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Biomedical subjects

M R Taskinen

Publications and source records attributed to M R Taskinen.

At least 199 records · Page 11Linked to original sources
PubMed1988

Acute effects of ethanol and acetate on glucose kinetics in normal subjects.

We compared the effects of two ethanol doses on glucose kinetics and assessed the role of acetate as a mediator of ethanol-induced insulin resistance. Ten normal males were studied on four occasions, during which either a low (blood ethanol 4 +/- 1 mmol/l) or moderate (14 +/- 1 mmol/l) ethanol, acetate, or saline dose was administered. Both ethanol doses similarly inhibited (0.4-0.5 mg.kg-1.min-1, P less than 0.01) basal glucose production. The decrease in Ra was matched by a comparable decrease in glucose utilization (Rd), resulting in maintenance of normoglycemia. During hyperinsulinemia (approximately 70 microU/ml), glucose disposal was lower (1.2-1.7 mg.kg-1.min-1, P less than 0.01) in the moderate than the low-dose ethanol or saline studies. During acetate infusion, the blood acetate level was comparable with those in the ethanol studies. Acetate had no effect on glucose kinetics. In conclusion, 1) in overnight fasted subjects, ethanol does not cause hypoglycemia because its inhibitory effect on Ra is counterbalanced by equal inhibition of Rd;2) basal Ra and Rd are maximally inhibited already by small ethanol doses, whereas inhibition of insulin-stimulated glucose disposal requires a moderate ethanol dose; and 3) acetate is not the mediator of ethanol-induced insulin resistance.

Acetates↗
PubMed1988

Lipoproteins, lipolytic enzymes, and hormonal status in hypothyroid women at different levels of substitution.

Serum lipoproteins and postheparin plasma lipoprotein lipase and hepatic lipase (HL) activities were determined in 23 hypothyroid women treated with graded doses of thyroxine (T4) (50, 100, and 150 micrograms/day), each given for 3 weeks. Since the sex hormone-binding globulin (SHBG) and thereby serum sex steroid concentrations are sensitive to thyroid status, we also measured serum testosterone, estradiol, and SHBG at each time. Stepwise T4 treatment resulted in gradual improvement in thyroid status. Concomitantly, serum low density lipoprotein (LDL) cholesterol decreased in a linear fashion from a mean of 4.72 +/- 0.31 (+/- SEM) to 3.21 +/- 0.18 mmol/L (P less than 0.001) after the largest dose. In contrast, serum high density lipoprotein (HDL) cholesterol decreased, although not in a dose-dependent fashion, from 1.61 +/- 0.07 to 1.44 +/- 0.05 mmol/L (P less than 0.001) after the largest dose. Serum SHBG increased along with improvement of thyroid function, but this increase did not have major impact on the changes in LDL during T4 treatment, as judged by multiple regression analysis. Thus, serum LDL correlated independently only with T4 (r = -0.38; P less than 0.001). The serum HDL changes were almost exclusively due to those in the HDL2 subfraction, and these were related to HL activity, which increased from 13.4 +/- 1.76 to 18.9 +/- 2.08 U/L after the largest dose. We conclude that thyroid hormones regulated serum HDL (HDL2) cholesterol mainly through their effect on HL.

Adult↗
PubMed1988

Effects of endogenous sex steroids on serum lipoproteins and postheparin plasma lipolytic enzymes.

Sex steroids influence serum high density cholesterol (HDL) concentrations through their effects on postheparin plasma hepatic lipase activity. This enzyme is remarkably sex steroid sensitive; its activity is increased by treatment with androgens and androgenic progestins but decreased by estrogens. Hepatic lipase also is regulated by endogenous estradiol, but less is known about its regulation by endogenous androgens. We measured serum lipoproteins and postheparin plasma hepatic lipase and lipoprotein lipase activities in relation to sex steroids in 13 boys in whom testicular sex steroid production was stimulated by 4 injections of hCG given at 3-day intervals. Serum testosterone, but not estradiol, concentrations increased in 8 boys (group I, prepubertal and early pubertal boys), whereas in 5 boys both testosterone and estrogen concentrations increased concomitantly (group II, pubertal boys). Postheparin plasma hepatic lipase activity increased by 34% (P less than 0.001) in group I, but did not change in group II. Serum HDL cholesterol concentrations did not change during hCG stimulation. However, postheparin plasma hepatic lipase activity correlated inversely with serum HDL (r = -0.34; P less than 0.05) and HDL2 cholesterol levels (r = -0.51; P less than 0.001), and the changes in HDL2 levels and hepatic lipase activity were inversely related (r = -0.63; P less than 0.05). Postheparin plasma lipoprotein lipase activity decreased during hCG stimulation. Its activity was positively related to HDL (r = 0.47; P less than 0.05) and HDL2 cholesterol levels (r = 0.54; P less than 0.001). These results suggest that endogenous androgens and estrogens are involved in the regulation of postheparin plasma lipase activities and serum HDL cholesterol concentrations.

Adolescent↗
PubMed1988

Short-term effects of prednisone on serum lipids and high density lipoprotein subfractions in normolipidemic healthy men.

To study the effects of short term low dose prednisone administration on serum lipids and lipoproteins we measured the concentration and composition of serum lipoproteins; serum apoproteins (apo) A-I, A-II, and B; and plasma lipolytic enzymes before and during prednisone administration (30 mg/day for 7 days) in eight normal men. We also measured insulin binding to adipocytes. Serum high density lipoprotein (HDL) cholesterol increased significantly after 2 days of prednisone administration; the maximal increase was 27% (P less than 0.01 after 5 days). The rise of HDL cholesterol was accounted for by that of HDL2 cholesterol. There were marked changes in the distribution of HDL particles; HDL2 increased, whereas HDL3 decreased. These changes were also apparent after 2 days of prednisone administration and were maximal at 5 days [mean, 1.58 +/- 0.12 (+/- SE) vs. 2.00 +/- 0.14 g/L (P less than 0.001) for HDL2; 1.82 +/- 0.11 vs. 1.61 +/- 0.06 g/L (P less than 0.05) for HDL3], and they were due to opposing changes in cholesterol, phospholipids, and proteins in the HDL subfractions. The change in HDL2 protein correlated inversely with that in HDL3 protein (r = -0.73; P less than 0.05). Notably, prednisone did not change the apo A-I concentration, but that of apo A-II decreased (0.32 +/- 0.02 vs. 0.27 +/- 0.01 g/L; P less than 0.05). Consequently, the lipid to protein ratio of HDL increased. Prednisone induced no significant changes in very low density or low density (LDL) lipoproteins. Adipose tissue LPL activity did not increase until after 7 days of prednisone intake (1.10 +/- 0.28 vs. 3.43 +/- 1.02 mumol FFA/g.h; P less than 0.05), and the same was true for muscle LPL (0.49 +/- 0.14 vs. 0.82 +/- 0.11 mumol FFA/g.h; n = 4; P = 0.06). Specific insulin binding was normal, but both basal and maximal insulin-stimulated glucose transport decreased significantly. In summary, prednisone induces changes in serum HDL which are characterized by redistribution of particles within HDL density toward less dense particles and a quantitative rise of lipids in the HDL2 fraction.

Adipose Tissue↗
PubMed1988

Interrelationships among insulin's antilipolytic and glucoregulatory effects and plasma triglycerides in nondiabetic and diabetic patients with endogenous hypertriglyceridemia.

We tested the hypothesis that the previously observed association among hypertriglyceridemia, hyperinsulinemia, and insulin resistance could be explained by a defect in insulin's antilipolytic effect. Insulin action was measured in 10 nondiabetic and 8 diabetic patients with hypertriglyceridemia (fasting plasma triglyceride 800 +/- 154 and 1105 +/- 445 mg/dl, respectively, P NS; fasting plasma glucose 99 +/- 3 and 161 +/- 12 mg/dl, respectively, P less than .001) and in 8 weight-matched normolipemic nondiabetic individuals (fasting plasma triglyceride and glucose 110 +/- 21 and 91 +/- 3 mg/dl). The slope of the decay in plasma free fatty acid (FFA) during insulin infusion was used as an index of insulin's antilipolytic effect. Insulin stimulation of glucose uptake in vivo during intravenous hyperinsulinemic clamp and in vitro in adipocytes were measures of insulin's glucoregulatory action. Both glucoregulatory and antilipolytic effects were similarly reduced in both hypertriglyceridemic groups compared with normal subjects. The plasma triglyceride concentration correlated positively with the slope of FFA suppression by insulin (r = .81, P less than .0001) and the fasting FFA concentration (r = .65, P less than .0001). In multiple linear regression analysis, insulin's antilipolytic effect and the fasting FFA concentration explained 83% of the variation in the plasma triglyceride concentration. These associations were independent of insulin's glucoregulatory effect and the fasting plasma insulin concentration. The data indicate that patients with endogenous hypertriglyceridemia are resistant to both the antilipolytic and glucoregulatory actions of insulin and that increased flux of FFA as a result of the latter, rather than hyperinsulinemia, is responsible for elevation of very-low-density lipoprotein production.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1988

Role of apolipoproteins E and C in type V hyperlipoproteinemia.

Type V hyperlipoproteinemia is characterized by elevations of chylomicron (CM) and very low density lipoprotein (VLDL) triglycerides. The development of this lipid disorder involves a multitude of metabolic derangements including deficient clearance of triglycerides and/or their increased output aggravated by obesity, diabetes, alcohol intake, or use of some hormones. Some studies have suggested that the apolipoprotein E4 phenotype is involved in this dyslipoproteinemia but this concept is still a matter of controversy. Therefore, we determined the apoE phenotype in 21 patients with severe hypertriglyceridemia classified as type V. Their apoE4 gene frequency was 0.595 which is 2.6-fold higher (P less than 0.001) than that in the Finnish population. Correspondingly, their apoE3 gene frequency was lower than that in the normal population. No differences were noted in plasma lipoproteins of the apoE4 phenotypes and the other type V subjects. The apolipoprotein C-II and C-III distribution was similar to that in normolipidemic subjects. The results suggest that apoE4 may be involved in the development of type V hyperlipoproteinemia.

Adult↗
PubMed1987

Lipoprotein lipase in diabetes.

Lipoprotein lipase has a central role in the metabolism of both triglyceride-rich particles and high density lipoproteins, and it is one determinant of both serum triglyceride and HDL concentrations. In man the enzyme activity in both adipose tissue and skeletal muscle is insulin dependent, and therefore it varies in diabetes according to ambient insulin level and insulin sensitivity. In insulin deficiency (untreated Type 1 diabetes) the enzyme activity in both adipose tissue and muscle tissue is low but increases upon insulin therapy. In chronically insulin-treated patients with good control, the enzyme activity in postheparin plasma is increased. In untreated Type 2 diabetic patients, the average enzyme activity in adipose tissue and postheparin plasma is normal or subnormal. Therapy with oral agents or insulin, resulting in good glycemic control, is followed by an increase of LPL activity in both adipose tissue and postheparin plasma. In both Types 1 and 2 diabetes, changes of LPL activity are associated with relevant alterations in lipoprotein pattern. In insulin deficiency with low LPL, serum total and VLDL triglyceride levels are elevated, and HDL concentration is reduced. In chronically insulin-treated patients with high LPL activity, VLDL triglyceride concentrations are normal or subnormal, and HDL level is increased. In untreated Type 2 diabetic patients subnormal LPL activity may contribute to the elevation of serum triglycerides and to the reduction of HDL level.

Diabetes Mellitus↗
PubMed1987

Alcohol-induced changes in serum lipoproteins and in their metabolism.

The effects of alcohol intake on serum lipids and lipoproteins depend on the dose and mode of alcohol intake, individual susceptibility, genetic variables, and dietary factors. Therefore the changes of lipoprotein pattern are different among moderate and heavy drinkers. Moderate intake of alcohol increases the concentrations of apolipoproteins (apo) AI, apo AII, and high-density lipoprotein subfraction (HDL3) in plasma without any effects on other lipoproteins. If alcohol intake exceeds 60 to 80 gm per day, the synthesis of very low-density lipoprotein (VLDL) particles is stimulated. Even short-term use of alcohol stimulates lipoprotein lipase (LPL) activity in adipose tissue, and consequently the concentration of VLDL in plasma stays normal or is even subnormal. If alcohol intake continues in excessive amounts, the increased transport rate of VLDL particles as a result of high LPL activity results in the up regulation of HDL2. This is clearly evident in chronic alcoholics. Low or subnormal low-density lipoprotein (LDL) levels are another characteristic of the lipoprotein pattern in chronic alcoholics. The increase of HDL (HDL2) and reduction of LDL levels could well explain the reduced risk of coronary heart disease in chronic alcoholics, whereas the causal factors remain open among moderate drinkers.

Alcoholism↗
PubMed1987

Coordination of very low-density lipoprotein triglyceride and apolipoprotein B metabolism in humans: effects of obesity and non-insulin-dependent diabetes mellitus.

To understand the relationship between very low-density lipoprotein (VLDL) triglyceride and VLDL apolipoprotein (apo) B, we studied their metabolisms simultaneously in 53 subjects with a range of obesity and glycemia. Obese subjects had increased production of both VLDL apo B and VLDL triglyceride and more VLDL of normal composition. Compared with nondiabetics, diabetic subjects had decreased clearance of both VLDL apo B and VLDL triglyceride, increased production of VLDL triglyceride but not of VLDL apo B, and more VLDL of abnormal composition. Production of both VLDL apo B and VLDL triglyceride were significantly correlated with plasma insulin concentrations, and rates of clearance of both were inversely correlated with plasma glucose. There was no direct correlation between total plasma free fatty acid concentration and production of either VLDL triglyceride or VLDL apo B, but VLDL triglyceride production was found to account for only a very small proportion of the nonoxidative component of free fatty acid turnover. We suggest that in obese subjects hyperinsulinemia induces overproduction of both VLDL apo B and VLDL triglyceride. In diabetes VLDL is increased in part because of decreased clearance; the altered composition is the result of the increase in VLDL-triglyceride production independent of apo B. The increase in VLDL triglyceride production may be mediated through plasma free fatty acids or glucose, although assessment of the relationship between these precursors and VLDL triglyceride is confounded by the fact that only a small portion of free fatty acids or glucose is converted to VLDL triglyceride.

Adult↗
PubMed1987

Integrated study of low density lipoprotein metabolism and very low density lipoprotein metabolism in non-insulin-dependent diabetes.

The metabolisms of VLDL, IDL, and LDL and their interconversions have been studied in ten obese untreated male Pima Indian diabetics compared to 16 age-, sex-, and weight-matched nondiabetics. VLDL was elevated in the diabetics and had abnormal composition, as indicated by a significantly higher ratio of triglyceride/apo B. Fractional catabolic rates for both VLDL apoB and VLDL triglyceride were lower in diabetics, and diabetics had increased production of VLDL triglyceride but not VLDL apoB compared to obese nondiabetics. A higher proportion of VLDL apoB was removed without conversion to LDL in diabetics. LDL cholesterol and apoB were higher in diabetics, but production of LDL apoB was not different from nondiabetics. Fractional catabolic rate for LDL apoB, however, was significantly lower in the diabetics. The data indicate that the triglyceride-rich VLDL in non-insulin-dependent diabetics are less readily converted to LDL, whereas the elevated LDL in this group of diabetics is due to impaired clearance. Thus, decreased conversion of VLDL to LDL and impaired LDL clearance are two opposing phenomena which may influence the LDL concentration of diabetics in either direction. Thus, despite minimal changes in LDL concentration, there are multiple defects in the metabolism of LDL in non-insulin dependent diabetes which may contribute to the increased atherogenesis in this disorder.

Adolescent↗
PubMed1987

Basal and postprandial lipoprotein lipase activity in adipose tissue during caloric restriction and refeeding.

The effect of a ten-day caloric restriction period and of subsequent refeeding on adipose tissue lipoprotein lipase (LPL) activity was studied in 14 moderately obese women. The enzyme assays were made from subcutaneous fat taken from three separate regions (gluteal, femoral, and abdominal) after overnight fasting and from one region also after a standard meal. There was a close correlation between the activities measured from the different subcutaneous sites. The caloric restriction was followed by a decrease of the basal LPL activity to one fifth of the value recorded during the isocaloric diet. However, the relative postprandial increase of LPL activity was greater during the low-calorie diet than during the isocaloric diet. During refeeding the basal LPL activity rose but remained at a lower level than before the caloric restriction. The postprandial LPL response was markedly exaggerated after ten days of refeeding (21% increase before dieting and 250% after refeeding). The changes of LPL during caloric restriction and subsequent refeeding were not correlated to plasma insulin levels. The mechanism of the exaggerated LPL response to meal during refeeding remains obscure.

Adipose Tissue↗
PubMed1987

Enzymes involved in triglyceride hydrolysis.

The lipolytic enzymes LPL and HL play important roles in the metabolism of lipoproteins and participate in lipoprotein interconversions. LPL was originally recognized to be the key enzyme in the hydrolysis of chylomicrons and triglyceride, but it also turned out to be one determinant of HDL concentration in plasma. When LPL activity is high, chylomicrons and VLDL are rapidly removed from circulation and a concomitant rise of the HDL2 occurs. In contrast, low LPL activity impedes the removal of triglyceride-rich particles, resulting in the elevation of serum triglycerides and a decrease of HDL (HDL2). Concordant changes of this kind in LPL and HDL2 are induced by many physiological and pathological perturbations. Finally, the operation of LPL is also essential for the conversion of VLDL to LDL. This apparently clear-cut role of LPL in lipoprotein interconversions is contrasted with the enigmatic actions of HL. The enzyme was originally thought to participate in the catalyses of chylomicron and VLDL remnants generated in the LPL reaction. However, substantial in vitro and in vivo data indicate that HL is a key enzyme in the degradation of plasma HDL (HDL2) in a manner which opposes LPL. A scheme is presented for the complementary actions of the two enzymes in plasma HDL metabolism. In addition, recent studies have attributed a role to HL in the catabolism of triglyceride-rich lipoproteins, particularly those containing apo E. However, this function becomes clinically important only under conditions where the capacity of the LPL-mediated removal system is exceeded. Such a situation may arise when the input of triglyceride-rich particles (chylomicrons and/or VLDL) is excessive or LPL activity is decreased or absent.

Animals↗
PubMed1986

High density lipoproteins in postprandial lipemia. Relation to sex and lipoprotein lipase activity.

Twelve subjects (6 women, 6 men) were given 120 g fat orally for 2 h to study its effect on serum high density lipoproteins (HDL), HDL subfractions and apoproteins A-I and A-II. In addition, we measured the fasting activity of adipose tissue lipoprotein lipase (LPL). The HDL2 mass concentration increased significantly in women (216 +/- 10 vs 232 +/- 12 mg/dl, P less than 0.01) but not in men (114 +/- 10 vs 119 +/- 11 mg/dl, NS). The changes of the HDL2 mass in women were due to significant increases of phospholipids, and both apoproteins A-I and A-II. In men, only HDL2 phospholipids rose slightly. The HDL2 cholesterol remained unchanged postprandially. Both fasting and maximal postprandial concentrations of HDL2 correlated positively with adipose tissue LPL activity (r = +0.63, P less than 0.05 and r = +0.61, P less than 0.05). The concentration of HDL3 remained unchanged postprandially but compositional changes were observed. Thus, the HDL3 phospholipids increased slightly in both sexes whereas the HDL3 cholesteryl esters fell significantly. The postprandial changes of HDL2 and HDL3 phospholipids were evident in both zonal ultracentrifugation and equilibrium ultracentrifugation. In addition, 5 women received intragastric fat infusions with or without extra soya phospholipids, lecithin. The HDL2 mass concentration increased after both infusions. In 4 of the 5 subjects the overall increment of the HDL2 phospholipids was larger after the phospholipid-rich emulsion than after phospholipid-poor one. This difference was obvious in zonal profile of HDL subfractions which revealed also a slight increase of HDL3 phospholipids after both infusions. In conclusion, the response of HDL2 to fat meal is more pronounced in women than in men and it seems to be dependent on fasting LPL activity which is higher in women than in men. Further, the alterations in postprandial composition of HDL subfractions can be modified by the composition of fat meal.

Adipose Tissue↗
PubMed1986

Rapid decrease in high density lipoprotein subfractions and postheparin plasma lipase activities after cessation of chronic alcohol intake.

Regular intake of alcohol is associated with elevated levels of high density lipoproteins (HDL). Opinions differ, however, on the HDL subfraction which is preferentially influenced by alcohol. In the present study we measured the HDL subfraction lipid and protein concentrations and postheparin plasma lipase activities in chronic alcohol users immediately after cessation of drinking and sequentially during one week of total abstention. The HDL2 mass concentration decreased significantly already during two abstinent days the decline continuing until the 8th day. At this time the mean HDL2 concentration had decreased by 38% from the initial value (P less than 0.05). The HDL2 cholesterol, phospholipid and protein concentrations decreased in approximately similar proportions, whereas the HDL2 triglyceride increased by 40%. The HDL3 mass concentration decreased by 13% but this change was not significant. Also in HDL3 the cholesterol, phospholipid and protein contents decreased to a similar extent but the triglyceride content rose. The postheparin plasma lipoprotein lipase activity decreased by 41% and the hepatic lipase by 37% during the abstention. It is concluded that in chronic alcoholics HDL2 accounts for the major part of the increase in HDL.

Adult↗
PubMed1986

Insulin resistance is a prominent feature of patients with pancreatogenic diabetes.

To compare in vivo insulin action in patients with diabetes secondary to pancreatic diseases (n = 9) to that in type I diabetic patients (n = 13) and in normal subjects (n = 8), we measured insulin-mediated glucose disposal by the euglycemic insulin clamp technique. Five of the nine patients with pancreatogenic diabetes had undergone total pancreatectomy. Similar plasma glucose (approximately 4.8 mmol/l) and insulin (approximately 70 mU/l) levels were maintained in all groups. The rate of glucose metabolism in the pancreatogenic diabetic patients (3.77 +/- 0.55 mg/kg/min) was 47% lower (P less than 0.001) than in normal subjects (7.05 +/- 0.57 mg/kg/min) and 21% lower (P less than 0.05) than in type I diabetic patients (5.54 +/- 0.39 mg/kg/min). The rates of glucose uptake were similarly reduced in totally pancreatectomized patients and in those with pancreatogenic diabetes due to other causes. During hyperinsulinemia induced by the clamp, glucose production (measured using 3-3H-glucose infusion) was completely suppressed in both the pancreatogenic diabetic patients and the normal subjects indicating that the impairment of in vivo insulin action was localized to the peripheral tissues. However, basal glucose production was elevated in the pancreatogenic diabetic patients (2.75 mg/kg/min, P less than 0.001) compared to the normal subjects (1.79 +/- 0.07 mg/kg/min). Glucose production rates were comparable in the totally pancreatectomized patients and in the other patients with pancreatogenic diabetes. The fasting plasma insulin level was, however, lower in the totally pancreatectomized (3.2 +/- 1.6 mU/L, P less than 0.05) than the other pancreatogenic (11.5 +/- 3.7 mU/L) diabetic patients. To examine the mechanisms of peripheral insulin resistance in the pancreatogenic diabetic patients, insulin binding and action were measured in isolated adipocytes. The pancreatogenic diabetic patients displayed normal insulin binding as well as normal rates of glucose transport and oxidation in adipocytes. In conclusion, patients with pancreatogenic diabetes demonstrated marked insulin resistance. Thus, impaired regulation of glucose production is a more likely explanation for the special clinical features of pancreatogenic diabetes than enhanced glucose utilization.

Adipose Tissue↗
PubMed1986

Postheparin plasma lipoprotein and hepatic lipase activities in hyperinsulinemic infants of diabetic mothers and in large-for-date infants at birth.

To study postheparin plasma lipase activities in nonfed newborn infants immediately after birth and to investigate the possible influence of fetal hyperinsulinemia on lipoprotein lipase activity, we measured lipoprotein and hepatic lipase activities in 55 macrosomic newborn infants: group I consisted of 21 infants born to mothers with insulin-dependent diabetes. The infants were hyperinsulinemic at birth and had hypoglycemia and poor lipolysis at the age of 2 h. Group II consisted of 18 infants born to mothers with gestational diabetes. Group III consisted of 16 large-for-date infants born to nondiabetic mothers. The mean postheparin plasma lipoprotein lipase activities at 2 h of age were similar (mean 36 mumol free fatty acids/ml/h; SEM 15) in groups I-III. Lipoprotein lipase activity correlated negatively with cord-serum triglycerides (range 0.13-1.2 mmol/liter) but did not correlate with serum insulin (range 5.4-524 microU/ml) or C-peptide (range 0.6-21.0 micrograms/liter). Hepatic lipase activity was somewhat higher in group I (mean 68 mumol free fatty acids/ml/h; SEM 23) than in groups II and III (mean 55 mumol free fatty acids/ml/h; SEM 14). Hemoglobin Alc was the only important factor explaining the difference in hepatic lipase activities between groups. Lipoproteins and apolipoproteins A-I, A-II, and B were similar in all three groups. We conclude that in large-for-date infants lipoprotein lipase is active at birth without exogenous fat induction, and that these infants are capable of hydrolyzing fat, their main source of energy, immediately after birth. In addition, we conclude that postheparin plasma lipoprotein lipase activity is not affected by fetal hyperinsulinemia.

Apolipoprotein A-I↗