The antilipolytic effect of insulin was investigated in obese subjects before and after 7 days of total fasting, and 1 h after oral refeeding with 100 g glucose. Isolated fat cells were prepared from subcutaneous gluteal adipose tissue and incubated in vitro. Specific insulin receptor binding and insulin inhibition of basal and isoprenaline-stimulated lipolysis were determined. During the fasting period, a 15% increase (P < 0.05) in high-affinity insulin binding and a concomitant 3–4-fold increase in insulin sensitivity were noted, and there was a marked enhancement of the maximum insulin-induced inhibition of basal lipolysis, from 4 to 10 μmolof glycerol/107 cells/2 h. The maximum insulin-induced inhibition of isoprenaline-induced lipolysis was similar before and after fasting, about 10 μmol/107 cells/2 h. Glucose refeeding induced a 30% decrease (P < 0.02) in high-affinity insulin binding and a 20–60-fold decrease (P < 0.01) in the sensitivity of the antilipolytic effect of insulin under basal conditions and in the presence of isoprenaline. The maximum antilipolytic effect of insulin, however, was not altered by glucose refeeding. Thus, in the basal state, maximum antilipolytic effect was larger after refeeding as compared with that before fasting. The high-affinity insulin binding and insulin sensitivity were significantly lower after refeeding than before fasting. Before the fasting period, neither the insulin binding nor the antilipolytic effect ofthe hormone was altered by oral glucose. It is concluded that fasting and glucose refeeding are associated with marked alterations in the antilipolytic effect of insulin on human fat cells of obese subjects. Antilipolysis is enhanced during fasting due to a combination of receptor and postreceptor alterations of insulin action. Glucose refeeding induces an acute state of insulin resistance (within 1 h) due to a decrease in insulin receptor binding and insulin sensitivity without achange in antilipolysis at the intracellular level. Insulin inhibition of basal and catecholamine-stimulated lipolysis is influenced in different ways by fasting and refeeding.

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