TY - JOUR
T1 - Adipocyte glycogen synthase and pyruvate dehydrogenase in obese and type II diabetic subjects
AU - Mandarino, L. J.
AU - Madar, Z.
AU - Kolterman, O. G.
AU - Bell, J. M.
AU - Olefsky, J. M.
PY - 1986
Y1 - 1986
N2 - To determine whether 1) insulin stimulates pyruvate dehydrogenase (PDH) and glycogen synthase (GS) in isolated human adipocytes and 2) adipocytes from subjects with obesity or noninsulin-dependent diabetes mellitus (NIDDM) are resistant to the effects of insulin, PDH and GS were assayed in adipocytes from 11 control, 8 obese, and 9 NIDDM subjects. Basal PDH activities were 123 ± 20, 129 ± 21, and 128 ± 25 pmol pyruvate oxidized/min per 2 x 105 adipocytes in these groups. Insulin stimulated PDH activity to a maximum of 223 ± 38 pmol/min per 2 x 105 in adipocytes from control subjects, but did not significantly increase values from obese subjects. Insulin significantly decreased PDH activity in cells from NIDDM subjects (99 ± 20 pmol/min per 2 x 105 cells, P < 0.05). PDH activity assayed with high magnesium and calcium concentrations was significantly stimulated by insulin in adipocytes from control, but not obese or NIDDM subjects. GS assayed with 1 mM glucose 6-phosphate did not differ significantly among control, obese, or NIDDM subjects (446 ± 110, 451 ± 156, and 291 ± 35 pmol incoporated into glycogen, respectively). Insulin significantly stimulated glycogen synthase in all three groups (827 ± 179, 764 ± 177, and 569 ± 51 pmol incorporated) to a similar extent. Glycogen synthase assayed with 10 mM glucose 6-phosphate was decreased in NIDDM (1,335 ± 131 pmol incorporated) compared with obese or control subjects (2,512 ± 451 and 2,239 ± 230 pmol incorporated, respectively, P < 0.01).
AB - To determine whether 1) insulin stimulates pyruvate dehydrogenase (PDH) and glycogen synthase (GS) in isolated human adipocytes and 2) adipocytes from subjects with obesity or noninsulin-dependent diabetes mellitus (NIDDM) are resistant to the effects of insulin, PDH and GS were assayed in adipocytes from 11 control, 8 obese, and 9 NIDDM subjects. Basal PDH activities were 123 ± 20, 129 ± 21, and 128 ± 25 pmol pyruvate oxidized/min per 2 x 105 adipocytes in these groups. Insulin stimulated PDH activity to a maximum of 223 ± 38 pmol/min per 2 x 105 in adipocytes from control subjects, but did not significantly increase values from obese subjects. Insulin significantly decreased PDH activity in cells from NIDDM subjects (99 ± 20 pmol/min per 2 x 105 cells, P < 0.05). PDH activity assayed with high magnesium and calcium concentrations was significantly stimulated by insulin in adipocytes from control, but not obese or NIDDM subjects. GS assayed with 1 mM glucose 6-phosphate did not differ significantly among control, obese, or NIDDM subjects (446 ± 110, 451 ± 156, and 291 ± 35 pmol incoporated into glycogen, respectively). Insulin significantly stimulated glycogen synthase in all three groups (827 ± 179, 764 ± 177, and 569 ± 51 pmol incorporated) to a similar extent. Glycogen synthase assayed with 10 mM glucose 6-phosphate was decreased in NIDDM (1,335 ± 131 pmol incorporated) compared with obese or control subjects (2,512 ± 451 and 2,239 ± 230 pmol incorporated, respectively, P < 0.01).
UR - http://www.scopus.com/inward/record.url?scp=0022966997&partnerID=8YFLogxK
U2 - 10.1152/ajpendo.1986.251.4.e489
DO - 10.1152/ajpendo.1986.251.4.e489
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C2 - 3094377
AN - SCOPUS:0022966997
SN - 0193-1849
VL - 251
SP - E489-E496
JO - American Journal of Physiology - Endocrinology and Metabolism
JF - American Journal of Physiology - Endocrinology and Metabolism
IS - 4 (14/4)
ER -