Fat Tissue Expansion: Part II ~ Overview of How it Can Happen

In Part I, I laid out some terminology that we'll use in the discussion of how we get fat.  In this installment, I'm mostly going to list the various means by which fat tissue can expand, emphasis on the word can.  Because as future installments will lay out, while some of these mechanisms are plausible, some of these mechanisms contribute very little if at all to the fattening process. 

So what mechanisms might be involved in the expansion of fat tissue?  It is not controversial that fat tissue expands by two means:
  • Adipocytogenesis:  The growth of new fat cells, increased fat cell number
  • Adipocyte growth:  Increased size of adipocytes

Fat tissue also contains blood vessels and connective tissue, the amount and mass of which no doubt increases and decreases with expansion and contraction of the tissue.  I consider this to be a negligible component, or at the very least out of our control and proportional to adipocyte size & number, so won't really discuss this.  However there are two more related "components" of fat tissue that may be significant, likely moreso the greater the degree of obesity we're talking about:

  • Adiposopathy:  Macrophage infiltration of "sick fat"
  • Inflammation and lipid associated water (mostly extracellular)
Of the above, it is the adipocyte growth, often referred to as hypertrophy in the literature, that is likely the dominant factor in fat tissue expansion, especially in adults.  Fat cells grow when there is a net deposition of triglycerides in the fat cell.  So I'll be discussing:
  • Factors favoring triglyceride deposition in adipocytes, including hormonal forces
  • Factors suppressing lipolysis & NEFA release from adipocytes
  • Sources of lipids for deposition.
There are several possible sources of the lipids that can accumulate in fat cells to make us fatter.  These are listed below 
  • Dietary fat -- chylomicrons
  • Lipoprotein particles containing lipids -- mostly VLDL triglycerides and chylomicron remnants
  • Hepatic de novo lipogenesis -- the conversion of non-lipid substrates, mostly glucose, to fatty acids in the liver
  • Adipose de novo lipogenesis -- the above, but within the fat cells themselves
  • Recycled NEFA
My apologies that my HTML skills  do not allow a nested outline format for the topics of future posts.  I'll pretty much be going in order of the topics here ... and if at some point Blogger or my HTML skills allow, I'll come back and revise this.

In Part III, I'll look at the role of adipocyte number in the growth of  fat tissue


Harry said…
Thank you for this series Evelyn.

I think it is very important that people have an understanding of the basic underlying structures/processes that are involved in fat mass gain and loss.

Hopefully this will inoculate them from some of the more bizarre claims that do the rounds in the weight loss industry (e.g. 'don't eat carbs because they will all turn to fat in the liver').

madmax said…

I really love your blog and you bring a dose of sanity to the Paleo/LC world. But I'd like to make a suggestion as you embark on a series of science rich posts. Could you give a conclusion section like Paul Jaminet where you summarize your main points. Often it is difficult for non-science people to get past alot of the terminology. At least it is for me. I have a feeling that it would be appreciated by more people than just me.
Leila said…
I would love that, great idea!
CarbSane said…
Welcome madmax! This has been suggested before and it's a good suggestion. In this case the reasons for the introductory posts are to introduce the terminology, etc., but still I can see how a summary would be helpful. Believe it or not, most of my blogging is off the top of my head. So by the time I get through my posts, which tend to be lengthy, and do at least a cursory spell/grammar check it's time to hit the publish button b/c I've already spent a lot of time writing it up.

My intent with this series is to write it up into PDF format. Not sure how that's going to work at this point. As time permits I'll try and integrate some sort of summary at least in some posts.
Craig said…
I hope that as part of this series you will give a concise explanation for how weight/fat gain happens with overfeeding on a VLC diet. I have a pretty good idea of what happens to excess calories on a mixed diet, and a high carb diet. I'm less clear about the LC case. I gather there are routes that don't involve insulin, but I'm not sure if these have been demonstrated to be significant. Some overall perspective would be nice.
bentleyj74 said…

I know there have been several articles already regarding what you asked about but sadly my short term memory isn't worth the sieve it was printed on. Maybe someone else could give better direction or the search function could help? :)
CarbSane said…
I sure plan on it. In a nutshell, acylation stimulating protein, ASP, is perfectly capable of storing fat in your fat cells without elevated insulin or blood sugar levels.