1.

Fasting lipid profile  high cholesterol / electrophoresis  high LDL

Type 2: Familial hypercholesterolemia

2. Defective LDL receptor (AD)

3. LDL (Apo B-100) – LDL receptor  endocytosis

Intracellular LDL  Broken down into Amino Acid, Fatty Acid, and Cholesterol.

 cholesterol for plasma membrane, steroid H, & bile acids

 storage (acyl CoA cholesterol acyl transferase (ACAT))

4. Oversupply of cholesterol  First, decreases the synthesis of cholesterol by inhibiting

HMG-CoA reductase. Second, LDL- receptor is downregulated (high cytosolic C level

First, retains SCAP-SREBP complex in the ER membrane  prevents SREBP entering the

nucleus  can’t bind to SRE in the nucleus).

5. High LDL  oxidized LDL  + macrophage  foam cell  fatty streak & fibrofatty

atheroma

6. Blood sample analysis provided crucial information needed for accurate diagnosis. To see

the amount of TAG, Total Cholesterol

7. –

8. Decrease Total Cholesterol to <200mg/dL

–Diet: Reduce intake of Trans fat, and cholesterol.

Increase HDL by Omega 3 (linolenic).

Decrease Carbohydrates  Decrease TAG synthesis  Increase HDL.

9. Statin: competitive inhibitor of HMG CoA-reductase (liver)  less hepatic C synthesis 

low hepatic cytosolic free C  less VLDL assembly & more LDL receptors (less serum

LDL-C)

Cholestyramine: bile acid sequestering drugs / bind bile acids & bile salts in the intestine
 less dietary lipid digestion & bile acid & bile salts excretion  liver has to use free C
for de-novo synthesis of bile acids  low hepatic cytosolic free C & more hepatic LDL
 receptor synthesis  lower serum LDL

10. Farnesyl pyrophosphate (FPP-intermediate product of cholesterol synthesis) used for

nonsterol products (e.g. ubiquinone (CoQ)  mitochondrial dysfunction (ETC), dolichol
(N-glycosylation), & heme A)

11. Friedewald equation: LDL-C = total C – (HDL-C + TAG/5) = 494 - (42 + 325/5) = 387

mg/dL  high total C (<200 mg/dL) & high LDL-C (100-130 mg/dL)

12. Overnight fasting  no CM / non-fasting  CM present @ the origin

Type 1 : CM / 2a: LDL / 2b: LDL & VLDL / 3: CM remnants & IDL / 4: VLDL / 5: CM &

VLDL

13. Good C  HDL / bad C LDL

However, normal level of LDL is essential for transporting C&CE to the peripheral tissues

14. LPL deficiency  high CM & VLDL

15. – Ethanol + NAD+  Acetaldehyde + NADH

NADH ETC, Lipogenesis (TAG, Cholesterol)

16. TAG is 235mg/dL so hypertriacylglycerolemia (100-150 mg/dL) / LPL deficiency(TypeIa),

Apo C-2 deficiency(TypeIb), LPL inhibitor protein(TypeIc), VLDL overproduction(TypeIV/V)

 high CM & VLDL

17. –

Hormone: +Insulin/-Glucagon

Enzyme: - AMP Activated Protein Kinase (response to inc. AMP and Leptin)