las

Welcome all seeking refuge from low carb dogma!

“To kill an error is as good a service as, and sometimes even better than, the establishing of a new truth or fact”
~ Charles Darwin (it's evolutionary baybeee!)

Friday, June 11, 2010

Fatty Acid Re-esterification rates

Alterations in adipocyte free fatty acid re-esterification associated with obese and weight reduced man

This is a bit of a tough read, but the main conclusions are interesting.


ABSTRACT Using a newly developed in vitro technique, the rate of re-esterification of lipolyzed free fatty acids (FFA) in small fragments of human subcutaneous adipose tissue was measured. When related to simultaneous glycerol release, this measure permits the calculation of the molar ratios of glycerol and FFA leaving the adipocyte. In weight-stable, never-obese control subjects the molar ratio of FFA:glycerol leaving the adipocytes is 1.4:1. During fasting, this ratio climbs to 2.7:1, close to the theoretical maximum of 3.0:1. Adipocytes from weight-stable obese subjects do not differ significantly from adipocytes of control in regard to this ratio. However, the adipocytes of weight-stable reduced-obese (RO) subjects display a significantly higher FFA:glycerol ratio than the adipocytes of either control or obese subjects. The presence of this fasting-like physiology in adipose tissue from weight-stable RO subjects is of particular interest since these same individuals have other systemic metabolic and subjective findings compatible with caloric deprivation. 
So after significant weight loss, our fat cells have a "diet hangover" and behave as if in the calorie restricted state.  In the conclusions, the authors postulate that the relative FFA and glycerol levels may be involved in some signalling process causing hunger, overeating and weight regain.  How depressing as usual!

Also of interest:  Obese vs. Never Obese have similar ratios.  This would indicate that there's nothing about the Triglyceride/FFA cycling that's out of whack in the obese -- In other words, the fat didn't just accumulate because this cycle was dysfunctional.  Unfortunately when adiposity is reduced, the fat cells appear to get stuck in "starvation mode".  The RO groups were, however, some only weight stable for around one month prior to this study.  It would be interesting to know if there were differences over a longer period of time.

Some other interesting info in the discussion:

Taken together, these observations may be interpreted to suggest a change in the structure [and/or] function of the plasma membrane of adipocytes and/or interstitial space in RO subjects. Theoretically, an alteration which allowed more rapid mixing of outgoing and incoming FFA, would produce a decrease in the re-esterification of lipolyzed FFA. This model suggests that the surface of the adipocyte functions as a mixing pool for FFA fluxing in and out of the cell, resulting in a reciprocal relationship between lipolysis rate and FFA uptake (see above). This concept is consistent with recent work regarding mechanisms of uptake and release of FFA from adipocytes, in that uptake and release appear to occur at physically separate sites (25, 26).  Whether significant mixing of incoming and outgoing FFA occurs intracellularly has been a point of contention, with some investigators reporting little (27) or no (28) evidence for this in rats, and others suggesting that substantial mixing does occur in human adipose tissue (29). Our data suggest that while some intracellular mixing probably does occur in man, the major site is probably near or just beyond the surface of the plasma membrane.  Interestingly, in some adipocytes, particularly those of the RO, this mixing may be more rapid or more efficient than in the never obese.




  

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