusion of arteries and infarction and failure to remove Ab from brain

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14
Q

Lipoprotein: HDL

A

Scavenge cholesterol –> return to liver

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15
Q

CVD and Blood Cholesterol Level (TC)

A
  1. High TC/oxidized LDL –> higher chance of CVD
  2. Treatment:
    > LDL receptor to un-mutate (heterozygotes in adulthood especially)
    > PCSK9 (Degrade LDLR): must inactivate to reduce LDL (Evolocumab, alirocumab)
  3. Statins: inhibit HMG-CoA reductase –> no cholesterol –> lower LDL and inflammation; damages mito (muscle pain, memory loss, diabetes, 2x breast CA)
  4. Baby Aspirins:
    > Reduce blood clotting and inflammations; GI tract damage (10% ulcers)
  5. Controversial: replace trans and saturated fat with mono- and poly-unsaturated fat
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16
Q

Fat Tissues: Types

A
  1. White: Storage (Large fat droplet + small nucleus surrounded in membrane)
  2. Brown: mitochondria-rich; thermogenesis (energy dissipation)
    > Irisin (exercise induced): converts white to brown
17
Q

Adipose Tissue Turnover and Hormonal Control of Lipase

A
  1. Lipolysis: mobilization of stored fat in adipose tissue (cytokine- and hormone-regulated)
    > Insulin promotes storage; glucagon/stress promotes mobilization (conversion between FA + glycerol to TG)
  2. Hormone control:
    > Preprandial/between meals –> glucagon –> HSL –> FA release –> catabolic energy
    > Feeding –> Insulin –> no HSL –> less FA release –> less energy (anabolic)
18
Q

Adipose signals affecting diabetes

A
  1. Hyperglycemic: resistin, TNF-a, IL-6, cytokines, RBP4

2. Hypoglycemic: leptin, adiponectin, visfatin, omentin

19
Q

Types of Body Fat

A
  1. Subcutaneous: insulation (80%)
  2. Visceral: around organs
    > Upper body mostly; insulin resistance (Type II, CVD, HTN)
  3. Harmful: oxidation:
    > Rancid oils: PUFA most vulnerable; oxidized
    > Causes: UV exposure (PUFA should be kept in dark; Vitamin E counters)
    > Cis (bent backbone) Oleic Acid –(partial hydrogenation)–> Increased trans form Elaidic Acid –> MI risks increase (FDA wants to remove artificial trans fat)

BIBC 120 (9 decks)

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