Carbohydrates are first lines of energy source for tissues. If there is a decrease in the amount of carbohydrates, then other energy sources such as fatty acids and proteins are mobilized and undergo metabolism to produce energy. One of the byproducts of fatty acid metabolism are ketone bodies; therefore, a decrease in carbohydrates will lead to an increase in fatty acid metabolism and, subsequently, an increase in ketone bodies.

Glycogen stores will be depleted because liver will respond to the decreased glucose levels and break down glycogen to component glucose molecules. Low carbohydrate concentration will decrease blood glucose levels.

Pyruvate carboxylase is an enzyme involved in gluconeogenesis, which is the generation of glucose from non-carbohydrate carbon substrates. This enzyme aids in the formation of PEP (phosphoenolpyruvate) from pyruvate. It converts pyruvate to oxaloacetate in the mitochondrion, requiring the hydrolysis of one molecule of ATP.

Proteins are the most diverse group of macromolecule. They can be fibrous (structural) or globular (receptors, enzymes, signaling molecules, and more).

Cysteine (C) is the only amino acid of the group to possess an uncharged R group at normal blood pH levels.

Arginine (R) and lysine (K) have positively charged R groups, and are considered basic. Aspartate (D) and glutamate (E) have negatively charged R groups, and are considered acidic.

Alanine (A) is the only hydrophobic amino acid in the group.

Serine (S), threonine (T), glutamine (Q), and asparagine (N) have polar, uncharged R groups.

Low-density lipoproteins have the highest content of cholesterol and cholesterol esters. There are essentially five classes of blood lipoproteins: chylomicrons, very-low-density lipoproteins, intermediate-density lipoproteins, low-density lipoproteins, and high-density lipoproteins. Chylomicrons have the lowest density of the five classes of lipoproteins. This is because the have the highest proportion of triglycerides and the least lowest proportion of protein. Very-low-density lipoproteins are a bit more dense than chylomicrons; however, the relative amount of triglycerides is still high. Intermediate-density lipoproteins which are formed from the very-low-density lipoproteins have a higher density than very-low-density lipoproteins due to the fact that they have less than half of the amount of triglycerides as very-low-density lipoproteins. Low-density lipoproteins have the highest amount of cholesterol and an even lesser amount of triglycerides than intermediate-density lipoproteins. Lastly, high-density lipoproteins are the densest of the lipoproteins due to the fact that they have the highest amount of protein in relation to the amount of triglycerides they contain.

The dietary intake of carbohydrate, in excess of the fuel requirement of the liver, leads to their conversion into triacylglycerols. These triacylglycerols are packaged into very-low-density lipoproteins (VLDL's) and released into the circulation for delivery to the various tissues (primarily muscle and adipose tissue) for storage or production of energy through oxidation. VLDL's are, therefore, the molecules formed to transport endogenously derived triacylglycerols to extra-hepatic tissues. The fatty acid portion of VLDL's is released to adipose tissue and muscle in the same way as for chylomicrons, through the action of lipoprotein lipase.

A cell's necessity for cholesterol as a part of the cell membrane is accomplished by two ways: either it is synthesized from within the cell by the cell, or it is supplied by low-density lipoproteins and chylomicrons. The dietary cholesterol that goes into chylomicrons is supplied to the liver by the interaction of chylomicron remnants with the remnant receptor. In addition, cholesterol synthesized by the liver can be transported to extra-hepatic tissues if packaged in very-low-density lipoproteins (VLDL's). In the circulation VLDLs are converted to low-density liporoteins through the action of lipoprotein lipase.

Very-low-density lipoprotein (LDL) triglycerides are broken down by lipoprotein lipase forming intermediate density lipoproteins. Intermediate density lipoproteins can either be brought into the liver through a receptor-mediated event or it may be further digested to form low density lipoproteins. LDL may be brought into the liver also by a receptor-mediated even in the liver. 

High density lipoproteins (HDL's) are converted into spherical lipoprotein particles through the accumulation of cholesterol esters. This accumulation converts nascent HDL to HDL2 and HDL3. Any free cholesterol present in chylomicron remnants and intermediate-density lipoproteins can be esterified through the action of the HDL-associated enzyme, lecithin-cholesterol acyltransferase (LCAT). LCAT is synthesized in the liver and so named because it transfers a fatty acid from the second carbon position of lecithin to the hydroxyl group on the third carbon of cholesterol, generating a cholesterol ester and lysolecithin. The activity of LCAT requires interaction with apoA-I, which is found on the surface of HDLs.