Subcutaneous abdominal adipose tissue was removed from six normal weight patients (118–184 lb.) at laparotomy and six obese subjects (280–533 lb.) under local anesthesia and incubated in vitro. Glucose-C-14 incorporation into CO2, total lipids and glycogen were measured. Although insulin (10 mU./ml.) stimulated CO2 production from glucose in all twelve subjects (p < .001), the average increase was only 26.6 per cent (5.3 to 50.8). Radioactive glucose incorporation into total lipids was increased by insulin in eight of twelve subjects (average rise = 21.9 per cent; range, −45.5 to 107.1 per cent), but this failed to achieve significance. This small insulin effect on human adipose tissue reflects the experience of others. On the other hand, insulin-stimulated glycogen synthesis proved to be the most sensitive indicator of hormonal activity (mean rise = 231.9 per cent; range, 66.2 to 562.2 per cent). There was no significant difference in basal or insulin-stimulated glucose incorporation into CO2, total lipids or glycogen between the obese and normal weight subjects. The insulin effect on glycogen synthesis could not be correlated with either weight index or body fat in these twelve subjects. Basal conversion of glucose to CO2 was significantly correlated with these two measures of obesity (r = 0.6, p < .05). These data corroborate two other reports that obesity is associated with increased basal glucose metabolism by human adipose tissue in vitro. However, they fail to substantiate the postulate that adipose tissue of the obese is insensitive in insulin. These results and the fact that only approximately 5 per cent of basal or. insulin-stimulated glucose turnover in vivo involves adipose tissue suggest that insensitivity of the muscle mass and/or a circulating insulin antagonist should be more important in the insulin antagonism of obesity.

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