Answer = C. (Decreased hepatic VLDL synthesis)

Nicotinic acid = Niacin. Niacin works by:

1. Inhibiting lipolysis (hormone sensitive lipase) in adipose tissue)

2. Reducing hepatic VLDL synthesis

A: cholestryramine and other bile acid resins prevent the reuptake of bile acids from the gut. B: Statins inhibit HMG-CoA reductase, preventing the liver from making mevalonic acid, a precursor to cholesterol. C: Niacin (nicotinic acid) reduces hepatic VLDL synthesis and also inhibits lipolysis in adipose tissue by inhibiting hormone sensitive lipase. D&E: Fibrates upregulate lipoprotein lipase (LPL), increasing triglyceride clearance (VLDL and chylomicrons are full of triglycerides) and also activate peroxisome proliferator-activated receptor- alpha (PPAR-alpha) to induce HDL synthesis.

A: cholestryramine and other bile acid resins prevent the reuptake of bile acids from the gut.

B: Statins inhibit HMG-CoA reductase, preventing the liver from making mevalonic acid, a precursor to cholesterol.

C: Niacin (nicotinic acid) reduces hepatic VLDL synthesis and also inhibits lipolysis in adipose tissue by inhibiting hormone sensitive lipase.

D&E: Fibrates upregulate lipoprotein lipase (LPL), increasing triglyceride clearance (VLDL and chylomicrons are full of triglycerides) and also activate peroxisome proliferator-activated receptor- alpha (PPAR-alpha) to induce HDL synthesis.

1) label D (VLDL -->ILD --> LDL) = anything that increased LPL = Fibrates which use PPAR-alpha (Rx) are good at reducing [VLDL]; therefore, less VLDL means more ILD.

2) VLDL --> fatty acid oxidation = using fats (TAGs) for energy production Here PPAR-gamma plays a role= which are Thiazolidinediones (also called glitazones) are a class of medicines that may be used for the treatment of type 2 diabetes. They are also good at reducing serum TAGs

Note VLDL are very rich in TAGs

Could someone please explain which drugs (if any) are at D and E?