Effects of an oral and intravenous fat load on adipose tissue and forearm lipid metabolism

Abstract

We have studied the fate of lipoprotein lipase (LPL)-derived fatty acids by measuring arteriovenous differences across subcutaneous adipose tissue and skeletal muscle in vivo. Six subjects were fasted overnight and were then given 40 g of triacylglycerol either orally or as an intravenous infusion over 4 h. Intracellular lipolysis (hormone-sensitive lipase action; HSL) was suppressed after both oral and intravenous fat loads ( P < 0.001). Insulin, a major regulator of HSL activity, showed little change after either oral or intravenous fat load, suggesting that suppression of HSL action occurred independently of insulin. The rate of action of LPL (measured as triacylglycerol extraction) increased with both oral and intravenous fat loads in adipose tissue ( P = 0.002) and skeletal muscle ( P = 0.001). There was increased escape of LPL-derived fatty acids into the circulation from adipose tissue, shown by lack of reesterification of fatty acids. There was no release into the circulation of LPL-derived fatty acids from skeletal muscle. These results suggest that insulin is not essential for HSL suppression or increased triacylglycerol clearance but is important in reesterification of fatty acids in adipose tissue but not uptake by skeletal muscle, thus affecting fatty acid partitioning between adipose tissue and the circulation, postprandial nonesterified fatty acid concentrations, and hepatic very low density lipoprotein secretion.

Regulation of Dietary Fatty Acid Entrapment in Subcutaneous Adipose Tissue and Skeletal Muscle

“…Adipose tissue TAG extraction increased after the meal, reflecting an increased rate of action of LPL, as we have shown previously (7,22,23). The extraction of labeled fatty acids from the TAG fraction was particularly clear, since they start from a zero baseline, and the tracers are contained mainly in the chylomicron fraction, which is the preferred substrate for LPL action (24 -26).…”

“…Tissue-specific studies, based mostly on arteriovenous difference measurements, suggest that release of plasma TAG-fatty acids as NEFAs occurs in adipose tissue, but perhaps not in other tissues such as skeletal muscle (6,7). That would imply that the adipocyte is not simply a "sink" to take up excess fatty acids, but that fatty acid uptake is regulated by some means, and that the adipocyte's handling of fatty acids derived from circulating TAG might be fundamentally different from that of other tissues.…”

Integrative physiology of human adipose tissue

“…This is clearly an unphysiological situation, but if it is mimicked acutely by intravenous infusion of a TG emulsion, producing no detectable increase in plasma insulin, there is a marked decrease in NEFA release from adipose tissue, reflecting a suppression of HSL activity. 168,169 This experiment seems to imply that there is some signal that responds to increased nutrient availability to regulate net fat storage independently of insulin, and in this case presumably also independently of the SNS.…”

Nitric Oxide and β-Adrenergic Stimulation Are Major Regulators of Preprandial and Postprandial Subcutaneous Adipose Tissue Blood Flow in Humans

“…Adipose tissue blood flow (ATBF) seems to exhibit its highest degree of modulation in response to food intake, illustrated by either glucose 1 or mixed-meal 2 ingestion, whereas fat alone does not elicit a blood flow response. 3 The actual stimulus for this nutrient-related increase in ATBF is, however, not fully understood, but the postprandial increase in ATBF coincides with the increase in insulin concentration in plasma and with the suppression of nonesterified fatty acids (NEFAs). 2 Enhancement of ATBF may have importance in metabolic physiology in that the extraction of plasma triglycerides (TGs) increases with increasing blood flow.…”