The Remarkable 'Shrinking' Fat Cell

July 2011, Xtend-Life Expert

Summary

In my blog on ‘Fatty Foods for a Flat Stomach’, I said I would write about the fascinating fat burning process. Do you wonder where the fat ‘goes’ when it’s burnt? And why does it seem to ‘reappear’ so quickly...at least far more quickly than it disappears!? Let’s take a look...

In my blog on ‘Fatty Foods for a Flat Stomach’, I said I would write about the fascinating fat burning process. Do you wonder where the fat ‘goes’ when it’s burnt? And why does it seem to ‘reappear’ so quickly...at least far more quickly than it disappears!? Let’s take a look...

Where and How Much Fat is Stored and in What Form?

Fat is stored throughout the body in fat cells or adipocytes in the form of triglycerides. ‘Tri’ means ‘three’ because the glyceride consists of three individual fatty acids bound together in a single large molecule.

Adipocytes can increase both in size (hypertrophy) and in number (hyperplasia). Middle age with the dreaded ‘middle age spread’ is an example of this.

Numbers of Adipocytes: They are more likely to increase in number during late childhood and early puberty, pregnancy, and adulthood when excess weight is gained.

Some people are genetically predisposed to have more adipocytes than others, so women have more fat cells than men. An infant usually has about 5 - 6 billion fat cells. A healthy adult with normal body composition has about 25 to 30 billion fat cells, while an obese adult can have as much as 250 to 300 billion!

Size of Adipocytes: The average size of an adult fat cell is about 0.6 micrograms, but they can vary in size from 0.2 micrograms to 0.9 micrograms. An overweight person's fat cells can be up to three times larger than a person with ideal body composition.

Adipocytes are more likely to increase in size when:

  • You over eat repeatedly so leading to a constant calorie surplus
  • You eat nutrient poor, empty processed foods such as sugar and chemical filled processed junk
  • Your hormones are out of balance &/or malfunctioning.

So the adipocytes expand or contract/shrink dependent on the amount of stored fat (triglycerides) and how effectively it is burned or metabolised.

How are Triglycerides Metabolised?

Triglycerides are not burned in the adipocytes. They must be liberated or released from the fat cell into the bloodstream as free fatty acids (FFA's) through a complex hormonal/biochemical process involving:

  1. Lipolysis – fat metabolism
  2. The Citric acid /Krebs cycle - the chemical conversion of carbohydrates, fats and proteins into carbon dioxide and water to generate a form of usable energy
  3. The interaction between leptin, insulin and glycogen

Yes....complex!

So what triggers the release of FFAs and ensures that the three hormonal/biochemical processes mentioned above function effectively? There are several triggers, the more they all work together the better:

  1. An energy deficit - eating less calories than are burnt
  2. Consumption of fat burning foods
  3. Intense exercise
  4. An enzyme called hormone sensitive lipase (HSL) which prompts the lipolysis / fat breakdown.
  5. Another enzyme called lipoprotein lipase (LPL), then helps the FFA's get inside the mitochondria of the muscle cell, where the FFA's can be burned for energy in the form of ATP (adenosine triphosphate).

Role of Leptin, Insulin and Glycogen in Fat Metabolism

The relationship between the protein hormones leptin and insulin (+ co-factor chromium) and the blood sugar glucose is critical in determining the effectiveness of fat metabolism.

Leptin is largely responsible for the accuracy of insulin signalling. Indeed, some claim that leptin, is the fat loss ‘control’ hormone because other important metabolic hormones like insulin, the appetite regulating neuropeptide-Y and ghrelin, and the thyroid hormones are very dependent on leptin.

Basically, leptin is secreted by fat cells, and high leptin levels = heightened fat burning and metabolism, whereas low leptin levels = decreased fat burning and metabolism. So there is a direct, linear relationship between how much body fat and leptin you have: the more fat, the more leptin, and vice versa.

If you have ever wondered why weight loss plateau’s happen this is why...With every pound of fat you lose, leptin levels fall, making it even more difficult to lose the next pound.

But then you might argue, if leptin is so metabolic, why are ‘fat’ people, well, ‘fat’?

Good question!

Insulin and Leptin Resistance

The answer is because like insulin resistance, there is leptin resistance. This is caused by prolonged high body fat levels and high calorie intakes slamming insulin receptors. These receptors become so desensitized to insulin that leptin no longer ‘works’.

When leptin doesn’t work properly, insulin signalling is also less effective and glucose metabolism becomes impaired. Over time this leads to excessive insulin, insulin resistance and diabetes, because excess insulin:

  • Impairs chromium production which prompts the body to take sugar (glucose) from the bloodstream and store it as fat.
  • Inhibits the release and utilization of stored body fat for energy so forcing the body to burn carbohydrates for energy instead of stored fat.

As you can see, the relationship between leptin, insulin and glucose is critical to your fat burning ability. Yet few doctors are taught to pay attention to this critical contribution of leptin, or even know much about it.

Why? Perhaps you know....

Yes, it’s because there are no known drugs to regulate leptin. Therefore there's no incentive to spend money to educate physicians about its key role in health and disease.

The only known effective way to re-establish proper leptin signalling is via a healthy lifestyle and especially, a natural unprocessed diet.

This after all is at the root of fat metabolism isn’t it!

As I have shown, when you lose weight you don't actually "lose" fat cells, you "shrink" or "empty out" fat cells. That means you must be forever diligent. To stay lean with small or empty fat cells you have to eat clean and stay active!

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