Monday, November 26, 2007

Getting fat, staying fat

Fat gets in to fat cells from lipoproteins in the blood stream. Dietary fat is transported in chylomicrons, big fat ladened lipoproteins made by the gut wall. Their production is as random as fat consumption is variable.

Our the bodies never just move fat molecules intact. They are always broken down in to fatty acids, moved across cell membranes in this form, and then reassembled in to triglycerides for long term storage.

The enzyme which performs this break down process is called lipoprotein lipase. Lipoprotein lipase is thus essential for fat storage. That's important.

Fat breakdown, for use as an energy supply, is performed by a completely different lipase, this time it is hormone-sensitive lipase. This enzyme acts on the stored triglycerides inside fat cells and releases free fatty acids in to the blood stream. This is a highly regulated process, finely tuned to supply the energy needed by the body. It is very different from the bulk transport of dietary fat in lipoproteins. As such, the fatty acids can be transported in free form called non esterified fatty acids (attached to albumin in plasma) and simply released as they are needed. Hormone-sensitive lipase is crucial to fat breakdown. That's important too.

It is very obvious, from its name, that hormone-sensitive lipase is under hormonal control. The only hormone which turns off this lipase is insulin.

This paper (From way back in 1964, this is not new information. Physiologists asked very basic questions in those days) shows clearly that insulin, at levels way too low to do anything related to glucose, stops the release of fatty acids from fat tissue. So anything which raises insulin levels blocks fat break down. Carbohydrate raises insulin levels. Insulin blocks fat breakdown. Carbohydrate blocks fat breakdown.

Back to that other lipase, the one that puts the fat in to fat cells in the first place. Is that under any sort of control? Of course it is, our bodies control everything. Guess which hormone controls lipoprotein lipase.

Yes, insulin again.

So insulin has two effects on body fat. It puts it on and keeps it on.

But dietary fat, the primary source of the fat we store, has absolutely no effect on blood insulin levels what so ever. You can eat a block of lard and not budge your insulin levels one iota (or a cup of cream, much more enjoyable). What causes us to store dietary fat, as a big bum or tum, is dietary carbohydrate, because it elevates blood insulin level more than any other food source.

So the take home message from this post is that insulin is the key hormone for fat storage. Dietary carbohydrate makes you store dietary fat, and eating carbohydrate stops you burning stored fat.

It makes you think of those Swedish children. Eating sugar makes them fat, eating saturated fat keeps them slim. Now you know why.

If only nutritionists understood this.


PS does eating half a kilo of lard per day make you put on weight? Possibly, as there is a basal rate of lipoprotein lipase activity irrespective of insulin levels. More importantly, have you ever tried to actually eat 500g of lard in a day? Palatability apart, if you did actually succeed, you would feel dreadful and I doubt you would be tempted to repeat the experience. The vast majority of people on mildly ketogenic high fat diets seem to stabilise their food intake somewhere between 1500 and 2500kcal/day. That is appropriate for weight loss or weight stability, depending on your baseline weight and activity level.


Chris said...


with respect to your PS on this post, have you ever looked at the role of Acylation Stimulating Protein (ASP)?

There is an article here for example:

I came across this in reading something the other day where the author was saying that while fat will not give an insulin response, Insulin is not the only hormone to worry about with respect to storing fat.

ASP he said is activated by chlyomicrons in the blood without any increase in insulin and eating fat even in the complete absence of insulin will affect both fat sorage and breakdown.

Two papers he pointed to are at


Any thoughts?

Peter said...

Hi Chris,

Thanks for that, haven't chance tonight to check the refs but it doesn't surprise me. Within a given macronutrient framework calories do seem to matter, you CAN gain weight LC if you eat enough fat. It can be quite difficult, but you can do it. Even kids on ketogenic diets grow, though perhaps not as well as those eating a little more carbs.

I'll have a read soon



Peter said...

And looking at the other end of the process, adipose tissue breakdown, hormone sensitive lipase is not the only system available. HSL knockout mice do do lipolysis, just not very well.... I guess that's evolution for you!


Chris said...

thanks for the comments.

Reading further ASP only really acts in terms of fat storage. Fat mobilisation and oxidation seem much more limited by insulin. Maybe it is just at the extremes of intake that ASP becomes an issue.

blackberrythorn said...

This is all very interesting but leaves me no further in making your son's birthday cake. Sculpt something suitably geeky out of lard perhaps?

Peter said...

Hmmmm, well I picked your comment up a day too late to suggest that something based on marscapone cheese, topped with 85% cocoa chocolate diluted with butter and cream over a base of ground nuts set in butter tends to taste better...... Add judicious glucose powder or a little honey to flavour, not too much.

Of course I was just going to give him steak when he gets up tonight.... Oh, maybe I should make the cake?????? Good idea.


Unknown said...

Peter, have you heard of the Chinese Restaurant effect that Dr. Bernstein describes in his book, The Diabetes Solution? He says that overeating through the mechanism of stretching the stomach and gut will stimulate insulin (and glucagon, adna bunch of other stuff as well). It's relevant for Type I diabetics as glucagon is released with huge amounts of eating, which can not balanced with insulin. Overeating is a stimulant for insulin release. What do you think?