TY - JOUR
T1 - Regional postprandial fatty acid metabolism in different obesity phenotypes
AU - Guo, Zengkui
AU - Hensrud, Donald D.
AU - Johnson, C. Michael
AU - Jensen, Michael D.
PY - 1999/8
Y1 - 1999/8
N2 - To examine if postprandial splanchnic/hepatic free fatty acid (FFA) delivery is increased in upper-body (UB) obesity, and to determine the adipose tissue depots responsible for the greater postprandial FFA availability, we measured systemic and regional uptake and release of FFAs ([1-14C]palmitate) before and during a 5-h frequent-feeding mixed meal in eight UB and eight lower-body (LB) obese women. Postabsorptive FFA flux and splanchnic FFA delivery were not different in UB and LB obese women; however, postprandial FFA concentrations (257 ± 45 vs. 81 ± 12 μmol/l, P < 0.0001), FFA flux (8.5 ± 1.2 vs. 3.9 ± 0.8 μmol · kg-1 fat-free mass · min- 1, P < 0.0001), splanchnic FFA delivery (275 ± 45 vs. 88 ± 24 μmol/min, respectively, P < 0.005), and estimated hepatic FFA delivery were greater in UB than LB obese women. Non-splanchnic UB adipose tissue FFA release was greater in UB than in LB obese women (276 ± 71 vs. 97 ± 37 μmol/min, respectively, P < 0.05) and accounted for the greater postprandial FFA availability in UB obesity. Postprandial leg glucose uptake was less in UB than in LB obese women (8.4 ± 5.1 vs. 22.9 ± 2.6 μmol · kg-1 leg fat- free mass · min-1, P < 0.05). We conclude that the elevated postprandial FFA release observed in UB obese women originates from the nonsplanchnic UB fat, not visceral fat. These results suggest that visceral fat may be a marker for, but not the source of, excess postprandial FFAs in obesity.
AB - To examine if postprandial splanchnic/hepatic free fatty acid (FFA) delivery is increased in upper-body (UB) obesity, and to determine the adipose tissue depots responsible for the greater postprandial FFA availability, we measured systemic and regional uptake and release of FFAs ([1-14C]palmitate) before and during a 5-h frequent-feeding mixed meal in eight UB and eight lower-body (LB) obese women. Postabsorptive FFA flux and splanchnic FFA delivery were not different in UB and LB obese women; however, postprandial FFA concentrations (257 ± 45 vs. 81 ± 12 μmol/l, P < 0.0001), FFA flux (8.5 ± 1.2 vs. 3.9 ± 0.8 μmol · kg-1 fat-free mass · min- 1, P < 0.0001), splanchnic FFA delivery (275 ± 45 vs. 88 ± 24 μmol/min, respectively, P < 0.005), and estimated hepatic FFA delivery were greater in UB than LB obese women. Non-splanchnic UB adipose tissue FFA release was greater in UB than in LB obese women (276 ± 71 vs. 97 ± 37 μmol/min, respectively, P < 0.05) and accounted for the greater postprandial FFA availability in UB obesity. Postprandial leg glucose uptake was less in UB than in LB obese women (8.4 ± 5.1 vs. 22.9 ± 2.6 μmol · kg-1 leg fat- free mass · min-1, P < 0.05). We conclude that the elevated postprandial FFA release observed in UB obese women originates from the nonsplanchnic UB fat, not visceral fat. These results suggest that visceral fat may be a marker for, but not the source of, excess postprandial FFAs in obesity.
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U2 - 10.2337/diabetes.48.8.1586
DO - 10.2337/diabetes.48.8.1586
M3 - Article
C2 - 10426377
AN - SCOPUS:0032793212
SN - 0012-1797
VL - 48
SP - 1586
EP - 1592
JO - Diabetes
JF - Diabetes
IS - 8
ER -