(Versión en español: pinchar aquí)
In general, insulin stimulates net fat deposition.
I’ve mentioned before my opinion on the carb-insulin hypothesis of obesity (see) . In short , I think, wether it is correct or not , it provides a way of thinking that leads to better decisions about what to eat. Moving from asking how many calories a food has to what effect that food has on our blood glucose and insulin, is positive. That is my view.
Although I’ve already written about the role of insulin in the adipocytes elsewhere, I will insist a little now.
First, in the article”Integrative physiology of human adipose tissue” we find the following schematic diagram illustrating the process of fat absortion and release in adipocytes (yellow circle) :
In the figure caption we can read: “In general, insulin stimulates net fat deposition“. We can see in the scheme how on one hand insulin stimulates the uptake of fatty acids (indicated by two + signs) into the adipocyte, while on the other hand it suppresses the mobilization of the fat already inside of the adipocyte (indicated with a – sign in the scheme). In the text of the article we find the following explanations :
In human adipose tissue, the capacity for de novo lipogenesis (DNL) appears to be low, and the contribution of DNL generally to metabolism appears not to be significant except perhaps under conditions of overfeeding with a high-carbohydrate diet
However, during normal, eucaloric conditions it seems that most of the TG deposited in adipose tissue arises from the pathway mediated by lipoprotein lipase (LPL)—hydrolysis of circulating lipoprotein-TG, followed by uptake of the fatty acids, and esterification to glycerol 3-phosphate. Both the activities of adipose tissue LPL and the pathway of esterification are stimulated by insulin, leading to a very energy-efficient pathway for storage of dietary TG in the postprandial period.
The pathway of fat mobilisation is exquisitely sensitive to suppression by insulin. The half-maximal insulin concentration for suppression of fat mobilisation in humans is around 90 pmol/l,16 whereas that for glucose production is around 200 pmol/l. When insulin is infused to moderately high physiological concentrations, there is therefore complete suppression of nonesterified fatty acid (NEFA) release from subcutaneous adipose tissue. This is brought about by a dual action, inhibition of hormone-sensitive lipase (HSL) by dephosphorylation, and stimulation of the re-esterification of fatty acids by the pathway described earlier.
The role of insulin as a fattening hormone seems to be undisputed. From other sources:
The major effects of insulin on […] lipid metabolism: (a) it decreases the rate of lipolysis in adipose tissue and hence lowers the plasma fatty acid level, […] (c) it increases the uptake of triglycerides from the blood into adipose tissue and muscle, […]
The buffering of fatty acids by insulin is mainly regulated by the suppression of lipolysis and NEFA release from the adipose tissue via a decrease in the activity of hormone-sensitive lipase (HSL) and adipose triglyceride lipase (ATGL), and the increase of triglyceride clearance through an increase in the activity of lipoprotein lipase (LPL).
In short, the effect of insulin is moving triglycerides from the blood into the adipocyte, and suppressing their release from the adipocyte. Is insulin important when talking about why we get fat? No doubt.
Is the caloric intake important for fat deposition? I have already (see) answered that, with another question, how does the adipocyte know that we have eaten too much and moved too little that day? Is there a receptor in the adipocyte that tells it to absorb or not to absorb fat as a function of how much we ate? What is the consequence of eating too much on a cellular level? Because, you know, fat deposition only exists at the cellular level, not in Neverland.
Does all that mean the carb-insulin hypothesis is true? No, it doesn’t. But it suggests that it makes more sense than “eat less and move more”.