[quote]red04 wrote:
[quote]anonym wrote:
[quote]LoRez wrote:
I’m guessing it hasn’t really been studied, but I’m wondering how visceral vs subq fat are added and lost/removed. Does the visceral fat remain after losing the subq fat, or do you lose them relatively in proportion to each other?[/quote]
Awkward bump, just so this question is easier for me to quote tomorrow.[/quote]
Someone already posted a study where 7% SubQ and 6.9% Visceral fat were lost, that seems ‘relatively in proportion.’ The opposition to this study centered around the sample population as I believe they were obese+sedentary to begin wtih, but I might be mixing up studies now.[/quote]
Thanks for keeping me up to speed. This thread kinda took off over the past several days.
Without going back and looking at the study (as I cannot be trusted to do that reliably), I’ll just say that the evidence concerning changes in subQ and visceral fat seems to indicate that a) visceral fat loss is preferentially seen in the early stages of weight reduction, and b) that this effect is diminished, or lost entirely, upon greater degrees of weight loss.
There are several reasons as to why this may be, and they typically revolve around the compositional and functional differences of the tissues. In this regard, visceral fatty tissue is seen to exhibit a higher rate of basal fatty acid flux than what is observed in subcutaneous fat, an effect which is believed to be compounded by a greater affinity for the lipolytic effects of catecholamines (via an increased proportion of B-adrenergic receptors versus the alphas) and a comparatively greater resistance to the anti-lipolytic effects of insulin (via lower insulin receptor affinity). So, visceral fatty tissue appears to have a very high turnover rate compared to subcutaneous fat, which is oftentimes found to be resistant to catecholamine-induced lipolysis in the overweight/obese populations.
This would explain the significant changes in various biomarkers after moderate weight loss (e.g., Lim et al), which are commonly seen to be comparable to what is experienced even after extensive weight reduction occurs. Note that visceral fat reduction doesn’t necessarily improve peripheral insulin sensitivity, however.
The reasons for all that ^ are still the subject of a fair bit of speculation. While it is known that visceral fat exhibits endocrine effects characterized by higher output of various adipokines associated with pro-inflammatory/diabetic/atherogenic states (e.g., IL-1B, -6, -8; TNF-a; MCP-1; RBP-4l CRP), it is still a point of contention as to whether or not these biochemical factors are of greater importance than anatomical location (compared to subQ fat, fatty acid efflux from visceral tissue makes a beeline to the liver via the hepatic portal vein, which is believed to induce insulin resistance through mechanisms I don’t really want to get into right now).
Beyond that, contention still exists as to whether or not subQ fat is STILL the determining factors simply because, despite a lower output of adipokines on a per-cell basis and the systemic dilution of non-esterified fatty acids (NEFAs, or free fatty acids), there is just so much more of it in the body. In any event, there is something called the “portal theory” which nowadays attempts to reconcile both the immunological effects of adipokines iwht the physiological ramifications of excess NEFA uptake, with newer evidence incorporating the significance of the bacteria which comprise our GI tract (as large parts of the small bowel also drain into the portal vein).
It’s all still a work in progress and is beyond the scope of this thread, I guess.
