I was forced to review some Biochemistry concepts. With all the negative connotation about dietary fats, it is still a necessary constituent of our diet.
To answer the second commentor's question:
Triglyceride is different from cholesterol. A TG (triglyceride) molecule consists of a glycerol attached to 3 fatty acids. It is the form in which fatty acids, whether synthesized de novo from dietary sources are stored in all cells, but mainly in adipocytes (fat cells).
Cholesterol is an extremely important biological molecule that has roles in membrane structure as well as being a precursor for the synthesis of the steroid hormones and bile acids. Both dietary cholesterol and that synthesized de novo are transported through the circulation in lipoprotein particles. The same is true of cholesteryl esters, the form in which cholesterol is stored in cells.
Fatty acids in triglycerides and cholesterol are synthesized utilizing acetyl-coA.
The interrelated pathways in which fatty acids are used in the body for synthesis of some important chemicals is also coupled with carbohydrate pathways. The whole system is so complex, even I had a hard time trying to see again the whole picture (actually I only got to appreciate the interrelationships of all the metabolic pathways when I was already reviewing for the board. During the lessons in our first year in medicine, we studied each pathway separately, which was hard enough. To understand even a bit of the whole puzzle required that we constantly refer to another pathway from time to time.)I won't even try to talk about these pathways using ordinary language...that's just impossible.
For those interested, I leave here the links to informations on cholesterol and triglycerides:
I would like to highlight the following from the site above:
ACC (Acetyl-Coa carboxylase) is the rate limiting (committed) step in fatty acid synthesis....Insulin stimulates ACC and FAS (fatty acid synthase) synthesis, whereas, starvation leads to decreased synthesis of these enzymes. Adipose tissue lipoprotein lipase levels also are increased by insulin and decreased by starvation. However, in contrast to the effects of insulin and starvation on adipose tissue, their effects on heart lipoprotein lipase are just the inverse. This allows the heart to absorb any available fatty acids in the blood in order to oxidize them for energy production. Starvation also leads to increases in the levels of fatty acid oxidation enzymes in the heart as well as a decrease in FAS and related enzymes of synthesis....Adipose tissue contains hormone-sensitive lipase, that is activated by PKA-dependent phosphorylation leading to increased fatty acid release to the blood. The activity of hormone-sensitive lipase is also affected positively through the action of AMPK. Both of these effects lead to increased fatty acid oxidation in other tissues such as muscle and liver. In the liver the net result (due to increased acetyl-CoA levels) is the production of ketone bodies. This would occur under conditions where insufficient carbohydrate stores and gluconeogenic precursors were available in liver for increased glucose production. The increased fatty acid availability in response to glucagon or epinephrine is assured of being completely oxidized since both PKA and AMPK also phosphorylate (and as a result inhibits) ACC, thus inhibiting fatty acid synthesis.
Insulin, on the other hand, has the opposite effect to glucagon and epi leading to increased glycogen and triacylglyceride synthesis. One of the many effects of insulin is to lower cAMP levels which leads to increased dephosphorylation through the enhanced activity of protein phosphatases such as PP-1. With respect to fatty acid metabolism this yields dephosphorylated and inactive hormone sensitive lipase. Insulin also stimulates certain phosphorylation events. This occurs through activation of several cAMP-independent kinases. Insulin stimulated phosphorylation of ACC activates this enzyme.... When carbohydrate utilization is low or deficient, the level of oxaloacetate will also be low, resulting in a reduced flux through the TCA cycle. This in turn leads to increased release of ketone bodies from the liver for use as fuel by other tissues. In early stages of starvation, when the last remnants of fat are oxidized, heart and skeletal muscle will consume primarily ketone bodies to preserve glucose for use by the brain....extrahepatic tissues (tissues other than liver) have access to ketone bodies as a fuel source during prolonged starvation....
The production of ketone bodies occurs at a relatively low rate during normal feeding and under conditions of normal physiological status. Normal physiological responses to carbohydrate shortages cause the liver to increase the production of ketone bodies from the acetyl-CoA generated from fatty acid oxidation. This allows the heart and skeletal muscles primarily to use ketone bodies for energy, thereby preserving the limited glucose for use by the brain.
The most significant disruption in the level of ketosis, leading to profound clinical manifestations, occurs in untreated insulin-dependent diabetes mellitus. This physiological state, diabetic ketoacidosis (DKA), results from a reduced supply of glucose (due to a significant decline in circulating insulin) and a concomitant increase in fatty acid oxidation (due to a concomitant increase in circulating glucagon). The increased production of acetyl-CoA leads to ketone body production that exceeds the ability of peripheral tissues to oxidize them. Ketone bodies are relatively strong acids (pKa around 3.5), and their increase lowers the pH of the blood. This acidification of the blood is dangerous chiefly because it impairs the ability of hemoglobin to bind oxygen.
So for those who tend to be swayed by the different dietary fads, I suggest you just know your TCR and follow the pyramid guide. That will be simpler and will make more sense...GO BACK TO THE BASICS.
Oh...and please, don't forget the physical activity (actually this is taken into consideration when you compute for your TCR).