This is a really good question. I did read an interesting article along similar lines as this question a few days ago that might help a bit with the confusion. It doesn't directly answer all of your questions, but some of the commentary will explain the mechanisms a bit.

The ‘Healthy Obese’ and Their Healthy Fat Cells
http://well.blogs.nytimes.com/2013/10/09/the-healthy-obese-and-their-healthy-fat-cells/?smid=fb-share

Lastly, wikipedia has a nice article on fatty acid metabolism which discusses how fat is stored in the body as well:
http://en.wikipedia.org/wiki/Fatty_acid_metabolism

The neutral lipids stored in adipocytes (and in steroid synthesizing cells of the adrenal cortex, ovary, and testes) in the form of lipid droplets, with a core of sterol esters and triacylglycerols surrounded by a monolayer of phospholipids, are coated with perilipin, a protein that acts as a protective coating from the body’s natural lipases, such as hormone-sensitive lipase.[4][5] However, when hormones such as epinephrine are secreted, or when insulin levels drop in response to low blood glucose levels, this triggers an intracellular secondary messenger cascade that phosphorylates hormone-sensitive lipase to break triglycerides into glycerol and free fatty acids for use in metabolism, a process called lipolysis.

The reference that gives the above quote in the Wiki article links to a really cool couple of graphs of how it works:
http://pharmaxchange.info/press/2013/10/mobilization-and-cellular-uptake-of-stored-fats-triacylglycerols-with-animation/

Thanks for asking this! It's a really interesting topic.

A message goes to cells to say, "dude, we need you to release some krakens"?

I imagine some fat cells more readily shed their stuff while others cling on to the fat.

Do most of our fat cells get collectively smaller over time (I read it's rare for us to shed the actual cell, only its contents)?

Thank you in afvance for indulging my nerd

You pretty much nailed it!

Lipid is released from adipocytes (fat cells; basically just cells that store lipid) when the body needs energy that is not provided by easily metabolized energy from the diet (ie calories). The lipid is broken down into smaller units that provide energy for other cells. Fat cells never go away, just get smaller (or bigger as the case may be). Certain adipocytes have more receptors on their surface to receive signals to mobilize lipid -- for instance in women, subcutaneous fat on the lower body has fewer receptors so is much slower to be metabolized than fat elsewhere.

I don't know the ins and outs of it, just the big picture stuff. But I agree it's very interesting!

Also, from now on, I'm going to refer to fat loss as the release of the krakens... LOL

The amazing thing to me is that we know any of this stuff at all. How did we figure it out?

I also liked the part about how we would have to carry around 38 lbs of carbs to equal the energy of 10 lbs of fat. Kind of makes you appreciate fat!

Some of the advances in biochemical research has been nothing short of phenomenal in the last 50 years. I bet if you dig around and follow the trail of papers in the last link I posted above, you'd find out how they did it. Cool stuff!

Thanks so much for this discussionand the research!

Jsl_mfp, I agree...it is amazing this science is known.

Our daily internal processes seem so complex. Yesterday I had an endurancelifting day on legs, and also logged 15k steps. Despite eating a bit below my cut, todayI still gained a bit. I'm guessing water, but I'd love to know and see the whole breakdown of that process. Sort of like that 80s movie innerspace

Yes. Your muscle will retain water to heal. That's why it's constantly said in the forums to rely more on measurements versus the scale because how easily it fluctuates.

Tagging to have a read and see if I have anything to add, but unlikely considering who has posted. Sorry - missed this earlier.

On a slightly related and interesting tangent, lower body fat in women is actually supposed to be good for you, so don't try to lose it all (in my case that seems to be impossible). It is cardioprotective, associated with better lipid profiles and lower risk of diabetes.

I first read that as lower + bodyfat, instead of lower body + fat - and wondered why the second part of the sentence didn't jell with the first.

Sorry for the confusion . I actually didn't realize I was posting in this group at the time (since I came to it from a link in my newsfeed) or I would have said gluteofemoral fat. I feel like I can use bigger words in this group than in the forums.

On a slightly related and interesting tangent, lower body fat in women is actually supposed to be good for you, so don't try to lose it all (in my case that seems to be impossible). It is cardioprotective, associated with better lipid profiles and lower risk of diabetes.

I first read that as lower + bodyfat, instead of lower body + fat - and wondered why the second part of the sentence didn't jell with the first.

Sorry for the confusion . I actually didn't realize I was posting in this group at the time (since I came to it from a link in my newsfeed) or I would have said gluteofemoral fat. I feel like I can use bigger words in this group than in the forums.

:flowerforyou:

Am I also correct in my understanding that our quantity of fat cells is determined by our size/weight/athleticism up until early 20s with teenage years being significant?

I'm thinking about my daughters here, as if this is the case, and they are encouraged to be healthy and fit during this time it would both 'set' the fat cells that they possess and set good habits (activity and intake) for the rest of their lives?

I'm already astonished (they are 6 and 4) at how different they are - the elder will gladly sit all day in front of the TV if allowed, concentrate for ages doing amazing drawings etc while the younger gets bored with the TV quickly, prefers helping (cooking/cleaning/whatever) and will race from kitchen to sofa and back again over and over just for the giggles, loves being outdoors..

Yes, there was a big paper out in the journal Nature in 2008 to this effect (unfortunately I could only access the abstract):

http://www.ncbi.nlm.nih.gov/pubmed/18454136

They suggested that fat gain in adulthood is due to hypertrophy (increase in size of the cell) rather than hyperplasia (increased number of cells). I don't know the practical significance of this in terms of the likelihood of overweight children to more easily gain weight as adults or if that has been teased apart from the learned/behavioral side of things.

Another interesting paper criticizes the conclusions of that study for only looking at abdominal fat:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2964201/#!po=7.89474

This is a good paper. They claim that while abdominal fat cells tend to get bigger, femoral fat cells multiply in number even in adulthood (and this study looked at an over feeding period of 8 weeks, so it really didn't take much). 

It's interesting that in the link sapienspisces posted above, it's the large fat cells that are metabolically abnormal and associated with greater health risks (http://well.blogs.nytimes.com/2013/10/09/the-healthy-obese-and-their-healthy-fat-cells/?smid=fb-share).

So actually, adipocyte hyperplasia (meaning making more fat cells rather than overfilling the ones you already have) is a good thing and they postulate that hyperplasia of femoral adipocytes may be protective to the extent that they prevent hypertrophy of abdominal fat stores which is tied to cardiovascular and metabolic disease.

From the discussion:

Our data suggest that the ability of healthy adults to expand lower-body fat via hyperplasia may prevent or delay abdominal s.c. fat-cell hypertrophy, presumably by sequestering the excess fat (Fig. 2B). An alternative mechanism is that some individuals display an overall adipose hyperplastic response to energy overload. This response was most evident in the women who had larger adipocytes at baseline, in whom the average size of mature adipocytes decreased in both depots with fat gain (Fig. 2B and Fig. S1). This finding supports the recently reported link of high rates of adipogenesis with smaller size of abdominal s.c. adipocytes, lower waist-to-hip ratio, and more favorable metabolic profile (20). . . . Our observations are consistent with the overflow hypothesis, which implicates lower-body fat as a primary adipose tissue compartment for expansion, the capacity of which may determine the degree to which secondary (upper-body s.c. and visceral) adipose tissue compartments grow during fat gain (22)."

I love it when it all comes together!