give up cigarettes.)
Hormone-sensitive lipase, on the other hand, reaches into fat cells and releases fatty acids into the bloodstream when they are needed—for example, if you’re doing a long aerobic exercise session and your legs need some fuel. Its ability to liberate fat is really intense. Consider this: there’s a protein called perilipin that shields fat from the fat-burning effects of hormonesensitive lipase. Mice that don’t have any perilipin to protect their fat from hormone-sensitive lipase don’t get fat, no matter what they eat! 15 The fatburning effect of hormone-sensitive lipase is that intense.
Insulin and glucagon have profound effects on both lipoprotein lipase and hormone-sensitive lipase. Can you guess what effects they have? By now it should come as no surprise: insulin stimulates lipoprotein lipase (the fat-storing enzyme) and inhibits hormone-sensitive lipase (the fat-releasing enzyme). If you want your fat cells to let go of fat, you want all the hormone-sensitive lipase activity you can scrounge up—you certainly don’t need high levels of insulin turning down the volume. Glucagon, on the other hand, has exactly the opposite effect on these enzymes. It inhibits the fatstoring enzyme and stimulates the fat-releasing one. This is just one more way that restoring a healthy balance between insulin and glucagon helps you to lose weight.
Fat Cells Know How to Protect Their Existence!
When you do lose weight, you stack the hormonal deck in your favor even more. We used to believe that fat cells were inert little sacks of blubber that basically didn’t do anything metabolically—they just took up space and held on to a gazillion calories’ worth of energy that never got burned up fast enough. We now know that fat cells are anything but inactive. They are actually endocrine glands that release a host of hormones—including estrogen—and other substances that can have a profound effect on our weight.
Many of the hormones that are released by the fat cells have one major purpose—to keep those fat cells in business! In this way, you might say that fat actually perpetuates its own existence by releasing hormones that make it harder for the body to get rid of it.
One of the hormones released by fat cells is resistin . The more fat cells you have, the more resistin gets released into your body. Mice given extra dosages of resistin develop insulin resistance in two days; 16 and, as we’ve just seen, insulin resistance is a major obstacle to fat loss. Another substance released by the fat cells is TNF-alpha 1, also known as tumor necrosis factor. This is a good guy: it’s part of the immune system’s arsenal, and, as you can tell by the name, it’s involved in destroying tumors. But TNFalpha 1 is also found in fat tissue, and in the circulatory system it appears to act like a hormone. In low amounts, it inhibits the ability of insulin to lower blood sugar, essentially making insulin’s job harder to accomplish and thereby forcing the pancreas to put out even more insulin to get the job done. 17 Once again, a hormone-like compound released by the fat cells raises insulin and makes fat loss difficult. As you can see, the fat cells themselves contribute to the difficulty in losing weight by releasing substances that offer “fat-protection insurance”—chemicals that, in essence, help your fat cells stay in business. By lowering your fat stores with a low-carbohydrate diet, you will also lower the amounts of these fat-protecting substances in the bloodstream.
A Low-Carb Diet Helps Reduce Insulin Resistance
When you are insulin-resistant, your cells stop making insulin receptors to import sugar and fat into the cells. This process is called down-regulation. Receptors are like job recruiters. When the market is flooded with unemployed workers, companies don’t have to go hunting for job applicants, because there are so many knocking at the door. When you’re insulinresistant, you’ve got a
Hormone-sensitive lipase, on the other hand, reaches into fat cells and releases fatty acids into the bloodstream when they are needed—for example, if you’re doing a long aerobic exercise session and your legs need some fuel. Its ability to liberate fat is really intense. Consider this: there’s a protein called perilipin that shields fat from the fat-burning effects of hormonesensitive lipase. Mice that don’t have any perilipin to protect their fat from hormone-sensitive lipase don’t get fat, no matter what they eat! 15 The fatburning effect of hormone-sensitive lipase is that intense.
Insulin and glucagon have profound effects on both lipoprotein lipase and hormone-sensitive lipase. Can you guess what effects they have? By now it should come as no surprise: insulin stimulates lipoprotein lipase (the fat-storing enzyme) and inhibits hormone-sensitive lipase (the fat-releasing enzyme). If you want your fat cells to let go of fat, you want all the hormone-sensitive lipase activity you can scrounge up—you certainly don’t need high levels of insulin turning down the volume. Glucagon, on the other hand, has exactly the opposite effect on these enzymes. It inhibits the fatstoring enzyme and stimulates the fat-releasing one. This is just one more way that restoring a healthy balance between insulin and glucagon helps you to lose weight.
Fat Cells Know How to Protect Their Existence!
When you do lose weight, you stack the hormonal deck in your favor even more. We used to believe that fat cells were inert little sacks of blubber that basically didn’t do anything metabolically—they just took up space and held on to a gazillion calories’ worth of energy that never got burned up fast enough. We now know that fat cells are anything but inactive. They are actually endocrine glands that release a host of hormones—including estrogen—and other substances that can have a profound effect on our weight.
Many of the hormones that are released by the fat cells have one major purpose—to keep those fat cells in business! In this way, you might say that fat actually perpetuates its own existence by releasing hormones that make it harder for the body to get rid of it.
One of the hormones released by fat cells is resistin . The more fat cells you have, the more resistin gets released into your body. Mice given extra dosages of resistin develop insulin resistance in two days; 16 and, as we’ve just seen, insulin resistance is a major obstacle to fat loss. Another substance released by the fat cells is TNF-alpha 1, also known as tumor necrosis factor. This is a good guy: it’s part of the immune system’s arsenal, and, as you can tell by the name, it’s involved in destroying tumors. But TNFalpha 1 is also found in fat tissue, and in the circulatory system it appears to act like a hormone. In low amounts, it inhibits the ability of insulin to lower blood sugar, essentially making insulin’s job harder to accomplish and thereby forcing the pancreas to put out even more insulin to get the job done. 17 Once again, a hormone-like compound released by the fat cells raises insulin and makes fat loss difficult. As you can see, the fat cells themselves contribute to the difficulty in losing weight by releasing substances that offer “fat-protection insurance”—chemicals that, in essence, help your fat cells stay in business. By lowering your fat stores with a low-carbohydrate diet, you will also lower the amounts of these fat-protecting substances in the bloodstream.
A Low-Carb Diet Helps Reduce Insulin Resistance
When you are insulin-resistant, your cells stop making insulin receptors to import sugar and fat into the cells. This process is called down-regulation. Receptors are like job recruiters. When the market is flooded with unemployed workers, companies don’t have to go hunting for job applicants, because there are so many knocking at the door. When you’re insulinresistant, you’ve got a
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