Femoral adipose tissue may accumulate the fat that has been recycled as VLDL and nonesterified fatty acids

Abstract

Objective: Gluteo-femoral, in contrast to abdominal, fat accumulation appears protective against diabetes and cardiovascular disease. Our objective was to test the hypothesis that this reflects differences in the ability of the two depots to sequester fatty acids, with gluteo-femoral fat acting as a longer-term "sink."

Research design and methods: A total of 12 healthy volunteers were studied after an overnight fast and after ingestion of a mixed meal. Blood samples were taken from veins draining subcutaneous femoral and abdominal fat and compared with arterialized blood samples. Stable isotope-labeled fatty acids were used to trace specific lipid fractions. In 36 subjects, adipose tissue blood flow in the two depots was monitored with (133)Xe.

Results: Blood flow increased in response to the meal in both depots, and these responses were correlated (r(s) = 0.44, P < 0.01). Nonesterified fatty acid (NEFA) release was suppressed after the meal in both depots; it was lower in femoral fat than in abdominal fat (P < 0.01). Plasma triacylglycerol (TG) extraction by femoral fat was also lower than that by abdominal fat (P = 0.05). Isotopic tracers showed that the difference was in chylomicron-TG extraction. VLDL-TG extraction and direct NEFA uptake were similar in the two depots.

Conclusions: Femoral fat shows lower metabolic fluxes than subcutaneous abdominal fat, but differs in its relative preference for extracting fatty acids directly from the plasma NEFA and VLDL-TG pools compared with chylomicron-TG.

FIG. 1.

ATBF and systemic concentrations in the fasting and postprandial states. A: ATBF. n = 36. B: Arterialized plasma glucose and plasma insulin. C: Plasma NEFAs. D: Arterialized plasma TG. For B, C, and D, n = 12.

FIG. 2.

Tissue-specific responses in the fasting and postprandial states. A: Plasma creatinine. B: Adipose tissue glucose uptake. C: Adipose tissue NEFA release. D: Adipose tissue TG extraction. RM-ANOVA shows the following: creatinine, main effects of site (P = 0.004) and time (P = 0.007); glucose uptake, main effect of time (P = 0.01), no effect of site or time × site interaction; NEFA release, main effects of time and of site (P < 0.01) with time × site interaction (P = 0.02); TG extraction, main effects of time (P = 0.01) and site (P = 0.052) (interaction, P = 0.07).

FIG. 3.

Measures of net fatty acid retention in adipose tissue in the fasting and postprandial states. A: Net transcapillary flux of fatty acids. B: Percentage re-esterification of fatty acids. Both A and B were calculated from mass balances as in research design and methods. RM-ANOVA shows the following: net transcapillary flux, main effect of time (P = 0.001) and time × site interaction (P = 0.019); percentage re-esterification, main effect of site (P = 0.02) and time (P < 0.001). C and D: Relationships between the two adipose depots in the fasting (C) and postprandial (D) states. The data are percentage re-esterification of fatty acids (as in B) in subcutaneous abdominal (abdo.) (x-axis) and femoral (y-axis) adipose tissue. C: Mean basal values. D: Average values over the postprandial period. The correlation between depots was significant for each period (see the text for statistics).

FIG. 4.

Tracer-based measurements of chylomicron- and VLDL-TG extraction by the two adipose tissue depots. A: Extraction of chylomicron-TG. B: Net flux (expressed as release) of nonesterified [U¹³C]palmitate from adipose tissue (“spillover”). C: Extraction of VLDL-TG. D: Net flux (expressed as release) of nonesterified [²H₂]palmitate across adipose tissue (negative values therefore show net uptake). RM-ANOVA shows the following: chylomicron-TG extraction, main effects of time (P = 0.03) and site (P = 0.03); [U¹³C]palmitate flux, main effects of site (P = 0.025) and time (P < 0.001); VLDL-TG extraction, no significant effects; [²H₂]palmitate flux, main effect of time (P = 0.02) with no effect of site (P = 0.20) or time × site interaction.

FIG. 5.

Net transcapillary flux of labeled palmitic acid in the fasting and postprandial states. Units are nmol · 100 g⁻¹ · min⁻¹. A: Net transcapillary flux of [U¹³C]palmitate, i.e., net uptake or release of chylomicron-derived palmitate, including uptake via the LPL pathway and spillover as shown in Fig. 4B. B: Net transcapillary flux of [²H₂]palmitate, i.e., net uptake or release of NEFA- and VLDL-TG–derived palmitic acid, including uptake via the LPL pathway, and direct uptake and spillover as shown in Fig. 4D. RM-ANOVA shows the following: net transcapillary flux of [U¹³C]palmitate, main effects of site (P = 0.042) and time (P < 0.001); net transcapillary flux of [²H₂]palmitate, main effect of time (P = 0.012), no effect of site (P = 0.67) or time × site interaction (P = 0.13).