A B S T R A C T The role of insulin in the regulation of human adipose tissue lipoprotein lipase was evaluated. Adipose tissue heparin-releasable lipoprotein lipase (thought to be related to peripheral clearance of plasma triglycerides) was low in insulin-deficient, untreated hyperglycemic diabetic subjects (P <0.001) and treatment of hyperglycemia returned the activity to normal. In chronic hyperinsulinism, represented by obesity, heparin-releasable activity among control subjects was correlated to percent of ideal body weight (r = 0.53, P < 0.05) and to fat cell size (r = 0.61, P < 0.02).Acetone-ether powder lipoprotein lipase activity (presumed to reflect total tissue enzyme) was also related to percent of ideal body weight (r = 0.76, P < 0.001 for controls; r = 0.67, P <0.05 for diabetics) and to fat cell size (r = 0.71, P <0.01 for controls; r = 0.85, P <0.01 for diabetics. Postprandial-stimulated insulin secretion was related to diet-induced changes in lipoprotein lipase in control subjects; both were dependent upon the amount of dietary carbohydrate. In contrast, the diabetic patients with low insulin responses, failed to increase lipoprotein lipase activity with feeding. The changes in heparin-releasable (r = 0.66, P <0.01) and acetone-ether powder (r = 0.69, P <0.01) activity during feeding were related to the percent increase in plasma insulin.Thus, insulin appears to be important in the regulation of human adipose tissue lipoprotein lipase activity. Elevated insulin levels in obesity and increased insulin secretion after eating were associated with increased lipoprotein lipase activity. Defects in insulin secretion, both in postabsorptive and postprandial states, are asThis study represents a part of the clinical investigation by the late Dr. Olavi J. Pykdlist6 during a fellowship at the Veterans Administration Hospital in Seattle, Wash.

A B S T R A C T The rise in plasma triglyceride (TG) levels associated with estrogen administration has been thought to arise from impaired clearance because of the uniform suppression of post-heparin lipolytic activity (PHLA). Recently PHLA has been shown to consist of two activities: hepatic TG lipase and extrahepatic lipoprotein lipase (LPL). To determine whether estrogen might induce a selective decline in one of these activities, both hepatic TG lipase and extrahepatic LPL were measured in postheparin plasma from 13 normal women before and after 2 wk of treatment with ethinyl estradiol (1 ,ug/kg per day). Hepatic TG lipase and extrahepatic LPL were determined by two techniques: (a) separation by heparin-Sepharose column chromatography, and (b) selective inhibition with specific antibodies to post-heparin hepatic TG lipase and milk LPL. Estrogen uniformly depressed hepatic TG lipase as measured by affinity column (-68±12%, mean±SD, P < 0.001) or antibody inhibition (-63±11%, P < 0.001). Extrahepatic LPL was not significantly changed by affinity column (-22±40%) or antibody inhibition (-3+42%). Direct measurement of adipose tissue LPL from buttock fat biopsies also showed no systematic change in the activated form of LPL measured as heparin-elutable LPL (+64+164%) or in the tissue form of LPL measured in extracts of acetone-ether powders (+21±77%). The change in hepatic TG lipase correlated with the change in PHLA (r = 0.969, P < 0.01). However, neither the change in PHLA nor hepatic TG lipase correlated with the in-

To determine whether adipose tissue lipoprotein lipase (LPL) plays a role in the regulation of triglyceride (TG) metabolism in hypothyroidism, the activity of the enzyme was measured in the subcutaneous adipose tissue of six hypothyroid patients before and during therapy with L-thyroxine. The activity of the activated form of the enzyme, measured as heparin elutable LPL, was lower in hypothyroid patients (1.54 +/- 0.93; mU/10(6) cells; mean +/- SD) than in controls (3.26 +/- 1.49; P less than .02) and increased (163 +/- 89%; P less than .01) with treatment to levels comparable to the controls. The total activity of LPL, measured in ammonium hydroxide extracts of acetone ether tissue powders, was in the low normal range in the hypothyroid patients (0.68 +/- 0.42), but not significantly different from normal (1.10 +/- 0.58) and did not increase significantly (92 +/- 105%), with treatment. Plasma post heparin lipolytic activity (PHLA) was low in hypothyroidism and increased (111 +/- 78%; P less than .05) with treatment. These increases in PHLA correlated with the increases in the activity of heparin elutable LPL (r = .88, P less than .05). In all patients fasting plasma TG levels decreased (-43 +/- 25%; P less than .02) after treatment. Serial determination of heparin elutable LPL activity, PHLA, and plasma TG during L-thyroxine treatment revealed a correlation between the per cent changes in PHLA and heparin elutable LPL activity (r = .68, P less than .05), an inverse correlation between plasma TG levels and heparin elutable LPL (r = -0.53,P less than .05) and no correlation between plasma TG and PHLA (r = -0.05). These results suggest that the low PHLA and hypertriglyceridemia of hypothyroidism are related to low adipose tissue LPL activity. All these parameters return to normal after treatment with L-thyroxine and attainment of euthyroidism.

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