Put the Power of MHCP in Your Blood

Insulin Regulates Not Just Blood
Sugar But Fatty Acids As Well

The cinnamon extract MHCP mimics insulin with regard to glucose.
Does it do the same with regard to fatty acids?

By Aaron W. Jensen, Ph.D.

nsulin is one of the most intensively studied proteins in medicine. A wealth of research from laboratories throughout the world over the past 80 years has helped to elucidate the role that this hormone plays in regulating blood glucose (blood sugar) levels. We know that when insulin production is impaired - or, just as importantly, when our cells become resistant to the effects of insulin - our blood glucose levels can become dangerously elevated - a condition called hyperglycemia. The eventual result is the sinister disease diabetes mellitus, or diabetes for short. By far the most common form of this disease is type 2, or age-related, diabetes.

All cells in the body require glucose as a source of chemical energy - but to varying degrees. For most tissues, glucose is the primary energy source, and for the brain it is virtually the only source. And although glucose is the preferred energy source for the muscles, they (and many other tissues) are also equipped to use other fuels, notably fatty acids. These organic compounds, which are sometimes loosely referred to as fats, are components of true fats. They are derived from plant and animal fats in our diet and are precursors to the human fats made by our own bodies.

As you already know from the title of this article, insulin regulates not just glucose, but fatty acids as well. We'll soon see how it does that - but why is it important? Because fatty acids are among the most basic of all nutrients. Paradoxically, however, some are potentially harmful to our health (particularly our heart health), whereas others are decidedly beneficial to our health (again, particularly our heart health; for more information on these beneficial ones, see the article on omega-3 fatty acids in this issue).

A Tale of Two Dogs


Frederick Banting (right) with Charles Best and man’s best friend.
The role of insulin in diabetes was discovered in 1921-22 by the Canadian physiologist Frederick Banting and a medical student, Charles Best, who was his research assistant. Knowing that the pancreas was somehow connected with diabetes, and knowing that it exhibited hormone activity that was attributed to something called insulin (this mysterious substance had been discovered in 1916), Banting and Best took an extract from the pancreas of a healthy dog and administered it to a dog with diabetes. Presto! As long as the diabetic dog received the pancreatic extract from the healthy dog, its glucose levels were controlled and it enjoyed good health. But when the extract ran out, the dog's health failed, and it died.

Within a year, a pancreatic extract was successfully administered to a human diabetic patient, with excellent results: the patient's blood glucose levels improved dramatically, demonstrating that this was an effective method for treating diabetes.* Word of the seemingly miraculous treatment spread quickly, and Banting received the Nobel Prize in medicine and physiology in 1923. In 1925, insulin was finally isolated in pure crystalline form for the first time.


*Fortunately for diabetics, most animal insulin is almost identical to human insulin and is safe and effective for human use. Until the early 1980s, insulin isolated from pigs and cows was used in treating diabetes. In 1982, recombinant DNA technology was used to produce human insulin in the laboratory, and it has since become the most important source of insulin for medical use.


Insulin Opens the Cellular Gates to Glucose

You might think that by now we must know everything important about insulin - but you would be wrong. New discoveries are being made all the time. Earlier this year, e.g., researchers at MIT demonstrated that insulin regulates the levels of fatty acids in the blood, and it does so by a mechanism very similar to that for glucose regulation.1 Let's see how that mechanism works for glucose, and then we'll look at the fatty acids.

Insulin acts like a magic key. When it binds to insulin receptors on cell walls, a series of molecular events is initiated that opens microscopic gates (channels, actually) in the cell wall and allows glucose (and only glucose) molecules to enter the cell from the blood. The insulin receptor is a mediator in this process and is not itself the gate - it acts more like the gatekeeper. It's worth noting, by the way, that not all tissues require insulin to provide them with glucose, because many of them, such as the brain, consist of cells whose walls are permeable to glucose to begin with. The cells that require insulin for their glucose needs are primarily those of the muscles (heart, skeletal, and smooth) and adipose (fatty) tissues.


The cinnamon compound MHCP
acts as an insulin mimic -
it activates some of the
same pathways in our cells
that insulin does.


When insulin activates the receptors on cells such as these, a chemical message is sent through the cell that causes swarms of glucose transporter proteins (called Glut4) to congregate at the cell wall and embed themselves in it (some are already there, and the rest "come running," so to speak). Once there, they act as the gates, opening and closing the channels in such a way as to seize nearby glucose molecules and transport them into the cell. As a result, the concentration of glucose in the bloodstream falls, and the body is thus able to maintain a safe level of glucose in the blood.

Diabetes Is Easy to Avoid

A group of Harvard researchers monitored 84,941 women from 1980 to 1996 to determine the impact of diet and lifestyle on the incidence of type 2, or age-related, diabetes.1 Their results showed strikingly that the majority of diabetes cases in this population could have been avoided by simple changes in diet and lifestyle. The researchers investigated five risk factors for type 2 diabetes - weight, diet, exercise, smoking, and alcohol - and found that each of these had a significant impact on whether the women were likely to become diabetic.

The most significant risk factor was being overweight, as defined by the body mass index (BMI) score.* For this study, the ideal BMI was taken to be 23.0. Women with a BMI in the range 23.0-24.9 were 2.7 times more likely to develop diabetes than those with a value less than 23. For a BMI in the range 25.0–29.9, the risk increased to 7.6; for the range 30.0–34.9, it rose to 20.1, and for a BMI of 35.0 or greater, the risk of developing diabetes was a staggering 38.8. Thus, all else being equal, a 5'7" woman who weighs 225 pounds (BMI = 35.2) is roughly 40 times more likely to get diabetes than a woman of the same height who weighs 145 pounds (BMI = 22.7) Food for thought!


*BMI is a common measure of obesity based on height and weight. To calculate your BMI, divide your weight in pounds by the square of your height in inches, and multiply the result by 703. (In metric units, divide your weight in kilograms by the square of your height in meters.)


Other factors also increased the risk of diabetes, although to a much lesser extent than BMI. Those who smoked more than 15 cigarettes per day, e.g., had a 34% increased risk of developing diabetes.

Happily, there was good news about diet and lifestyle with respect to diabetes. Individuals with a healthy diet who exercised at least 7 hours per week, who had a moderate intake of alcohol, and who didn't smoke had an incidence of diabetes approximately 90% lower than those who did not fit this profile. (Here a healthy diet was defined by a low intake of trans-fatty acids, moderate sugar intake, high fiber intake, and a high ratio of polyunsaturated fat to saturated fat in the diet.)

This research clearly indicates that type 2 diabetes could largely be avoided through appropriate lifestyle modifications. Stop and consider that an estimated 1700 new cases of diabetes mellitus are diagnosed every day2 and that 15 million Americans already have the disease. We have the way to defeat diabetes, if only we have the will.

  1. Hu FB, Manson JE, Stampfer MJ, et al. Diet, lifestyle, and the risk of type 2 diabetes in women. N Engl J Med 2001;345:790-7.
  2. Kahn BB. Type 2 diabetes: when insulin secretion fails to compensate for insulin resistance. Cell 1998;92:593-

Insulin Regulates Fatty Acid Uptake Too

The MIT team found that insulin plays a similar role in regulating blood levels of fatty acids. Their research demonstrated that when insulin binds to the insulin receptor in mouse adipocytes (the fat-storage cells of adipose tissue), not only is Glut4 summoned and activated, but also a molecule called the fatty acid transporter protein (FATP), which swarms to the cell wall in vast numbers and does the same thing to fatty acids that Glut4 does to glucose: it brings them in, thereby causing their levels in the bloodstream to fall.

In their experiments, the researchers grew two groups of mouse adipocytes in a culture medium (a nutrient-rich broth) containing fatty acids that were labeled with radioactive tracer atoms. One group of cells received insulin, while the other (the control group) did not. After the cells were incubated with insulin for 60 minutes, they were removed from the culture medium and washed thoroughly. The researchers then measured the radioactivity of each group of cells - the cells would contain radioactive material only if the fatty acids had been transported through the cell walls. They discovered that, whereas both groups of cells absorbed fatty acids, the insulin-treated group took up 75% more of them than the control group. They concluded that insulin mediates improved fatty acid uptake in mouse adipocytes.

What About Humans?

So far, these experiments have been carried out only in specially grown cells in the laboratory. Could insulin serve a similar function in cells in the human body? It is a distinct possibility, but we must await further research to know for sure. Meanwhile, the MIT researchers' next objective is to determine the effect of insulin's activation of FATP on the overall levels of fat in the bodies of . . . mice.

It has long been known that one of insulin's primary functions in the human body is to promote the storage of fat in adipocytes. This is a valuable adaptive process to increase the availability of fuel for metabolic functions, because the stored fat can be mobilized in times of need to provide chemical energy in the form of fatty acids. The process works fine as long as the human body in question does not overeat and gets adequate physical exercise, which prevents the excessive accumulation of fat. Without exercise, however, fat tends to build up - and you don't need Paul Harvey to tell you the rest of that story.

MHCP, a Natural Insulin Mimic

The relationship between insulin, blood glucose levels, and diabetes is well documented. But is there any way to relieve the symptoms of diabetes other than with pharmaceutical approaches or insulin injections? It just so happens that there might be. One of the most exciting developments in this field is the discovery of a compound in cinnamon - methylhydroxychalcone polymer, or MHCP - that acts as an insulin mimic. This means that MHCP can activate at least some of the same pathways in our cells that insulin does (a pathway is a well-defined series of molecular processes leading to a specific outcome, such as glucose or fatty acid transport).

Using the same model as in the MIT study (mouse adipocytes grown in culture), researchers at the U.S. Department of Agriculture have demonstrated that MHCP encourages cells to take up glucose, in a manner similar to that initiated by insulin.2 Furthermore, the results suggest that MHCP may act additively with insulin. Consequently, when insulin and MHCP are present together, the cellular response to elevated glucose levels may be to absorb even more glucose than usual. And the fact that MHCP can work by itself (in the absence of insulin) may be especially important when cells are insulin-resistant, as is true in many diabetic individuals.


Researchers are pursuing the
question of whether MHCP can
mimic insulin's regulation of
fatty acids as well as its
regulation of glucose.


MHCP appears to be an insulin mimic in activating at least two different pathways. One pathway leads to an increase in glucose absorption by our cells, as we've already seen. The second activates an enzyme called glycogen synthetase, which enables the liver and muscles to store glucose in the form of glycogen, a polymeric form of glucose. This is useful because it's an additional mechanism for controlling blood glucose levels and because it's important that a supply of glycogen be available at all times for quick conversion back to glucose when the body needs more of it, such as during exercise. Thus, both of these insulin-related functions activated by MHCP are important mechanisms that help to maintain healthy blood sugar levels.

Can MHCP Induce Fatty Acid Uptake Too?

Given the results of the MIT study, it is interesting to speculate that MHCP may also play an important role in regulating fatty acid levels in our blood. Knowing how fatty acids are removed from the blood is important, of course, but it is vital to know where they go and what they do. To what extent do they enter cells that use them as an energy source, and to what extent do they enter adipocytes and get converted to fats?

Although currently the relationship between insulin and fatty acids has been studied on mouse adipocytes growing in the laboratory, you can bet that researchers are pursuing the question of whether MHCP can mimic this important function of insulin as well. You can also bet that we will keep you informed of their results. Meanwhile, you can be sure that MHCP can help you maintain healthy blood sugar levels, thus keeping the threat of diabetes at bay.

References

  1. Stahl A, Evans JG, Pattel S, Hirsch D, Lodish HF. Insulin causes fatty acid transport protein translocation and enhanced fatty acid uptake in adipocytes. Devel Cell 2002 Apr;2:477-88.
  2. Jarvill-Taylor KJ, Anderson RA, Graves DJ. A hydroxychalcone derived from cinnamon functions as a mimetic for insulin in 3T3-L1 adipocytes. J Am Coll Nutr 2001;20(4):327-36.

Dr. Jensen is a cell biologist who has conducted research in England, Germany, and the United States. He has taught college courses in biology and nutrition and has written extensively on medical and scientific topics.


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