Exercise and Nutrition | Senior Safety

How diet and activity each play a role in fat cell metabolism and help to determine whether you gain or loss weight.

Thu, 02 Feb 2006 22:03:02 -0500

The ratio of two enzymes, LPL and HSL, effect whether your store fat and gain weight or release fat and lose weight.

To a large extent the main factor that determines whether or not we store fat in our bodies are two key enzymes. Since most of the factors that regulate the activity of the enzymes are always present these enzymes are always active and are like lights with a dimmer switch that never go off. So it is the relative ratio of the two enzymes, which determines whether triglycerides are stored in our fat cells or released from the fat cells to be used for energy.

The two key enzymes responsible for fat storage and fat removal, respectively, are lipoprotein lipase (LPL) and hormone-sensitive lipase (HSL). Lipoprotein lipase is the enzyme located outside cells and responsible for removing triglycerides (TG – fat) from the blood and helping to move it into the cell for fat storage. Hormone-sensitive lipase on the other hand is located within the cell and is activated to release TG from the cells into the blood for utilization elsewhere.

Some of the key controllable factors that stimulate LPL are

1) a high fat diet,
2) saturated fats,
3) trans fats (found in hydrogenated oils),
4) the hormones insulin and cortisol, and
5) caloric restriction.

Other factors influence LPL, but these are the ones we cannot control through diet, exercise, or stress reduction.

The key controllable factor that regulates HSL is exercise or activity. Exercise, being a stress, causes release of epinephrine (adrenalin), and stimulates the release of TG from adipocytes to be used for fuel. However, unlike psychological stress, the physiological stress of exercise causes most of the fat to be taken up by skeletal muscles and used for energy production.

When a stressor is psychological in nature and the energy demands are low - much of the fat goes to the liver and is repackaged and released back into the blood stream only to be re-stored in fat cells or in unfortunate cases the artery walls leading to atherosclerosis (cardiovascular disease).

Another benefit of exercise is an enhanced glucose tolerance and insulin sensitivity. With continued training there is a chronic lowering of circulating insulin levels. The post entitled: the role of exercise in treating type II non-insulin dependent diabetes, goes into the mechanism behind the improved insulin sensitivity brought about by activity. A benefit of lower insulin levels is a reduction of insulin’s stimulatory effect on LPL. So exercise lowers the ratio of LPL to HSL by both lowering the activity of LPL and raising the activity of HSL.

Combining exercise with diet modifications of reduced total-fats, saturated-fats, trans fats, higher mono-unsaturated fats, omega-3 fats, and increased fiber creates an environment which is more efficient at removing fat than storing it – ultimately leading to fat loss and weight loss.

The role of exercise in treating type II non-insulin dependent diabetes.

Wed, 01 Feb 2006 06:56:46 -0500

By improving glucose tolerance and insulin sensitivity, exercise is a key player in the prevention and treatment of adult-onset diabetes.

The majority of the 7+ million people with diabetes in this country are non-insulin dependent diabetic (NIDDM). Over eighty percent of all NIDDM patients are obese. In addition, a growing number of Americans have fasting blood glucose levels which would classify them as border-line diabetic.

While insulin-dependent diabetes (IDDM) results from the inability of a person's pancreas to produce the hormone insulin, NIDDM is associated with elevated insulin levels, resistance to the hormone, and poor glucose tolerance.

It is still debatable in the scientific community which comes first- does the insulin resistance associated with NIDDM cause obesity, or does obesity result in insulin resistance and later the development of NIDDM. Whatever the case, both types of NIDDM are to a large degree preventable and treatable through diet and exercise.

Insulin's primary role is to lower blood glucose levels. The two major target tissues of insulin are skeletal muscle and adipose (fat) tissue. Whenever someone eats a meal containing carbohydrates that food is digested and converted into glucose. The rise in blood glucose causes the release of insulin from the pancreas and the resultant uptake of glucose into muscle and fat cells.

Along with diet, exercise plays a key role in NIDDM treatment and in determining one's sensitivity to insulin. Fat cells contain only one type of glucose transport protein (a glut-4 transporter) which respond to insulin and increase glucose transport into the fat cell whenever insulin levels go up. Unfortunately, most of the glucose that enters the fat cell are converted to triglycerides and stored as fat.

Muscle on the other hand has two different types of glucose transport proteins, one insulin regulatable (a glut-4 transporter) and one which is insulin independent (a glut-1 transporter). The glut-1 transporter functions in the basal state (between meals), whenever the muscle is active, and for a period of time after exercise. This increased glucose transport which is stimulated by activity and exercise - by the glut-1 transporter and independent of insulin - is what improves glucose tolerance and insulin sensitivity in individuals who exercise regularly.

Because glut-1 transporters exist in IDDM individuals and require no insulin to transport glucose into the muscle cells, IDDM patients who exercise require a lower insulin dose than sedentary ones.

So now you can begin to understand how your workouts are not only improving you blood glucose and lipid levels they are modifying the activity of your glut-1 transporters and improving your blood glucose regulation and insulin sensitivity.

An added benefit of improved insulin sensitivity, and lower basal and post-meal insulin levels, is that you'll not only have less glucose transported into your fat cells and less conversion into fat, but you will also have a lower activity of the enzyme lipoprotein lipase and less of a stimulus for TG storage in your fat cells. But that is another story for another post.

FDA advisory panel receives a failing grade with recommendation on Orlistat (Xenical).

Thu, 26 Jan 2006 15:40:47 -0500

Release of Xenical to over-the-counter status sends wrong message to the public - use drugs rather than taking personal responsibility.

This past Monday, January 23rd 2006, a joint advisory committee of the FDA voted 11-3 to change the status of Orlistat from a prescription weight loss drug to an over-the-counter (OTC) medication. If approved by the FDA (which is highly likely and generally the case when recommended to by their advisory panels) it will send a terrible message to the public in general and to the adults of the future - our kids.

With the change GlaxoSmithKleine and the FDA are supporting the use of a pill (in this case a fat blocking drug) rather than recommending taking personal responsibility for one's health by making wise dietary choices and increasing one's activity level.

The advisory boards' primary arguments for its reclassification to OTC status are greater weight loss on Orlistat compared to placebo groups and that over a ten-year period of release as a prescription drug no cases of severe medical side effects have been reported.

An important reason to stop its re-classification to OTC status and keep it a prescription medication is that in the studies on Orlistat's effectiveness, virtually all those who used the drug and lost weight regained the weight once the drug was discontinued. Without regulation and physician supervised release it is unknown whether future over-the-counter users will modify their diet and exercise along with taking the drug.

There is also the question as to whether side effects take a longer time to develop. Although eating saturated fat has been linked to a host of diseases including heart disease, cancer and diabetes it takes much longer than ten years of a high saturated fat intake for any of these diseases to progress to a life-threatening level.

Also unknown is if the new drug, which will be released under the name Alli (pronounced "Ally") and at half the dose of the prescription medication, is as effective. No long-term studies have been completed. As with all over-the-counter medications - there are questions of compliance to the manufacturer's warnings and recommendations. The possibility for abuse is obviously much greater.

It is unfortunate that the pharmaceutical, medical, and governmental agencies that profess to be watching over the health and well being of the American population don't take a stronger lead. While these groups get up on their "soap box" and preach for healthy eating, lifestyle modification, and restraint in drug use (both recreational and unnecessary drug use), they undermine that message with support of drug use and re-classifications like this which take the focus away from most American's diet and activity choices and places it on a quick fix approach. With this announcement they are basically sending a message which says "take this drug to lose weight ... don't change your eating habits, don't exercise, It's not what you eat. Its what you take to block what you eat."

Is that the correct message our physicians and regulators should be sending?