This week I received a letter asking how insulin causes us to gain weight and store fat. “How does too much insulin make one fat?,” commented the writer.
And the answer is: “We don’t exactly know yet.” But we’re figuring it out, a little at a time. The biochemists, who work at the cellular level, appear to be figuring it out first. The rest of us can tell firsthand that the information we get from TV advertisements and cereal boxes doesn’t help much. The fact that our epidemic of obesity and diabetes is getting worse all the time shows that this information isn’t accurate. If things continue to get worse no matter how hard you try, it’s time to reexamine the fundamentals. If you can’t stop your head from hurting no matter what you do, it’s time to stop banging it against a wall. There is a name for nutritional claims on food products. It’s called advertising.
OK, so what do we understand? We understand that insulin (and other enzymes) is released in response to some kind of signal that is sent to the pancreas (and other parts of the gut) when we start to eat. There is new evidence that this signal is actually sent in anticipation of eating, in other words, BEFORE the food actually enters our mouths. This is not a surprise to me. Our own language actually contains evidence of this phenomenon in the expression “mouth-watering.”
We understand that food causes your blood sugar to rise, as it should, and that the pancreas releases insulin in response to those rising blood sugars. The insulin escorts the sugar to cells, sugar is thus removed from the bloodstream, and blood sugars return to their pre-meal levels.
In a previous post, I discussed the fact that the faster you absorb your food, the faster your blood sugar rises, and the more insulin you need to catch the sugar and remove it from the bloodstream. Insulin is the fat-storage hormone; the more insulin we use, the more fat we store. Also, there is something about the RATE at which you absorb sugar that dictates how much insulin you are going to need. If all the sugar shows up at once, you need a load of insulin to catch it. If the sugar drips in bit by bit, you only need a little bit of insulin to catch it. You can read more about this at my post, “Eating Toast and Jelly for Breakfast Wastes Your Insulin.”
Where does the sugar go next? Some sugar molecules get used immediately by working muscles and thinking brains. Some go to our liver, where they are collected into strands of glycogen. Glycogen strands are like pearl necklaces whose pearls can be popped off later, one at a time, to keep our blood sugars normal between meals and while we sleep.
The rest of our blood sugar gets stored as fat. That makes sense. If you don’t need it now, and you have enough for later, then the rest should go into deep storage. Fat is deep storage. We store fat in the form of triglyceride, which is a molecule that consists of three fatty acid chains attached to a glycerol molecule. Glycerol is made from the sugar that comes from the carbohydrates in our diet. The more carbohydrate we eat, the more sugar becomes available to form glycerol. The more glycerol we make, the more triglyceride we make and the more fat we store. The amount of available glycerol dictates how much triglyceride we can make. So carbohydrate is an essential component of fat storage. That’s really important.
Remember that triglycerides are composed of 1 glycerol plus 3 fatty acids. The source of fatty acids is dietary fat. Our brains are designed to be able to use as fuel not only sugar, but also fatty acids. Interestingly, as far as insulin is concerned, fatty acids are a free ride. You don’t need insulin to catch fat the way you do to catch sugar. So after fat (in the food we eat) is digested and broken down into free fatty acids, those free fatty acids can either be used right away, or they can be attached to glycerol molecules to make triglyceride molecules. Then all those triglycerides are stored in body fat.
Triglycerides are a big molecule. They are too big to move across a cell membrane, so they must be transported across as individual components, and then reassembled into a triglyceride molecule inside the cell. This reminds me of the huge breakfront that we inherited from my husband’s grandparents and which has sat in my dining room all the years of my married life. It’s so big that we can’t get it through doorways, so when we have moved we have had to take it apart. The top detaches from the bottom in a very clever way that always gets my admiration. It’s an ingenious design that makes it simple to move what would be an unwieldy piece of furniture, and which would otherwise have been obliged to remain forever in the room in which it was built. In much the same way, triglycerides circulate in the bloodstream and accumulate in cells, but the fatty acids of which they are composed continually pass across cell membranes, cycling into triglycerides and back.
Now, let’s talk about insulin again. A great number of hormones in our bodies help to break down triglycerides and release fatty acids for use (as fuel). But not insulin. Insulin is the one hormone that facilitates triglyceride storage. In the presence of insulin, we will always store fat, and not release it. Insulin is the stimulus for fat storage. In order to release fatty acids, the level of insulin must be low. For fat cells to release their fatty acids, there must be a relative deficiency of insulin in the body. That makes sense, because our insulin levels should be high only when we have just eaten, and that is the one time when there is no need to break down fat to obtain nutrition.
Therefore, because the high-insulin state prevents mobilization and use of fatty acids, it becomes impossible to lose weight in the presence of large amounts of insulin. We store fat independent of our food intake, and we gain weight when insulin exerts its effect on body fat. More as the story develops…