BACKGROUND AND AIMS: Although whole-body insulin resistance in obesity is established, information on insulin action in peripheral tissues, especially adipose tissue (AD), is limited. This study was undertaken in morbid obesity to investigate insulin action on glucose disposal in AD and muscle (M). SUBJECTS AND METHODS: A meal was given to 30 obese (age 34 +/- 1 yr, body mass index 47 +/- 1 kg/m(2)) and 10 nonobese women (age 39 +/- 4 yr, body mass index 23 +/- 1 kg/m(2)). Samples for glucose and insulin were taken for 360 min from veins draining the abdominal subcutaneous AD and forearm muscles and from the radial artery. Blood flow (BF) was measured in AD ((133)Xe) and M (plethysmography). RESULTS: The area under the curve divided by time (AUC(0-360 min)/360 min) in obese vs. nonobese was as follows: 1) arterial glucose was similar 6.04 +/- 0.2 vs. 5.67 +/- 0.1 mm), but insulin was increased (65.5 +/- 6.6 vs. 28.7 +/- 1.7 mU/liter, P = 0.0004); 2) BF was decreased (3 +/- 0.2 vs. 4.4 +/- 0.3 ml/min per 100 ml tissue in M, P = 0.002 and 1.8 +/- 0.1 vs. 3.7 +/- 0.3 ml/min per 100 ml tissue in AD, P < 0.0001); 3) glucose uptake was decreased (0.9 +/- 0.1 vs. 2.3 +/- 0.4 micromol/min per 100 ml tissue in M, P = 0.002 and 0.45 +/- 0.1 vs. 1.1 +/- 0.17 micromol/min per 100 ml tissue in AD, P = 0.01); 4) fractional glucose extraction was decreased in M (5 +/- 1 vs. 9 +/- 1%, P = 0.03), but was similar in AD (3 +/- 1 vs. 3.6 +/- 1.4%); 5) glucose uptake (per total fat mass) was increased (0.275 +/- 0.04 vs. 0.12 +/- 0.02 mmol/min, P = 0.027). CONCLUSION: In morbid obesity, the sensitivity of glucose metabolism to insulin is impaired in M, due to defects in insulin-stimulated glucose use and decreased BF, and in AD, at least in part, due to decreased BF. However, increased total fat mass provides a sink for the excess of glucose and compensates for insulin resistance.
BACKGROUND AND AIMS: Although whole-body insulin resistance in obesity is established, information on insulin action in peripheral tissues, especially adipose tissue (AD), is limited. This study was undertaken in morbid obesity to investigate insulin action on glucose disposal in AD and muscle (M). SUBJECTS AND METHODS: A meal was given to 30 obese (age 34 +/- 1 yr, body mass index 47 +/- 1 kg/m(2)) and 10 nonobese women (age 39 +/- 4 yr, body mass index 23 +/- 1 kg/m(2)). Samples for glucose and insulin were taken for 360 min from veins draining the abdominal subcutaneous AD and forearm muscles and from the radial artery. Blood flow (BF) was measured in AD ((133)Xe) and M (plethysmography). RESULTS: The area under the curve divided by time (AUC(0-360 min)/360 min) in obese vs. nonobese was as follows: 1) arterial glucose was similar 6.04 +/- 0.2 vs. 5.67 +/- 0.1 mm), but insulin was increased (65.5 +/- 6.6 vs. 28.7 +/- 1.7 mU/liter, P = 0.0004); 2) BF was decreased (3 +/- 0.2 vs. 4.4 +/- 0.3 ml/min per 100 ml tissue in M, P = 0.002 and 1.8 +/- 0.1 vs. 3.7 +/- 0.3 ml/min per 100 ml tissue in AD, P < 0.0001); 3) glucose uptake was decreased (0.9 +/- 0.1 vs. 2.3 +/- 0.4 micromol/min per 100 ml tissue in M, P = 0.002 and 0.45 +/- 0.1 vs. 1.1 +/- 0.17 micromol/min per 100 ml tissue in AD, P = 0.01); 4) fractional glucose extraction was decreased in M (5 +/- 1 vs. 9 +/- 1%, P = 0.03), but was similar in AD (3 +/- 1 vs. 3.6 +/- 1.4%); 5) glucose uptake (per total fat mass) was increased (0.275 +/- 0.04 vs. 0.12 +/- 0.02 mmol/min, P = 0.027). CONCLUSION: In morbid obesity, the sensitivity of glucose metabolism to insulin is impaired in M, due to defects in insulin-stimulated glucose use and decreased BF, and in AD, at least in part, due to decreased BF. However, increased total fat mass provides a sink for the excess of glucose and compensates for insulin resistance.
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