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C H A P T E R 4 7 Lipid-lowering agents

Dietary fats 1

To heart—enter circulation and reach periphery—stored as fat

8

-used as energy -absorbed into circulation -atheroma develops

-injured vessel -inflame vessel -becomes remnants

Stomach 2

Liver processes fats to LDLs, HDLs—enter circulation and reach periphery

9

Small intestine 3

Gallbladder contracts and relases bile into small intestine

4

Bile recycled to liver 5

6a

Bile breaks fat into micelles

Micelles absorbed into small intestine wall, packaged as chylomicrons

6b

Chylomicrons absorbed into lymphatic system

7

FIGURE 47.1  Metabolism of fats in the body.

unit in the formation and maintenance of cell mem- branes. Cholesterol is usually provided through the diet and the fat metabolism process just described. If dietary cholesterol falls off, the body is prepared to produce cholesterol to ensure that the cell membranes and the endocrine system are intact. Every cell in the body has the metabolic capability of producing cholesterol. The enzyme hydroxymethyl- glutaryl-coenzyme A (HMG-CoA) reductase regulates the early, rate-limiting step in the cellular synthesis of cholesterol. If dietary cholesterol is severely limited, the cellular synthesis of cholesterol will increase. Hyperlipidaemias When the levels of lipids in the blood increase, hyperlip- idaemia occurs. This can result from excessive dietary intake of fats or from genetic alterations in fat metab- olism leading to a variety of elevated fats in the blood (e.g. hypercholesterolaemia, hypertriglyceridaemia, alterations in LDL and HDL concentrations). Cultural variations related to lipid levels have also been identified (see Box 47.4).

Cultural considerations

BOX 47.4

Rosuvastatin and Asian people Rosuvastatin reaches higher serum levels in Asian people than in other populations. Higher serum levels are associated with an increased risk for rhabdomyolysis. It is recommended that this drug be reserved for use in non-Asian people. Dietary modifications are often successful in treating hyperlipidaemia that is caused by excessive dietary intake of fats. Drug therapy is needed if the cause is genetically- linked alterations in lipid levels or if dietary limits do not decrease the serum lipid levels to an acceptable range. The NHF (2012) recommends the following standard goals for lipid levels: LDLC <1.8; HDLC >1.0;TG <2.0; and NHDLC <2.5. Antihyperlipidaemic agents such as bile acid sequestrants, HMG-CoA inhibitors, fibrates, niacin, cholesterol absorption inhibitors and, in some cases, hormones (in women) may be used.These drugs are often used in combination and should be part of an overall healthcare regimen that includes exercise, dietary restrictions and lifestyle changes. See the Critical thinking scenario for additional information on treating hyperlipidaemia.