The SubQ Belly Fat to Visceral Fat shuffle - Keto Coach Thomas DeLauer explains!



TLDR version: We don’t burn subcutaneous belly fat directly, but it’ll be re-purposed and moved to deeper into the body to replace the visceral fat that we do burn.

Many of us (esp midlifers whose metabolisms naturally slow a bit) will see a temporary scary increase in visceral fat/belly measurements while on the long & winding road to recomposing the belly - even though being very compliant with LCHF dietary practice, exercise, etc. The belly rids our watery squishy ready-to-go subcutaneous fat by shuttling it into visceral fat before we can burn it!

I’ve been pondering my Squish City belly, knowing that change is happening - but then alarmed at an apparent increase in belly size though my subcutaneous fat is very squishy and obviously changing for the better. Listening to DeLauer talk about the process set my mind at ease, and encourages me to continue doing 18-24 hour natural IF a few days a week along with LCHF/keto. DeLauer’s video talk:


  1. Klempel MC , et al. (n.d.). Intermittent fasting combined with calorie restriction is effective for weight loss and cardio-protection in obese women. - PubMed - NCBI. Retrieved from…

  2. Fasting induces a subcutaneous-to-visceral fat switch mediated by microRNA-149-3p and suppression of PRDM16. (2016, May 31). Retrieved from…

  3. Plasticity of adipose tissue in response to fasting and refeeding in male mice. (n.d.). Retrieved from…

  4. Fasting induces a miRNA-mediated subcutaneous to visceral fat switch. (2016, 1). Retrieved from…



I’m very TL;DR when it comes to videos due to bandwidth constraints etc. so I appreciate you digging out the source material. Going by your description, I’m not seeing the stated conclusion in the studies you linked from the video. One of the studies [Plasticity of adipose tissue… pdf] states what I believe is the opposite, or at least that visceral fat is used first and subcutaneous second, but the visceral should not increase during this process.

Fasting preferentially consumes lipids in visceral adipose tissues, whereas refeeding recovers lipids predominantly in subcutaneous adipose tissues, which indicated the significance of plasticity of adipose organs for fat distribution when subject to food deprivation or refeeding.

Another study [Intermittent fasting combined with calorie restriction…] has an evaluation of visceral vs subcutaneous fat in male mice with a picture (Figure 3) which shows more loss in visceral than subcutaneous.


A. Abdominal visceral fat (58 cm2) and subcutaneous fat (245 cm2) before the intermittent fasting calorie restriction
B. Abdominal visceral fat (17 cm2) and subcutaneous fat (173 cm2)

And finally the study[Fasting induces a subcutaneous-to-visceralfat switch…pdf] is talking about the metabolic shift from WAT to beige (browning) of subcutaneous fat, not the physical relocation of the fat.

I’m not sure what I’m missing here??

My take on this is that visceral fat is used first during weight loss, in much the same way MCTs go directly to the liver through the portal vein. The FFA released from your subcutaneous fat during low enough insulin conditions is processed through the liver with the leftovers being recirculated or rexported. At that point, where the fat goes (if it’s not used by muscle etc.) should be into subcutaneous fat. There might be a roadblock exporting fat from the liver with a large influx of FFA during fasting given insufficient choline for the amount of fat being processed.

A lot of visceral-intestinal fat (mesenteric) can be inflamed fat which contains fluids that can’t be easily distinguished from the adipose tissue.


Hmmm, I think there are different phases to it… and DeLauer springboards off the research by reframing into a LCHF/keto physiology context, and the video also adds a perspective on gene triggering context.

Yes, excess visceral fat is dealt with first during fat loss, leaving the baseline visceral fat - which is essential and highly functional brown fat. Then, inactive adipose is metabolically converted into visceral/brown fat, which then gets burned - maybe it doesn’t move per se?

The metabolic shift involved is fascinating - maybe it’s that subQ fat repurposes itself and baseline healthy brown/visceral fat increases at the same time due to the fact that the brown fat is full of circulation channels?

I’ve heard from a few well fat-adapted keto-compliant folks around here about their visceral fat increasing (whether via DEXA or measurement of upper belly) - and I know that metabolic changes in midlife (esp female) multiply the visceral fat. But DeLauer’s talk elicited my thought that there could well be a LCHF/keto recomp that recruits the visceral/brown fat as a physiological stabilizer/buffer/processor? I do know the body likes buffers/filters, etc. Makes sense to me on an intuitive level, but I’m not biochemistry-informed enough to compute both your analysis, DeLauer’s, and the studies lolol.

If you can give it a listen Carol, maybe the new insights on genetic stuff will provide the missing link? My post is just a brief-brief, and you know much more than I do about the LCHF/keto fat-burning adaptations. I’d love to understand what’s what with this, as the LCHF/keto midlife-middle is quite a conundrum and want to feel more optimistic about it the weird the SubQ Squish City and incredibly slow processes behind the scenes… :thinking:


Will do. I might wait for a period of high ketones to attempt this feat. :joy:

(Erin Macfarland ) #5

This is fascinating thank you for sharing!


Thanks a million! Yes, always good to wait for the excellent ketobrainz for such tasks.

(Troy) #7

Interesting :smile:

White Fat to Brown Fat
Brown Fat to White

Gene A to Gene B
Gene B to Gene A

Summary -
Work out in a Fasted State
This ALWAYS works for me and I will continue to do so

I’m turning in my paper to Thomas Now🤣

(Kristen Ann) #8

Ahhh this explains so much! My stomach measurements were increasing as everything else was decreasing. I stopped measuring bc I hated how weird my stomach looked and I preferred to ignore it. Thanks for sharing.


First of all, when looking at mouse studies involving fasting, keep in mind that 48 - 72 fasts in mice are a near death experience for them. It would be the equivalent of a much longer fast in humans.

This study revealed enhanced mitochondrial biogenesis in visceral adipose tissue caused by fasting, as evidenced by the increased mitochondrial numbers and the expression of Pgc-1α in visceral adipocytes. Ucp-1 is not only a BAT-selective gene but also a thermogenic marker.

I think where DeLauer goes off track is with the notion that increased thermogenesis via the browning of white fat in subcutaneous belly fat is the same thing as “burning fat” to get rid of it. Brown fat uses thermogenesis by increasing the number of mitochondria that generate heat energy via uncoupling. The fat cells do not go away or “burn up” - they use glucose for energy to keep us warm.

When the WAT becomes more metabolically active, it is using up energy to produce heat. Fat only goes away by releasing fatty acids into the bloodstream to be metabolized by the liver into glucose, ketones and ultimately CO2 and water. Fat cells themselves don’t go away just because they are empty, and new ones are only created from progenitor cells as old ones die off in a ~10 year cycle.

Here’s Dr. Bikman to explain the process of browning and uncoupling:

What miR-149-3p has to do with it is based on the browning of inguinal fat (iWAT) in fasted mice. They take this as a starting point to do some experiments exposing newly forming fat cells to different levels of miR-149-3p in a lab, and seeing how they turn out when they grow up. They did not “give the subjects a drug”. They are manipulating cells in a dish. Only the inguinal cells are receptive to this manipulation which results in the ability to brown when the need arises later in life. (humans also have a brown fad pad between the shoulder blades)

Part 1:

Here, we show that after 24-h fasting, the subcutaneous adipose tissue of mice acquires key properties of visceral fat. During this fast-induced ‘visceralization’, upregulation of miR 149-3p directly targets PR domain containing 16, a key coregulatory protein required for the ‘browning’ of white fat.


To identify whether miR-149-3p alters the function of subcutaneous adipocytes, we isolated SV cells from the ingWAT of mice and induced their differentiation into beige adipocytes …
In cultured inguinal preadipocytes, overexpression of miR-149-3p promotes a visceral-like switch during cell differentiation.

Now we get to the cold-reaction vs. fasting and how the fat cells react in the body. Cold therapy increases the browning of cells (look up Wim Hof, the Iceman) but fasting conserves energy by whitening fat cells. So you have two opposing forces dependent on energy regulation and the need to stay warm.

If you watch all the way to the end of the video, he says it’s a “play on words”.


So, browning instead of burning… I like it in cooking, makes me think this whole topic smells like browned clarified butter :joy:

The opposing forces dependent on energy regulation and heating is really interesting. From what I’ve been reading today, there is both “constitutive” brown fat we’re born with and “recruitable” brown fat, the kind that gets accessed through super slow strength training or weight-bearing activity (which is both aerobic and anaerobic). Mitochondrial furnace activation is part of this process…

I read somewhere that a protein called irisin may be playing a role to transform white fat to brown.

Seems like the browning of SubQ fat is part of metabolic healing in the belly, as it’s more active - and more brown fat in the belly along with very squishy belly SubQ could go together as a very good sign of recomposition (or, sometimes it’s just that DEXA scans are inaccurate or measurements are off due to bloating).

I’ll watch that Bikman video, thanks so much Carol!