Why do we get fat

Chapter 20 Fat: Where did it come from and where is it going? (2)
The LPL activity in fat cells below the waist of women is relatively high, while the activity on visceral fat cells is low, which is why they tend to gain weight around the buttocks.After menopause, LPL activity in women's abdominal fat catches up with that of men's, so they also tend to accumulate excess fat around their waists.When a woman becomes pregnant, LPL activity increases in the buttocks, where calories are stored to meet the needs of raising a baby later.Storing fat below the waist and around the hips also balances the weight of the growing fetus in the womb.After a woman gives birth, the LPL activity below the waist decreases, and the excess fat acquired before disappears, at least most of the fat disappears; but the LPL activity on the breast breast increases, enabling women to use these fats to produce milk to feed their babies.

LPL also happens to be the best answer to the question "why don't we lose fat when we exercise".We already know that LPL activity is slightly lower on our fat cells and slightly higher on our muscle cells.This causes the fat in the adipose tissue to be released, we burn it off in the muscle cells that need fuel, and we become slightly leaner.So far so good.But when we exercise, the situation is reversed.At this time, the LPL activity on the muscle cells decreases, while the LPL activity on the fat cells rises rapidly, and the fat cells begin to restore any fat lost during exercise.We're getting fatter again.This also explains why exercising makes us hungry.It's not just our muscles that desperately need protein to recover and rebuild after a workout, our fat is also actively being restored.The rest of the body tries to compensate for this loss of energy, so our appetite increases.

Since insulin is the master regulator of fat metabolism, it is not surprising that it is also the master regulator of LPL activity.Insulin activates LPL on fat cells, especially abdominal fat cells, which "upregulates" LPL.The more insulin we secrete, the more LPL activity on the fat cells increases, and the more fat is transferred from the blood to the fat cells for storage.Insulin also suppresses LPL activity on muscle cells to ensure that muscle cells don't have many fatty acids to burn.Insulin also "tells" muscle cells and other cells in the body not to burn fatty acids, but to keep burning blood sugar so that blood sugar levels don't get too high.This means that when fatty acids escape from fat cells, if insulin happens to be high, those fatty acids are not taken up by muscle cells to be used as fuel.These fatty acids eventually return to the fat tissue.

Insulin also affects an enzyme we haven't discussed -- hormone-sensitive lipase, often shortened to HSL.This enzyme may be crucial when discussing how insulin regulates the amount of fat we store.Just as LPL acts to make fat cells (and us) fatter, HSL acts to make fat cells (and us) leaner.It does this primarily through its ability to break down triglycerides within fat cells into fatty acid molecules.In this way, these fatty acids can enter the blood circulation and be consumed.The more active the HSL in the body, the more fat we release to burn and the less fat we store.While insulin increases the activity of LPL, it also inhibits the activity of HSL.

All it takes is a little insulin to accomplish the feat of cutting HSL, trapping bulk fat in fat cells.When insulin levels rise, even by a tiny bit, fat builds up in the fat cells and doesn't get out.

Insulin also kicks in a new skill in the fat cells -- causing them to take in glucose, which increases the amount of glucose that the fat cells metabolize.The same is true for insulin in muscle cells.There is more glucose in fat cells, and the glucose metabolism is more vigorous, and one of the products of glucose metabolism is glycerol.At this time, these newly added glycerol molecules can synthesize triglycerides with fatty acids, and fat cells store more fat.

To make sure we have enough room to store all of our fat, insulin also has a function: it orders the creation of new fat cells in case our existing ones are full.Insulin also signals liver cells not to burn fatty acids, but to reassemble them into triglycerides and send them back to fat tissue.

In short, all insulin does in this case is increase the fat we store and decrease the fat we burn.

The same can be said for the action of insulin which makes us fat.This happens when insulin levels throughout our body are elevated.

This is why people with diabetes often gain weight when they are treated with insulin.The authoritative journal of diabetes "Joslin's Diabetes Mellitus" (Joslin's Diabetes Mellitus) clearly wrote that obesity is caused by "the direct production effect of insulin on obese tissue". In 2008, "The New England Journal of Medicine" (The New England Journal of According to a study in the Journal of Medicine, patients with type 3.6 diabetes gained an average of 9 kg after receiving intensive insulin therapy; almost a third of diabetic patients gained [-] kg over a period of three and a half years.

Since insulin levels in the blood are primarily determined by the sugars we eat, it is these sugars that ultimately determine how much fat we accumulate.What follows is a chain reaction of events.

1. You want to eat a meal that contains sugar.

2. You start secreting insulin.

3. Insulin signals fat cells to stop releasing fatty acids (via HSL) and start taking more fatty acids from circulation (via LPL).

4. You feel hungry, or get hungrier.

5. You start eating.

6. You secrete more insulin.

7. Sugars are digested and enter the blood circulation as glucose, resulting in an increase in blood sugar levels.

8. You secrete more insulin.

9. Fat from food is stored in fat cells as triglycerides, some of which are converted to fat in the liver.

10. Fat cells get fat, and so do you.

11. Fat stays in fat cells until insulin levels drop.

If you wonder if there are other hormones that make us fat, the answer is: no, with few notable exceptions. A presumably exception is the hormone that stimulates acylation-stimulating proteins, discovered in the late 20s, but which is secreted by adipose tissue itself, and the process is partly regulated by insulin.

One way of thinking about hormones is that they tell the body to do certain things—grow and develop (somatropin), reproduce (sex hormones), flee or fight (adrenaline).They also provide usable fuel for these diverse activities.They have another job, too, in that they signal fat tissue to mobilize fatty acids to make available fuel.

For example, we respond to threats by releasing adrenaline, which prepares us to either flee or fight.However, if there is a lion charging at you in front of you, you know you have to run, but you lack the emergency fuel to run faster or farther (possibly both) than the lion, and the lion will grab you.So when you see a lion, you release adrenaline; the adrenaline, which may be busy with other things, immediately sends a signal to the fatty tissue to get the fatty acids into the bloodstream quickly.Ideally, these fatty acids will provide all the fuel you need to escape.In this sense, all hormones except insulin prompt adipose tissue to release fat.They make us thin, at least temporarily.

However, if insulin levels are high in the bloodstream, other hormones have great difficulty making fat tissue release fat.Insulin acts far more than other hormones, and it is very necessary.Because if there's a lot of insulin around, that means there should be a lot of sugar around to burn, indicating higher blood sugar levels.That way, we don't need or want fatty acids that get in the way.As a result, other hormones can release fat from adipose tissue only when insulin levels are low.Other hormones work by stimulating HSL to break down triglycerides, but HSL is so sensitive to insulin that other hormones cannot overcome this property.

The hormone cortisol is a particular exception.This is a hormone that we secrete when we are dealing with mental stress or anxiety.The real function of cortisol is to put fat in and out of adipose tissue.It puts in fat by stimulating LPL (lipoprotein lipase), like insulin does, and it also puts in fat by triggering or exacerbating what's called "insulin resistance," which I'll get into in the next chapter elaborate.When you become resistant to insulin, the body has to secrete more insulin and store more fat.

So, cortisol makes us store fat both directly (via LPL) and indirectly (via insulin).But then, like other hormones, it causes fat cells to release fat, mainly by stimulating HSL.So, when insulin is high, cortisol, along with insulin, makes us fat; but when insulin is low, cortisol, along with all the other hormones, make us lean.This may explain why some people gain weight when they are stressed, anxious or depressed, or overeat, while others do the opposite.

For more than 40 years, we have been engaged in such metabolic research.We now know that if we want to be lean we have to pull fat out of adipose tissue and burn it off - and one of the things we have to do is lower our insulin levels.If we can keep insulin levels reasonably low, we can burn fat.If we can't lower insulin levels, we won't be able to burn fat.

When we secrete insulin, or have abnormally high levels of insulin in our blood, fat accumulates in adipose tissue, so we gain weight.This is what science tells us.

Where does fat come from, where does it go, and which hormones are regulating it? We have already understood the general situation.During the day, when we digest our meals, we gain fat because sugar intake raises insulin levels; we burn fat until the next meal and at night while we are asleep.Ideally, the fat gained during the fat storage phase is balanced by the fat burned during the fat burning phase.The fat we gain during the day is burned off at night, and insulin essentially controls this cycle.As I said, when insulin levels go up, we store fat; when insulin goes down, we call on fat for fuel.

This means that anything that causes us to secrete more insulin than normal, or keep insulin levels high for longer than normal, will prolong the fat storage cycle and shorten the fat burning cycle.In the hours after a meal, as blood sugar levels drop to pre-meal levels, we rely on fatty acids for fuel.

However, insulin inhibits the outflow of fatty acids from fat cells, which tells other cells in the body to preferentially burn sugars.So, if insulin levels stay high, we don't have available fat for fuel.We also can't use the sugars that were previously stored in the liver and muscle tissue because insulin locks them up too.

As a result, cells find themselves severely starved of fuel, and we can literally feel their plight: starvation.We either ate earlier than usual, or more than usual, or both in tandem.That's it, anything that makes us fat will make us eat more, and that's the result of insulin.

At the same time, as we store more fat, our body size increases, which further increases our need for fuel.As a result, our appetites also increase—especially sugar cravings, since this is the only nutrient our cells can still burn as fuel when insulin levels are high.This is a vicious circle that we should try our best to avoid.If you think about it carefully, when we have a tendency to gain weight, we will be driven by the body to seek out those foods rich in sugar, isn't it?

(End of this chapter)