Table 3.

Relative PC and PDH activities determined from adipocyte exposure to U¹³C-glucose

A.
	Σmn C2-4 fragment (mean ± SEM)			Σmn C2-5 fragment (mean ± SEM)
	Control		SGA	Control		SGA
Baseline	0.056 ± 0.003		0.073 ± 0.001C	0.060 ± 0.003		0.084 ± 0.001C
Rosi Treatment	0.073 ± 0.002*		0.096 ± 0.002*C	0.083 ± 0.003*		0.110 ± 0.002*C
B.
	PC (m2 152) (median with 25-75%)		PDH (m2 198 – m2 152) (median with 25-75%)		PC/PDH (median with 25-75%)
Control	SGA	Control	SGA	Control	SGA	Control
Baseline	0.015 (0.015-0.017)	0.018 (0.017-0.018)	0.009 (0.009-0.010)	0.017 (0.016-0.018)	1.66 (1.64-1.75)	0.92 (0.90-1.04)C
Rosi Treatment	0.019 (0.018-0.028)	0.025 (0.025-0.026)	0.021 (0.021-0.022	0.021 (0.021-0.022)	1.10 (1.10-1.19)*	1.17 (1.14-1.18)*i

^Cp < 0.05 compared with Control receiving the same treatment.

*p < 0.05 compared to the untreated state within the same group.

ⁱ interaction between SGA and rosiglitazone.

A) The Σmn representing the average fraction of ¹³ C atoms/molecule for the C2-4 fragment and C2-5 fragments are shown for cultures with and without rosiglitazone treatment. The data are presented as fractions of enrichment ± the SEM. Enrichment increased with rosiglitazone treatment in both Controls and SGA, while SGA maintained higher levels than Controls regardless of treatment. B) The PC and PDH pathway contributions are represented based on glutamate fragment enrichments. These data are presented as the median with the 25-75% interquartile ranges. At baseline, SGA demonstrated a lower PC/PDH ratio than Controls. With rosiglitazone, Controls decreased the PC/PDH ratio, while SGA increased it.