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Saturday, June 12, 2010

ASP action in vivo in humans

Coordinated release of acylation stimulating protein (ASP) and triacylglycerol clearance by human adipose tissue in vivo in the postprandial period

This paper demonstrated ASP actions in vivo for humans in the postprandial (post-meal) period.  ASP levels were measured locally to the adipocytes  (venous output side) and systemically in the arterially "supply" side.  This was important because many who would dismiss the action of ASP look at systemic ASP levels and claim no connection.  However, this paper demonstrated otherwise:


The objective of this study was to determine whether Acylation Stimulating Protein (ASP) is generated in vivo by human adipose tissue during the postprandial period.  After a fat meal, samples from 12 subjects were obtained (up to 6 h) from an arterialized hand vein and an anterior abdominal wall vein that drains adipose tissue. Veno-arterial (V-A) gradients across the subcutaneous adipose tissue bed were calculated.  The data demonstrate that ASP is produced in vivo (positive V-A gradient) with maximal production at 3–5 h postprandially. The plasma triacylglycerol (TAG) clearance was evidenced by a negative V-A gradient. It increased substantially after 3 h and remained prominant until the final time point. There was, therefore, a close temporal coordination between ASP generation and TAG clearance. In contrast, plasma insulin and non-esterified fatty acid (NEFA) had an early (1–2 h) postprandial change. Fatty acid incorporation into adipose tissue (FIAT) was calculated from V-A glycerol and non-esterified fatty acid (NEFA) differences postprandially.  FIAT was negative during the first hour, implying net fat mobilization. FIAT then became increasingly positive, implying net fat deposition, and overall followed the same time course as ASP and TAG clearance. There was a direct positive correlation between total ASP production and total FIAT (r 5 0.566, P , 0.05). These data demonstrate that ASP is generated in vivo by human adipocytes and that this process is accentuated postprandially, supporting the concept that ASP plays an important role in clearance of TAG from plasma and fatty acid storage in adipose tissue.—
Unfortunately, the "fat meal" was actually a somewhat balanced meal (although pretty low protein) relatively high in fat and carbs:  60 g fat, 85 g carbohydrate, and 13 g protein = 932 calories total   58% fat / 36% carb / 6% protein.  But there is something interesting in the timecourse of "fat storage" here.  Insulin and NEFA initially increased in the first 1-2 hr.  As stated above, fatty acid incorporation into adipose tissue (FIAT) was NEGATIVE in the first hour indicating net fat mobilization!  This seems an odd paradox, but this is not the first study I've read that demonstrated a release (at least initially) of fat from stores in response to a meal.  At least initially, insulin therefore does not trap fat in the fat cells or send fats on a one way street into the cells.  Other research I've blogged on here and here indicates that insulin can stimulate ASP production, although its action is much less potent than chylomicrons.  I've also blogged previously about the decreased anti-lipolytic effect of a large, truly high fat meal (very low carb) resulting in greater FA release from adipose tissue.

It seems to me that elevated NEFA/FFA (one of the markers of Metabolic Syndrome too often ignored in the low carb community) indicate a disturbed regulation of fat storage that is if anything tipped somewhat against fat accumulation.  At least to a point, esthetics aside, we really do want our caloric excesses to be accumulating in our fat cells, because the alternative is elevated fats and glucose in circulation (wreaking havoc) and/or accumulation in other places (e.g. liver, etc.) that can be "toxic" to such tissues.

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