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PubMedDate not supplied

Lipoprotein lipase in cultured pig aortic smooth muscle cells.

Acetone powder extracts prepared from cultured pig aortic smooth muscle cells and the culture medium from these cells (particularly when incubated with heparin) were shown to contain a lipolytic enzyme which was identified as lipoprotein lipase by the following criteria: 1) stimulation by apolipoprotein C-II; 2) an optimal activity at approximately pH 8.0; 3) inhibition by NaCl, and 4) binding to a heparin-Sepharose affinity column. In addition, we found that cultured arterial smooth muscle cells from guinea pig and rabbit secreted a similar lipase into the culture medium. In contrast, studies using cultured bovine aortic endothelial cells yielded no evidence for either the synthesis or secretion of lipoprotein lipase by these cells. The production of lipoprotein lipase by the smooth muscle cells of the artery may play a role in the process of atherogenesis.

Acetone↗
PubMed2003

1,1'-bis(anilino)-4-,4'-bis(naphtalene)-8,8'-disulfonate acts as an inhibitor of lipoprotein lipase and competes for binding with apolipoprotein CII.

Lipoprotein lipase (LPL) is dependent on apolipoprotein CII (apoCII), a component of plasma lipoproteins, for function in vivo. The hydrophobic fluorescent probe 1,1'-bis(anilino)-4,4'-bis(naphthalene)-8,8'-disulfonate (bis-ANS) was found to be a potent inhibitor of LPL. ApoCII prevented the inhibition by bis-ANS, and was also able to restore the activity of inhibited LPL in a competitive manner, but only with triacylglycerols with acyl chains longer than three carbons. Studies of fluorescence and surface plasmon resonance indicated that LPL has an exposed hydrophobic site for binding of bis-ANS. The high affinity interaction was characterized by an equilibrium constant Kd of 0.10-0.26 microm and by a relatively high on rate constant kass = 2.0 x 10(4) m(-1) s(-1) and a slow off-rate with a dissociation rate constant kdiss = 1.2 x 10(-4) s(-1). The high affinity binding of bis-ANS did not influence interaction of LPL with heparin or with lipid/water interfaces and did not dissociate the active LPL dimer into monomers. Analysis of fragments of LPL after photoincorporation of bis-ANS indicated that the high affinity binding site was located in the middle part of the N-terminal folding domain. We propose that bis-ANS binds to an exposed hydrophobic area that is located close to the active site. This area may be the binding site for individual substrate molecules and also for apoCII.

Anilino Naphthalenesulfonates↗
PubMed1987

Milk lipoprotein lipase activity during long-term administration of recombinant bovine somatotropin.

The effect of long-term administration of recombinant bovine somatotropin to dairy cows on milk lipoprotein lipase activity was investigated. Recombinant bovine somatotropin was administered daily to 32 cows (8/treatment). Treatments were 0 (control), 12.5, 25.0, and 50.0 mg/d or recombinant bovine somatotropin administered in once daily intramuscular injections. Treatments began at 28 to 35 d of lactation and continued until 294 d of lactation. Recombinant bovine somatotropin treatments had no significant effect on milk lipoprotein lipase activity; enzyme activity for each treatment was 97.87, 108.96, 99.96, and 92.43 units/ml of milk, respectively. A significant effect of the stage of lactation was unrelated to recombinant bovine somatotropin administration. Enzyme activity peaked at approximately 20 wk of the treatment or 25 wk postpartum. These results indicate that long-term administration of recombinant bovine somatotropin does not alter the processes that lead to lipoprotein lipase activity in milk.

Animals↗
PubMed1978

Effect of acute ethanol load on postheparin plasma lipoprotein lipase and hepatic lipase activities and intravenous fat tolerance.

This study aimed to examine the possibility that ethanol-induced rise of serum triglyceride concentration in man is partly due to an impaired removal of triglycerides from the circulation. Acute ethanol loads given to normal human subjects after an overnight fast reduced the postheparin plasma lipoprotein lipase activity by an average of 25% but did not influence the postheparin plasma hepatic lipase activity or fractional removal of Intralipid triglyceride. When alcolhol was administered to fed subjects in the evening the postheparin plasma hepatic lipase was significantly decreased in the next morning as compared to corresponding control value but the lipoprotein lipase and Intralipid clearance were not changed. It is concluded that the slight decrease of lipoprotein lipase during alcohol intoxication may contribute to the hyperlipemic effect of ethanol.

Ethanol↗
PubMed1989

Effect of tumor necrosis factor (TNF) on lipid metabolism in the diabetic rat. Evidence that inhibition of adipose tissue lipoprotein lipase activity is not required for TNF-induced hyperlipidemia.

Tumor necrosis factor (TNF) administration produces an increase in plasma triglycerides that may be due to inhibition of adipose lipoprotein lipase activity and/or a stimulation of hepatic lipogenesis. We now report that TNF administration to insulinopenic diabetic rats increases serum triglycerides (2 h, 2.4-fold; 17 h, 4.3-fold). Adipose tissue lipoprotein lipase activity was markedly decreased in diabetic animals compared with controls and was not further inhibited by TNF. Incorporation of tritiated water into fatty acids in the liver was increased 45% 1-2 h after TNF and 87% at 16-17 h. These results indicate that the TNF-induced increase in circulating lipid levels can occur in the absence of a TNF-induced inhibition of adipose tissue lipoprotein lipase activity. Moreover, the clearance from the circulation of triglycerides in chylomicrons was similar in control and TNF-treated animals; these results provide further evidence that the removal of triglyceride-rich lipoproteins is not altered in the TNF-treated animals. Our data suggest that the TNF-induced stimulation of hepatic lipid synthesis may play an important role in the increase in serum triglycerides. In addition, TNF administration to diabetic animals leads to an elevation in serum glucose levels (73% at 17 h) without a change in serum insulin levels. Thus, TNF stimulation of hepatic lipogenesis is independent of changes in insulin.

Adipose Tissue↗
PubMed1978

Synthesis of lipoprotein lipase in cultured avian granulosa cells.

Avian granulosa cells cultured as a homogeneous parenchymal population contain lipolytic activity. This activity is stimulated 2--5-fold by serum, inhibited 90% by 1 M NaCl and inhibited 80% by specific anti-lipoprotein lipase immunoglobulins. 85% of the activity binds to heparin-Sepharose 4B, and 70% of bound activity is eluted with 1.5 M NaCl. Thus, the lipolytic activity of cultured granulosa cells is lipoprotein lipase. Granulosa cells were shown to synthesize lipoprotein lipase in culture by incorporating [3H]leucine into the enzyme protein, as measured with an immunoadsorption technique. Finally, colchicine was shown to increase intracellular lipolytic activity, suggesting an inhibition of secretion of this enzyme by cultured granulosa cells.

Animals↗
PubMed1983

The response of plasma triglyceride, cholesterol, and lipoprotein lipase to treatment in non-insulin-dependent diabetic subjects without familial hypertriglyceridemia.

The effects of treatment on plasma total triglyceride, total cholesterol, and plasma postheparin lipase activities have not been evaluated in non-insulin-dependent diabetic (NIDD) subjects without a coexisting familial lipid disorder. In 49 untreated NIDD subjects, there was a linear relationship between glycosylated hemoglobin (GHb) and triglyceride (r = 0.35, P less than 0.02). This correlation was improved after adjusting for the effects of obesity by a partial correlation analysis. After therapy, there was a significant relationship between the change in GHb and the change in triglyceride. To determine whether changes in lipid removal from plasma may contribute to the decrease in plasma lipid concentrations during treatment, the plasma postheparin lipoprotein lipase and hepatic lipase activities were evaluated in a subgroup (N = 8) of these NIDD subjects before and after 1 and 3 mo of therapy. Plasma postheparin hepatic lipase activity in the NIDD subjects was not different from that observed in six normal control subjects and did not change during therapy. In contrast, plasma postheparin lipoprotein lipase activity was lower in the untreated NIDD subjects than in the control subjects. Analysis of the two phases (early and late) of the postheparin lipoprotein lipase activity in plasma showed that the abnormal early phase in untreated NIDD corrected to normal values in less than a month, but the late phase was not corrected until the 3-mo measurement. These findings suggest that some NIDD subjects have a defect in heparin releasable lipoprotein lipase activity, which is reversed with improved glycemic control.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1999

Erythropoietin supplement increases plasma lipoprotein lipase and hepatic triglyceride lipase levels in hemodialysis patients.

BACKGROUND: We reported in previous studies that plasma triglyceride levels, as well as remnant-like particles-cholesterol (RLP-C) and -triglyceride (RLP-TG) levels, were significantly lower in maintenance hemodialysis (HD) patients treated with erythropoietin (EPO) than in HD patients treated without EPO. However, little is known about the mechanisms underlying the improvements in abnormal RLP metabolism in HD patients. This study investigates whether EPO supplement therapy in cases of uremic anemia increases the plasma lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) levels in HD patients. METHODS: Twenty HD patients who had not previously received EPO were divided into two groups according to the stage of HD: 12 at the initial stage, defined as a mean HD duration of 0.35 +/- 0.68 months (range of 0 to 2.47 months), and 8 at the maintenance stage, defined as a mean HD duration of 114.1 +/- 91.9 months (range of 13.0 to 253.9 months). Fasting plasma was collected from the HD patients prior to the start of the EPO supplement therapy and at one month after the therapy. RLP-C levels were determined using a RLP-C JIMRO II kit. Fasting plasma was also collected from the HD patients 10 minutes after an intravenous injection of heparin (30 U/kg body wt). Plasma LPL levels were determined using an enzyme immunoassay, and HTGL levels were determined using a modified version of the Hernell et al method. RESULTS: Plasma RLP-C levels showed a tendency to decrease after the start of the EPO supplement therapy in HD patients at the maintenance stage. Plasma LPL levels were significantly higher in the two groups of HD patients one month after the start of the EPO supplement therapy than in the same patients prior to the start of the EPO supplement therapy. Plasma HTGL levels were significantly higher in HD patients at the maintenance stage one month after the start of the EPO supplement therapy than in HD patients at the maintenance stage prior to the start of the EPO supplement therapy. CONCLUSIONS: The results of this study suggest that the EPO supplement therapy may reduce plasma RLP-C levels by increasing the plasma LPL and HTGL levels in maintenance-stage HD patients.

Adult↗
PubMed1995

Homozygous deletion of exon 9 causes lipoprotein lipase deficiency: possible intron-Alu recombination.

We studied a homozygous deletion in the lipoprotein lipase gene at the molecular level. Comprising the end of intron 8, the whole of exon 9, and about two-thirds of intron 9, this 2.136-kb deletion caused complete lipoprotein lipase deficiency and severe hypertriglyceridemia (type I hyperlipoproteinemia). Intron 9 of a normal control subject was also sequenced in order to define the exact borders of the deletion. Up to now, only the first 0.721 kb of intron 9 had been sequenced. Thus the complete sequence of intron 9 (3.090 kb) is now available. Three Alu sequences were characterized in the normal intron 9, while the proband had only the third complete Alu sequence. The first Alu sequence was located in the deleted region, and only the left arm of the second was present, as the deletion began near its center. A stem-loop structure involving a 14-nt region towards the end of intron 8 and an Alu sequence in intron 9 might have led to the deletion. Sequence analysis showed that the three Alu sequences belonged to the 40-million-year-old Alu-Sa subclass.

Adult↗
PubMed1977

Postheparin plasma lipoprotein lipase and hepatic lipase in diabetes mellitus. Relationship to plasma triglyceride metabolism.

The activity of two triglyceride lipases was determined by an immunochemical method in the postheparin plasma of 60 diabetic patients and of 47 age- and sex-matched nondiabetic control subjects. The results were related to the type of diabetes, to plasma triglyceride and insulin concentrations, to removal of exogenous fat from the blood, and to turnover of VLDL-triglycerides . The mean postheparin plasma lipoprotein lipase (LPL) activity was decreased by 44 per cent (p less than 0.001) in patients with untreated ketotic diabetes and by 20 per cent (p less than 0.01) in patients with untreated mild to moderate nonketotic early-onset diabetes. Insulin treatment of ketotic diabetes resulted in a rapid increase in the activity of LPL and decrease in serum triglycerdie level, whereas sulfonylurea treatment of non-insulin-requiring diabetics did not significantly influence the enzyme activity. In insulin-treated chronic diabetics the average postheparin plasma LPL activity was not different from that of nondiabetic controls, but some of these patients had high LPL values. In normolipidemic maturity-onset-type diabetics the LPL activity was within normal range, but in those having hypertriglyceridemia the average LPL value was decreased by an average of 26 per cent (p less than 0.01). The LPL activity showed a significant negative correlation with the logarithm of serum triglyceride concentration (r = -0.62) and a positive correlation with fractional removal of Intralipid (r = +0.64) and fractional turnover of V triglyceride (r = +0.40). The activity of LPL was correlated to basal plasma insulin concen tration in the insulin-deficient diabetes r = +0.34) but not in patients with maturity-onset-type diabetes. The hepatic lipase (HL) activity of postheparin plasma was similar in diabetes and controls, with the exception of hypertriglyceridemic maturity-onset diabetics, who had higher mean HL activity than the corresponding control group (p greater than 0.01). The activity of HL was not related to triglyceride removal but showed a significant correlation to VLDL-triglyceride production rate. On the basis of these results it seems that a deficiency of LPL accounts for a great deal of the elevation of serum triglyceride in insulin-deficient human diabetes but has a smaller role in the pathogenesis of the hypertriglyceridemia that is associated with maturity-onset diabetes. The latter abnormality is caused mainly by an increased secretion of triglycerides into the blood even though a decreased LPL may contribute to development of hyperlipemia in cases with gross elevation of serum triglycerides.

Adolescent↗
PubMed1995

Common genetic variants of lipoprotein lipase that relate to lipid transport in patients with premature coronary artery disease.

Two common coding sequence mutations of lipoprotein lipase (serine447-ter, producing a carboxy terminal truncation; and asp9-asn variants) were studied in 329 Caucasian subjects, of whom 243 had angiographic features of premature atheroscelerosis (220 with coronary artery disease; 23 with coronary and peripheral artery disease). As expected, the mean levels of cholesterol, triglycerides, LDL-cholesterol, ApoB and Lp(a) were significantly higher in the arterial disease group than in the controls. HDL levels were lower in the patient group. With regard to the common mutations, plasma triglycerides and VLDL-triglycerides were lower in subjects possessing the Serine447-Ter mutation (p = 0.06 and < 0.05, respectively). When the lipid distributions were analysed by tertiles, the Ser447-Ter mutation was significantly less frequent in the highest tertiles for triglycerides (p < 0.02), and VLDL (p < 0.04). The Asp9-Asn substitution was significantly more frequent in the lowest tertiles for ApoAI (p = 0.05). Case-control analyses of genotypic distributions between the two groups with or without arterial disease did not show any significant differences. The possible functional effects of these common mutants of lipoprotein lipase are discussed.

Asparagine↗
PubMed2005

Relationship of lipoprotein lipase and hepatic triacylglycerol lipase activity to serum adiponectin levels in Japanese hyperlipidemic men.

OBJECTIVE: The aim of this study was to determine how lipoprotein lipase (LPL) and hepatic triacylglycerol lipase (HTGL) activity relate to serum adiponectin levels. RESEARCH DESIGN AND METHODS: Fifty-five hyperlipidemic Japanese men were recruited for this study. LPL and HTGL activity in post-heparin plasma (PHP) was measured using Triton X-100 emulsified-[14C] triolein. The remaining activity in the presence of 1M NaCl was defined as HTGL activity. Serum adiponectin levels were determined by an enzyme-linked immunosorbent assay system. RESULT: LPL activity had a positive relationship with HDL2, but had no relation with HDL3, while HTGL had positive relationship with HDL3, but had no relationship with HDL2. LPL activity showed a positive relationship [r = 0.345, p = 0.010] to serum adiponectin levels, while and HTGL activity showed an inverse relationship [r = - 0.365 p = 0.006]. Multiple regression analysis with LPL and HTGL as dependent variables and age, BMI, serum adiponectin and the homeostasis model assessment of insulin resistance (HOMA-IR) as independent variables showed LPL and HTGL's association to adiponectin did not persist after adjustments for these covariants. However, the association of LPL activity to HOMA-IR was found to persist after adjustments of age, BMI, and serum adiponectin. CONCLUSIONS: There was a co-linearity between insulin sensitivity and adiponectin as well as insulin sensitivity and LPL/HTGL activity.

Aged↗
PubMed1983

[Lipoproteins, apolipoproteins, lipoprotein lipase, hepatic triglyceride lipase and lecithin cholesterol acyltransferase in patients with nephrotic syndrome].

Chronic renal disease with secondary hyperlipidemia is highly atherogenic. In uremia and patients on chronic hemodialysis there is a high incidence of atherosclerotic complications whereas the incidence of atherosclerotic disease is relatively low in the nephrotic syndrome. This is surprising, as nephrosis produces type-II hyperlipidemia, which is usually highly atherogenic. In this study 10 patients (5 male, 5 female) with a newly diagnosed nephrotic syndrome were compared to 10 controls (5 male, 5 female). As laboratory parameters, lipids, lipoproteins (VLDL, IDL, LDL, HDL2 and HDL3 by rate zonal centrifugation) and the percentage composition of the major apolipoproteins in VLDL, HDL2 and HDL3, as well as lipoprotein lipase (LPL), hepatic lipase (HTGL) and lecithin-cholesterol-acyl-transferase (LCAT) were measured. In nephrotic patients significantly higher plasma levels of cholesterol, triglycerides, phospholipids, VLDL, IDL and LDL were found, whereas HDL-chol, HDL2 and HDL3 were unchanged. LPL and HTGL were both significantly impaired, whereas LCAT was distinctly increased. The percentage composition of apolipoproteins in HDL2 and HDL3 was normal. In nephrotic VLDL, apo-AI was distinctly increased at the expense of a decrease in apo-CII, and increased LCAT was explained by the relative rise of apo-AI in nephrotic VLDL. The increase in apo-AI in VLDL is discussed as a possible reason for the low atherogenic risk of secondary hyperlipidemia in nephrotic syndrome.

Adolescent↗
PubMed1997

Sepsis-induced regulation of lipoprotein lipase expression in rat adipose tissue and soleus muscle.

Hypertriglyceridemia of sepsis is associated with suppressed tissue lipoprotein lipase (LPL) activities. We investigated the effect of sepsis on lipoprotein lipase gene expression in epididymal fat and soleus muscle from control and septic rats in the fasted and fed state. After 24 h of sepsis, LPL activity decreased significantly in epididymal fat from fasted rats by 45% along with a 57% reduction in LPL mRNA levels and LPL mass. Transcription rate, measured by nuclear run-on assay, decreased by 70% in epididymal fat from fasted septic rats compared to fasted control rats. The synthesis rate of LPL in epididymal fat decreased by 31% while the LPL relative synthesis declined by 50% during sepsis. The turnover rate was not altered. Sepsis in fed rats did not lead to a significant decrease in LPL mRNA in epididymal fat but did lower LPL activity and LPL mass by 45%. The sepsis-induced suppression in soleus LPL activity, LPL mRNA levels, and LPL mass in the fasted state also was observed when septic rats were fed. The results indicate that during fasting sepsis, LPL expression in epididymal fat and possibly soleus muscle involves transcriptional regulation. During sepsis in the fed state, the regulation of LPL in adipose tissue may involve posttranslational mechanisms.

Adipose Tissue↗
PubMed1994

Lipoprotein lipase: structure, function and mechanism of action.

Lipoprotein lipase (LPL) plays a central role in the hydrolysis of circulating triglycerides present in chylomicrons, and very low density lipoproteins. The active form of the enzyme is a non-covalent homodimer which contains multiple functional domains required for normal hydrolytic activity including a catalytic domain, as well as sites involved in co-factor, heparin and lipid binding. Recent studies involving site-directed mutagenesis, the elucidation of the three dimensional crystallographic structure of different lipases, as well as analysis of the molecular defects that result in the expression of the familial chylomicronemia syndrome have provided new insights into the structure-function relationship of LPL. As a result, our understanding of structural domains involved in catalysis, heparin, lipid binding, and enzyme-cofactor interaction as well as the mechanism of action of LPL as an acylglycerol hydrolase has been greatly enhanced.

Chylomicrons↗
PubMed1985

Lipoprotein fractions, lipoprotein lipase and hepatic triglyceride lipase during short-term and long-term uptake of ethanol in healthy subjects.

In short-term experiments, healthy fasting persons were given a basic dose of 0.5 g of ethanol/kg body weight, followed by hourly maintenance doses of 0.15 g of ethanol/kg body weight. After 10 h there was a significant increase of triglycerides in the VLDL, LDL, and HDL, the main rise (from 42 to 92 mg/dl) being found in the VLDL triglycerides. Other subjects, who received nourishment isocaloric with ethanol, likewise showed a significant rise of triglycerides in all lipoprotein fractions. Chylomicron triglycerides increased from 9.3 to 35.5 mg/dl. There was no significant change in postheparin HTGL, but postheparin LPL activity decreased after 10 h from 17.9 to 12.2 mmol FFA/ml/h in the fasting subjects, and from 28.5 to 10.2 mmol/FFA/ml/h in the persons receiving food. In long-term experiments after 4 weeks of 70 - 80 g of ethanol and isocaloric food daily, triglycerides increased, especially in the VLDL (from 50 to 82 mg/dl). The increase in the HDL, however, was also significant. After 4 weeks of ethanol, the chylomicron triglycerides in the plasma of the fasting subjects reached a value of 29.3 mg/100 ml, LDL cholesterol decreased, and HDL cholesterol increased. After 4 weeks of ethanol there was an increase in the lipoprotein lipase of the adipose tissue.

Adult↗
PubMed1994

Effect of pancreas transplantation on lipoprotein lipase, postprandial lipemia, and HDL cholesterol.

Pancreas transplantation with systemic venous drainage of the graft causes elevated plasma levels of insulin, known to be a potent regulator of plasma lipoprotein metabolism. We studied 11 post-type I diabetic pancreas-kidney transplant recipients, 9 type I diabetic kidney transplant recipients displaying peripheral hyperinsulinemia due to subcutaneous insulin treatment, 11 nondiabetic kidney transplant recipients as controls for the effects of immunosuppressive medication, and 11 healthy control subjects, all matched for age, sex, and body mass index. We determined fasting lipids, lipoproteins and lipolytic enzymes, as well as postprandial lipid metabolism after a standardized oral fat load. High-density lipoprotein (HDL) cholesterol averaged 1.98 (0.40) mmol/L in pancreas-kidney transplant patients, clearly higher than that of kidney transplant recipients (1.52 (0.36) mmol/L, P < 0.05) or of controls (1.50 (0.38) mmol/L, P < 0.05). In pancreas-kidney transplant patients postprandial lipemia was lowest and lipoprotein lipase activity was highest (average 32% and 154%, respectively, of the mean of the controls) compared with nondiabetic kidney transplant recipients (P < 0.005, P < 0.05) and healthy controls (P < 0.001, P < 0.01). In type I diabetic kidney transplant recipients the levels of HDL cholesterol (1.88 (0.63) mmol/L), postprandial lipemia, and lipoprotein lipase activity were intermediate between pancreas-kidney transplant patients and healthy controls. The distinctly elevated HDL cholesterol in pancreas-kidney transplant patients can be readily explained by the low postprandial triglyceride levels resulting from a high activity of lipoprotein lipase. The very favorable lipid profile in post-diabetic pancreas-kidney transplant recipients could be expected to counteract the severe atherosclerotic risk of long-standing diabetes.

Adult↗
PubMed1994

Regulation of rat mammary-gland uptake of orally administered [1-14C]triolein by insulin and prolactin: evidence for bihormonal control of lipoprotein lipase activity.

The effects of insulin deficiency (streptozotocin-induced) or insulin plus prolactin deficiency on the disposal of orally administered [1-14C]triolein between oxidation to 14CO2, uptake by mammary gland and transfer to suckling pups were studied. Insulin deficiency decreased mammary-gland total weight (by 40%), but caused no change in total tissue DNA. A greater proportion of the [1-14C]triolein was oxidized to 14CO2 (120% increase) in the insulin-deficient rats, and there was a tendency for total transfer of [14C]lipid to mammary gland and suckling pups to be decreased. A parallel decrease in total mammary-tissue lipoprotein lipase activity occurred. Combined hormone deficiency caused more dramatic changes in all parameters measured. Replacement of insulin (24 h) in insulin-deficient rats decreased 14CO2 production, increased the uptake of [14C]lipid into the mammary gland and tended to increase total lipoprotein lipase activity. In contrast, administration of prolactin to insulin-deficient rats had no effect on any of the parameters measured. Replacement of insulin (24 h) in the combined hormone-deficient rats increased uptake of [14C]lipid and lipoprotein lipase approx. 3-fold, whereas prolactin again had no significant effects. Replacement of both hormones increased (6-fold) transfer of [14C]lipid to the pups, but did not increase overall uptake of [14C]lipid (mammary gland, milk clot and pups) above the value for insulin alone. It is concluded that insulin is the primary regulator of triacylglycerol uptake and of lipoprotein lipase activity in the lactating mammary gland of the rat and that the action of prolactin on these processes is indirect. Prolactin, but not insulin, appears to have a direct effect on milk lipid transfer to pups.

Animals↗