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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!)

Saturday, October 30, 2010

Response of plasma ASP to a prolonged fast

Response of plasma ASP to a prolonged fast - Abstract only unfortunately


OBJECTIVE: To determine the changes in the plasma level of acylation stimulating protein (ASP) during a one month total fast in female subjects with marked obesity.
DESIGN: Patients with marked obesity underwent a month total fast, before, during (2 weeks), and at the end of which, a variety of relevant metabolic parameters were measured.
SETTING: A metabolic unit of a teaching hospital.
SUBJECTS: 10 women with marked obesity were studied and the results compared with those in 16 age-matched controls.
MAIN OUTCOME MEASURES: Plasma ASP, lipoprotein lipids, apoB, free fatty acid, and ketone levels.
RESULTS: At baseline, fasting levels of ASP in the obese group were double that in control subjects (116 +/- 26 vs 53 +/- 30 nM P < 0.001). During the fast, ASP levels dropped progressively and were within the normal range at the end of the study (63 +/- 16 vs 53 +/- 30 nM pNS). In addition, there was a strong correlation between the plasma ASP at baseline before beginning the fast and the 4 week drop in ASP. That is, those subjects who had the highest starting ASP also had the largest 4 week drop in ASP (r2 = 0.644, P < 0.005). Of interest, as plasma ASP levels dropped, plasma free fatty acid and ketone levels rose and when all timepoints were considered, there was a significant inverse relation between plasma ASP and plasma free fatty acid (r2 = 0.295, P < 0.0002).
CONCLUSIONSThe pattern of responses during the fast is that of increasing mobilization of fatty acids from adipose tissue coincident with decreased activity of the pathway responsible for the storage of adipocyte triglyceride mass. The data are consistent, therefore, with the role proposed for ASP as a major determinant of the rate of triglyceride synthesis in human adipocytes and thus a potentially important factor in the pathophysiology of obesity.


It seems to me that it has been demonstrated in this, and other studies (that I've either shared or will as I get around to posting them) that ASP, as the highlighted conclusion above states, plays a major role in the Triglyceride/Fatty Acid cycle by controlling the the esterification (triglyceride synthesis from fatty acids + glycerol) rate.  This particular study demonstrates that ASP is not just involved transiently in the clearance of dietary fats (see, for example ASP action in vivo in humans), but rather has a basal/continual role in the on-going TAG/FA cycle.  Insulin primarily controls the release of fatty acids from the adipocyte, ASP seems to control the incorporation of fatty acids into triglycerides.  

On the GCBC Fact Check front:  Taubes ignored ASP and continues to ignore it.  It is worthwhile to note the date on this article:  1995.

Note that the obese women had higher fasting levels of ASP.  Fasting insulin tends to be elevated in the obese as well.  Taubes often repeats the carbs drive insulin drives fat storage.  That logic could similarly be applied to dietary fat, because as we know, fats (chylo) drive ASP drives fat storage.

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