The insulin:glucagon ratio (I/G ratio) varies widely based upon the types of food an individual consumes. The list, below, shows I/G ratios under a variety of feeding conditions.
It is the relationship between insulin and glucagon that dictates the direction of fuel flow into either storage or oxidation and this outcome dictates, ultimately, the chances of becoming obese.
Mr. Kreiger’s next assertion begins in his standard format:
MYTH: carbohydrate drives insulin, which drives fat storage
FACT: your body can synthesize and store fat even when insulin is low
His conception here is that the body has ways to store and retain fat even when insulin is low. He mentions the primary enzyme in the adipocyte, hormone-sensitive lipase, which cleaves the fatty acid moeity from its triglyceride backbone. He states the known fact that insulin suppresses the activity of hormone-sensitive lipase thereby slowing the breakdown of fat. This statement is the basis, he argues, that has caused some people to point fingers at carbohydrate for causing fat gain.
He follows this statement with the idea that fat will also suppress hormone-sensitive lipase even when insulin levels are low. Yet the research that he cites clearly shows the fatty acids in the adipocyte derived from LPL-triglycerides were not re-esterified as intracellular adipose fatty acids (see next paragraph).
LPL, or lipoprotein lipase, grabs circulating triglycerides or chylomicrons (digested fat) and cleaves a fatty acid from them releasing it into the circulation. This fatty acid has three fates depending on the nutritional and hormonal profile in the blood: 1) it can enter the fat cell and be esterified into a triglyceride, or 2) it can travel to the peripheral tissues as a source of fuel or 3) produce ketones in the liver.
Storage or oxidation of foodstuffs is determined primarily by the I/G ratio and both processes, storage and oxidation, will not occur simultaneously. The results of the study Mr. Kreiger refers to show that insulin was non-essential for hormone-sensitive lipase suppression.
The increase in 3-hydroxybutyrate, shows that the liver was actively oxidizing fatty acids and had become ketotic as a result. Combining this with the fact that fatty acids were not being re-esterified in the adipocyte shows that this experiment induced an increased oxidation of fatty acids, not storage of fat as Mr. Kreiger would have us believe. The exact process that he claims will not occur.
He asserts that the body will store fat in the absence of insulin. The body will only store fat if the environment induces increases in malonyl-Co A, while decreases in this substrate will lead to fatty acid oxidation.
Mr. Kreiger’s interpretation suggests that this paper supports the idea that when carbohydrate intake is low one will be unable to lose fat despite the fact that the paper actually shows that fat loss is occurring under the conditions of this experiment.
Earlier I alluded to the idea that one must have the background and training to be able to critically evaluate that which he reads. The authors of the study understand that insulin is a major regulator of hormone-sensitive lipase activity and point out that there was only a slight increase of insulin after the oral lipid load.
Clearly, they were miffed at this occurrence and suggested further reasons why hormone-sensitive lipase activity remained stable. They suggested the idea that catecholamine activity was responsible and may account for the suppression of hormone-sensitive lipase activity.
Their results show that insulin concentration after the oral load almost doubled after sixty minutes. To discount this rise underestimates the power of insulin in small increments, as shown above, to effect intracellular changes in enzymes.
The study only had six subjects which provide little statistical power to argue that a doubling of insulin was statistically significant. Further, they did not directly measure HSL levels but only measured a surrogate of HSL activity, the production of VLDL-triacylglycerol.
There was also no measurement of changes in glucagon which could have a direct effect on lipolysis. Clearly, the liver production of ketone bodies rose indicating the presence of glucagon whose primary role is to increase the liver’s ability to produce ketones. The source of ketones was fat derived from the fat cell or from LPL-derived free fatty acids arising from circulating triglycerides or chylomicrons.
So, in contrast to Mr. Krieger’s belief, fat was not stored in the fat cell, but was released into the circulation. The storage of fat is an unusual event unless accompanied by carbohydrates.
One more Mr. Kreiger Fact dismantled.
The results of this particular study, having nothing in common with the way that people actually eat, sheds no light on Mr. Kreiger’s assertions. They only support the idea that under these experimental conditions insulin was non-essential for hormone-sensitive lipase suppression or LPL activation and that the action of insulin may be important in the process of re-esterification of free fatty acids.
Mr. Kreiger takes a limited viewpoint of only considering hormone-sensitive lipase to the exclusion of considerations involving both insulin and lipoprotein lipase in the process of re-esterification of fatty acids.
Obviously, his considerations of the research data in this particular paper limit his understanding. If he possessed a larger perspective of basic biochemistry and physiology he would not need to rely on individual research papers rather than the whole volume of research that details the whole range of metabolic actions based on hormone and enzyme activities.