Let's begin with LPL lack of protein lipase. So sticking outside all of our fat cell membrane, our little receptors that secrete something called lipoprotein lipase and lpo isn't it enzyme that breaks down the bonds of fats, in other words, the triglycerides into these smaller fatty acids. And the reason why this is important is because on their own triglycerides are too big to enter the cell from the blood. the pores of the membrane are just too small to accommodate them. Now, because LPL breaks the bonds into smaller fatty acids, they are not small enough to flow from the blood. In fact, the cell so LPL literally Facts circulating fat into the cells.

Not insulin stimulates the action of LPL. In the presence of insulin, more fat is broken down sir, more of those triglycerides are broken down into small fatty acids, so that they can be sucked into the fat cell. And what is interesting is that some areas on our body have more LPL receptors than others. And it follows that the more LPL receptors that are on a cell and in an area, the more fat is going to flow into the cell in a particular area. And the more incident the cells are exposed to the more flat fat flows in not all cells have some LPR receptors, but some have very few like the back of the hand and some have many like tummies or bad And there's also a genetic influence as to where we have more LPR receptors. Some very lean people have more LPL on their muscle cells, rather than on their fat cells.

And for them, the fact that flows into the muscles is burned as fuel. But insulin also suppresses lpo muscle and stimulate appeal, in fact, so with a high carbohydrate diet, and therefore lots of insulin, the ability of the muscle cells to burn fat is reduced, and the flow of fat into the fat cells is enhance, so we get a double whammy. So to avoid our fat cells getting fatter, we need to keep insulin flow to a minimum. LPR sensitivity also changes in the presence of other hormones such as estrogen and testosterone. Estrogen suppresses LPs in the gut in Women, and as we hit menopause and Eastern levels drop off. If there is a high level of insulin stimulating LPL and the suppressive effects of estrogen are dropping off, then we're going to gain more fat on our belly as we age.

And I think for many of us, as we hit 40 and over, we notice that where are we gaining weight tends to be unhappy. Similarly, to stop during suppresses lpo activity in the get for men, so as men age and their testosterone drops off, they will also gain belly fat HSL or hormone sensitive lipase. Now conversely, HSL works inside the cell. So we're LPL has little receptors that stick out of the sell. HSL works within the cell, but it has a similar action to LP In that it also breaks the triglyceride bonds into their component glycerol and three fatty acids. So in a normal functioning cell, the HSL acts on the triglycerides, breaking them, breaking them up.

So they can flow out of the cell membrane of the fat cells to be burned as fuel. And we want the fat to flow out, and we want it to be burned as fuel. So it's important to have effective HSL in the cells, how insulin suppresses HSL in the cell, so it blocks the outward flow effect. So to summarize, incident stimulates LPL, thus increasing the inward flow effects and inhibit HSL which blocks the outward flow affects both results leave us in a situation Were we just gating and staying fat. But you can see again from this, that incident is a strong influencer. And if we can try that incident of course, we get a control what happens with our LPL and what happens happens with our HSL