Triglyceride Removal Research Articles

Effect of a 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibitor on triglyceride kinetics in chronically streptozotocin-diabetic rats

The effect of simvastatin (MK-733, Banyu, Tokyo, Japan), a new inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase on triglyceride kinetics, was studied in chronically streptozocin-diabetic rats. Diabetic rats, in whom diabetes was induced by a single intravenous injection of streptozotocin (40 mg/kg body weight) 2 months before the experiment, had significantly higher plasma glucose, triglyceride, and cholesterol levels compared with nondiabetic control rats, but triglyceride secretion rate was not increased. Both triglyceride secretion rate and plasma triglyceride level were significantly suppressed under nonfasting conditions in diabetic rats fed a (0.1%) simvastatin-containing diet for 10 days. After an overnight fast, their triglyceride secretion rate was not suppressed by this diet. However, their plasma triglyceride level was significantly (50%) suppressed, suggesting improved triglyceride removal from the circulation. In diabetic rats, the newly secreted triglyceride-rich lipoprotein particles were significantly cholesterol-enriched, but simvastatin had no effect on their lipid composition. These results suggest that the hypertriglyceridemia seen in chronically diabetic rats is mainly due to a triglyceride-removal defect, and that simvastatin reduces plasma triglyceride levels in these rats both by stimulating triglyceride removal and by reducing its entry into the circulation.

Differential metabolic responses to tumor necrosis factor with increase in age

Previous studies have shown varied responses to the effects of tumor necrosis factor (TNF) on glucose and lipid metabolism. To elucidate possible causes for this variation, the present study compared sequential changes in plasma glucose, lactic acid, triglyceride (TG), free fatty acids (FFA), and plasma insulin levels in 1.5- and 16-month-old, normal, fed, male rats, 1 to 6 hours after different doses of intravenous (IV) TNF. In addition, assessment was made of TNF injected intraperitoneally (IP) in precannulated and intact young (1.5 months) rats and of the dose-response (0.25 to50 μg/100 g rat) and the sensitivity to insulin in intact rats. Finally, the metabolic response and changes in serum insulin and corticosterone concentration after IP TNF were compared in 1.5-, 5-, and 16-month-old rats. Data show that metabolic responses vary with increase in age and experimental conditions. Dose-dependent decreases in plasma glucose (1.4 to 3.9 μmol/mL) and elevations in lactic acid (0.8 to 3.0 μmol/mL) were greater in 1.5- versus 16-month-old rats, were delayed in cannulated rats, and were preceded by hyperglycemia following larger IV doses. Plasma TG levels were elevated after TNF in all groups except precannulated rats, and also showed differences with age. In young rats, the elevation in TG peaked 2 hours after IP injection with return to baseline and was preceded by an elevation in FFA levels. In older rats, which were hypertriglyceridemic at base line, the elevation in TG by TNF occurred by suppressing the decrease in TG of controls, was not accompanied by an increase in FFA levels, was sustained for 5 hours, and was of greater magnitude than in young rats. Significant changes in plasma insulin did not occur in young and older rats after IV TNF. However, young rats had a significant decrease ( P < .02) in plasma insulin and an elevation in corticosterone levels after IP TNF, whereas older rats exhibited an increase in plasma insulin ( P < .02) and a comparable elevation in plasma corticosterone. Young rats also showed an increase in plasma insulin following IP TNF when hypoglycemia was prevented by the infusion of glucose. However, when insulin levels were held comparable (2.4 ng/mL), glucose uptake was enhanced ( P < .05) compared with controls. These findings indicate that mobilization of energy substrates occurs during the initial exposure to TNF, which is altered by the nutritional state of the rats and the dose and route of administration. In older rats, this metabolic response is modified in both magnitude and duration, possibly due to development of an increased resistance to insulin and differences in the effect of IP TNF on TG removal versus TG synthesis.

Effect of mild diabetes and dietary fructose on very-low-density lipoprotein triglyceride turnover in rats

Very-low-density lipoprotein (VLDL) triglyceride turnover was examined in mildly streptozotocin (25 mg/kg)-diabetic rats, using Triton WR1339. Diabetic rats fed standard rat chow showed mild hyperglycemia and suppressed levels of plasma insulin. Their triglyceride secretion was significantly suppressed despite an elevated level of plasma free fatty acids. However, the plasma triglyceride level of these diabetic rats was significantly elevated compared with nondiabetic controls. This suggested that the removal of triglyceride from the circulation, as well as its entry into the circulation, was impaired in mildly insulin-deficient rats. Glucose or fructose supplementation (10% in drinking water for 14 days) significantly increased the triglyceride secretion rate of diabetic rats. Especially, fructose supplementation increased plasma insulin to normal levels, but resulted in markedly elevated plasma triglyceride levels (three times higher than glucose-supplemented or chow-fed diabetic rats) despite similar triglyceride secretion rates between the two types of sugar-supplemented diabetic rat groups. This suggested an impairment of triglyceride removal by dietary fructose. The result obtained from chow-fed diabetic rats indicates that mild but significant insulin deficiency resulted in mild hypertriglyceridemia, linked to impaired triglyceride removal rather than to an overproduction of VLDL-triglyceride, despite elevated levels of plasma free fatty acids. Furthermore, fructose feeding induced prominent hypertriglyceridemia not only by stimulating triglyceride secretion, but also by suppressing triglyceride removal from the circulation of mildly diabetic rats.

Effect of long-term insulin deficiency and insulin treatment on the composition of triglyceride-rich lipoproteins and triglyceride turnover in rats

The effect of long-term (4 months) insulin deficiency on triglyceride turnover was examined using Triton WR1339 in rats. Triglyceride secretion rate was estimated in rats 2 weeks and 4 months after induction of diabetes with 40 mg/kg of streptozotocin. By the second week diabetic rats showed prominent hyperglycemia and the plasma insulin level was very low. In spite of a lower triglyceride secretion rate compared to non-diabetic control rats, diabetic rats showed normotriglyceridemia. Thus, the estimated fractional catabolic rate for plasma triglyceride was decreased in the diabetic rats of 2 weeks duration. By the fourth month diabetic rats still showed a suppressed triglyceride secretion rate but plasma triglyceride was markedly higher than in the non-diabetic control rats. Therefore, their estimated fractional catabolic rate for plasma triglyceride was severely suppressed. They also showed hyperglycemia and hypercholesterolemia. The triglyceride-rich lipoprotein particles obtained after Triton injection in long-term diabetic rats were significantly cholesterol-enriched and triglyceride-depleted compared to control rats. These changes were already present in 2-week diabetic rats but the magnitude was significantly smaller that those in long-term diabetic rats. All of these abnormalities (including triglyceride turnover and the particle composition) were almost normalized by 2 weeks of insulin treatment (6 units/day). Thus, it was concluded from the present data that duration of insulin deficiency is an important determinant of triglyceride removal rate from the circulation in rats. Further modification of lipid composition of triglyceride-rich lipoprotein particles by long-term insulin-deficiency could be one of the reasons for this removal defect. Furthermore, overproduction of triglyceride cannot be a cause of hypertriglyceridemia seen in long-term uncontrolled experimental diabetes.

Transport of free fatty acid and triglyceride in anhepatic rats

Without a liver the fractional plasma removal of free fatty acid is one third and chylomicron triglyceride one half of that in the intact rat. The intestine of the anhepatic rat converted enteral fatty acid to plasma triglyceride but was unable to do the same for plasma free fatty acid. This decrease in plasma free fatty acid removal and the inability to recycle the acid as triglyceride were, in part, responsible for the conversion of large fractions of plasma triglyceride flux to the plasma free acid in hepatectomized rats. Increased intravascular triglyceride lipolysis resulting from high circulating lipoprotein lipase concentrations and reduced plasma triglyceride removal were other factors shifting the partition of anhepatic plasma fatty-acid transport from the ester to the free. After the anhepatic plasma clearance of either free fatty acid or triglyceride, relatively more of both compounds was recovered in the lipid of actively metabolizing (heart and muscle) as opposed to storage (adipose) tissue when compared with controls. Sequential evaluations of the recovery of plasma free fatty acid and triglyceride in tissues of anhepatic rats demonstrated accumulation or storage solely in adipose tissue and only when the plasma fatty acid was in triglyceride. This observation and the large conversion of anhepatic circulating triglyceride to the free acid may, in part, explain the lack of an increase in adipose lipid with reduced hepatic mass. The data help explain the preferential use of a lipid fuel in liver disease and the difficulties in obtaining carbon storage in this condition.

Effects of dietary glucose or fructose on the secretion rate and particle size of triglyceride-rich lipoproteins in Zucker fatty rats

Effects of dietary carbohydrate on the secretion rate and particle size of triglyceride-rich lipoproteins were examined in Zucker fatty rats fed fructose and glucose and were compared with those of Zucker lean rats. Carbohydrates were supplied as 10% drinking solutions for 14 days. As compared with lean rats, Zucker fatty rats had hyperinsulinemia and hypertriglyceridemia associated with an increased rate of triglyceride secretion into the circulation. Feeding fructose and glucose to fatty rats produced an increase in plasma glucose levels, whereas plasma insulin concentrations did not show significant changes. Neither fructose nor glucose supplementation produced significant changes in the rate of triglyceride secretion. Despite this, plasma triglyceride concentrations in fructose-fed fatty rats were twice as high as those in glucose-fed rats or those receiving no supplementary carbohydrate. Particle diameters of lipoproteins of density between 0.96 and 1.006 were larger in fructose-fed fatty rats than in those receiving no sugar. The results suggest that feeding fructose, but not glucose, into fatty rats is associated with an impairment of triglyceride removal and a resultant increase in plasma triglyceride concentration, the latter of which is accompanied by an increase in triglyceride contents in each particle.

Effect of probucol on triglyceride turnover in streptozotocin-diabetic rats

The long-term effect of probucol on triglyceride turnover was examined in streptozotocin (40 mg/kg) diabetic rats. Two diabetic groups were prepared: one group received a probucolcontaining (1%) diet (probucol-treated diabetic) and the other standard diet (diabetic control) After 4 months of probucol diet, triglyceride turnover was estimated using Triton WR1339. In diabetic control rats, glucose, triglyceride and cholesterol concentrations in plasma and in the very low density lipoprotein (VLDL) fraction were markedly elevated and plasma insulin was suppressed compared to non-diabetic control rats. There was no significant difference in body weight, plasma glucose and insulin between the 2 diabetic groups. However, the probucol-treated diabetic group showed significantly suppressed levels of triglyceride and cholesterol in total plasma and in the VLDL fraction compared to each corresponding diabetic control value. On the other hand, there were no significant differences in triglyceride secretion rate between the 2 diabetic groups. Newly secreted VLDL particles after Triton injection from diabetic control rats were significantly cholesterol-enriched and triglyceride-depleted compared to those from non-diabetic control rats. However, the composition of those from probucol-treated diabetic rats was similar to that of non-diabetic control group. Prominent hypertriglyceridemia without increase in triglyceride secretion rate in diabetic control group indicates triglyceride removal defect in diabetic rats. Significant suppression of plasma triglyceride level without changes in the triglyceride secretion rate in the probucol-treated diabetic group suggests that probucol stimulated triglyceride removal in diabetic rats. Thus, probucol might normalize VLDL composition, thereby contributing to accelerated triglyceride removal from the circulation of streptozotocin diabetic rats without affecting glucose metabolism.

Glycation of very low density lipoprotein from rat plasma impairs its catabolism

Rat VLDL were glycated in vitro in the presence or absence of a reducing agent. Prior to glycation, the VLDL triglyceride was endogenously radiolabelled with [3H]-oleic acid. Post glycation the VLDL B-apoprotein was exogenously radiolabelled with [131]I. The double labelled VLDL was then injected into normal rats and the decline in plasma radioactivity of the two isotopes was used as a measure of triglyceride and particle clearance. VLDL glycated in either the presence or absence of reducing agent exhibited a significantly slower removal of triglyceride and apoprotein B compared to normal VLDL. The ability of glycated VLDL triglyceride to act as substrate for lipoprotein lipase and hepatic lipase was examined. Increasing concentrations of normal and glycated VLDL triglyceride were incubated with post-heparin plasma. The kinetics of triglyceride hydrolysis were determined in a manner analogous to Michaelis-Menten analysis. Glycated VLDL was found to be poorer than normal VLDL as a substrate for lipoprotein lipase. Glycation of VLDL appears to interfere with the lipolysis of its triglyceride. This may explain the delayed clearance of glycated VLDL triglyceride in vivo. Glycation also extended the mean plasma residence time of the VLDL particle. These factors may, in part, contribute to the hypertriglyceridaemia observed in subjects with diabetes mellitus.

Acquired Hyperlipidemia (Secondary Dyslipoproteinemias)

Acquired hyperlipidemia (secondary dyslipoproteinemias) results from underlying disorders that lead to alterations in plasma lipid and lipoprotein metabolism. Secondary dyslipoproteinemias may mimic primary forms of hyperlipidemia and can have similar consequences. They may result in increased predisposition to premature atherosclerosis or, when associated with marked hypertriglyceridemia, may lead to the development of pancreatitis and other features of the chylomicronemia syndrome. Diabetes mellitus and use of drugs such as diuretics, beta blockers, and estrogens are commonly encountered causes of secondary dyslipoproteinemia. Other conditions leading to acquired hyperlipidemia include hypothyroidism, renal failure, nephrotic syndrome, alcohol usage, and some rare endocrine and metabolic disorders. When secondary and familial forms of hypertriglyceridemia coexist, triglyceride removal mechanisms may be saturated and marked hypertriglyceridemia with fasting chylomicronemia might ensue. Treatment of the underlying condition, when possible, or discontinuation of the offending drugs usually leads to an improvement in the hyperlipidemia. Specific lipid-lowering therapy may be required in certain circumstances.

Long-term effects of bezafibrate on in vivo VLDL-triglyceride production in the rat

Long-term effects of bezafibrate on in vivo production of VLDL-triglyceride were studied in the rat. Bezafibrate given at a daily dose of 30 mg/kg body weight for 14 days produced a decrease not only in triglyceride by 51% but in cholesterol by 28% and phospholipid by 18%. Despite a marked reduction in plasma triglyceride concentrations, there was no significant change in the rate of VLDL-triglyceride secretion from the liver into the circulation between bezafibrate-treated and control animals (1113 ± 58 and 1234 ± 63 μg/min, respectively). In addition, bezafibrate produced no change in lipid composition in VLDL. These results suggest that bezafibrate enhances triglyceride removal from the circulation, which leads to reduction in plasma triglyceride.

Pathogenesis of the hypertriglyceridemia at early stages of alcoholic liver injury in the baboon.

To study the mechanism of alcoholic hypertriglyceridemia, baboons were pair-fed liquid diets containing 50% of energy as ethanol or as additional carbohydrate for 5-16 months. Alcohol-fed animals developed hypertriglyceridemia and early stages of alcoholic injury, namely fatty liver with or without perivenular fibrosis. In the fasting state, the triglyceride content was sixfold higher in very low density (VLDL) and intermediate density (IDL) lipoproteins and twofold higher in low density (LDL) and high density (HDL) lipoproteins. The increase in VLDL was markedly exaggerated in the postprandial state. To investigate the source of these increases, we determined net output or removal of serum triglycerides during circulation through either splanchnic or extrasplanchnic (lower extremities) vascular beds. In the splanchnic territory, there was net output of triglycerides in VLDL and net removal from the other lipoproteins. In alcohol-fed baboons, the output of VLDL-triglycerides into the hepatic (but not into the portal) vein tripled. This increase was mainly due to production of VLDL particles that were larger and had a flotation (Sf greater than 400) different from the Sf 20-400 which predominated in controls. This was associated with increased splanchnic removal of labeled chylomicron- or VLDL-triglycerides. In the lower extremities, there was an arteriovenous difference in VLDL-triglyceride concentration and this was increased in the alcohol-fed animals. Thus, the primary mechanism of the hypertriglyceridemia in alcohol-fed baboons was increased production of large, chylomicron-like VLDL by the liver, whereas both the extrasplanchnic extraction of VLDL-triglycerides and the splanchnic extraction of triglycerides from chylomicron- and VLDL-remnants were secondarily enhanced.

Increased turnover of very low density lipoprotein triglyceride during treatment with cholestyramine in familial hypercholesterolaemia

Kinetics of very low density lipoprotein (VLDL) triglyceride were determined in seven patients with heterozygous familial hypercholesterolaemia, using a 3H-glycerol technique. The study was repeated after 5-7 weeks of therapy with the bile acid-binding resin, cholestyramine. The rate of synthesis of VLDL triglyceride was increased by 85% (P less than 0.05) during resin therapy. Simultaneously, the fractional catabolic rate of VLDL was increased by 40% (P less than 0.02), so that only a moderate increase in plasma concentration was observed. Repeated measurements of VLDL size by electron microscopy (before, 1 week, and 5-7 weeks after initiation of therapy) indicated that a transient increase in VLDL size occurred in response to cholestyramine. The results are consistent with a stimulatory effect of bile acid sequestrants on VLDL triglyceride production and indicate that, in most subjects, a compensatory increase in VLDL triglyceride removal occurs.

Effect of dietary fructose on triglyceride turnover in streptozotocin-diabetic rats

The effects of fructose or glucose on plasma triglyceride kinetics in streptozotocin (40 mg/kg) diabetic rats were studied using Triton WR1339. To separate groups of diabetic rats fructose or glucose was supplied at 10% in drinking water. Diabetic rats without sugar supplementation (diabetic control) had significantly suppressed triglyceride secretion compared to non-diabetic controls. Neither fructose nor glucose supplementation increased the triglyceride secretion rate in diabetic rats. However, despite reduced secretion rates, plasma triglyceride levels in glucose-supplemented diabetic rats, diabetic controls and non-diabetic controls were essentially identical. This suggested that removal of triglyceride from the circulation was impaired in the diabetic rats. In contrast, fructose supplementation resulted in a more than 150% (significant) increase in the mean plasma triglyceride of diabetic rats. The observation of significant hypertriglyceridemia in spite of low triglyceride secretion rate in fructose-supplemented diabetic rats suggests that dietary fructose, but not glucose, interferes with triglyceride removal from the circulation of streptozotocin-diabetic rats. This impairment by dietary fructose is in addition to the impaired triglyceride removal associated with diabetes alone.

Effects of dietary sucrose on age-related changes in VLDL-triglyceride kinetics in the rat

The effects of sucrose feeding on in vivo kinetics of triglyceride metabolism were compared in rats aged 2 and 12 months. Sucrose was supplied as a 10% solution in their drinking water for 2 weeks. Although plasma triglyceride concentrations doubled with age, total triglyceride secretion rates for the whole rat (mg/min/rat) increased by 40%, suggesting a decrease in the efficiency of triglyceride removal from plasma with aging. The rate of triglyceride secretion per unit body mass (mg/min/kg body weight), however, decreased by 40% as the rats grew to 12 months of age. These age-related differences were statistically significant only in rats receiving supplementary sucrose. Feeding sucrose to rats of both ages doubled the secretion rates of triglyceride not only for the whole rat but also per unit body mass. However, it tripled triglyceride concentrations, implying that the sugar decreases the removal efficiency of plasma triglyceride equally in rats at either age. Fasting hypertriglyceridemia induced by sucrose supplement was much greater in old rats than in young rats (162 ± 30 vs. 80 ± 8 mg/dl). The present studies demonstrate that dietary sucrose enhances age-related changes in triglyceride kinetics in the rat.

Postprandial lipemia and chylomicron clearance in athletes and in sedentary men

To examine the effects of exercise on postprandial serum triglyceride (TG) metabolism, we measured oral and intravenous fat tolerance and chylomicron-TG half-life in highly trained endurance athletes and in a sedentary control group matched for body weight and fasting serum TG concentration. Postprandial lipemia was lower in athletes after meals containing 40 g fat (1.5 +/- 0.7 vs 2.6 +/- 1.5 mmol.L-1.8 h-1, p less than 0.001) or 140 g fat (2.5 +/- 1.2 vs 6.1 +/- 1.9 mmol.L-1.8 h-1, p less than 0.001). The disappearance of an intravenous bolus of Intralipid was faster in athletes (5.4 +/- 1.2%/min) than in sedentary men (4.3 +/- 0.8%/min, p less than 0.01). The half-life of chylomicron-TG was shorter in athletes (3.0 +/- 0.8 min) than in sedentary men (4.0 +/- 1.0 min, p less than 0.05). These findings indicate that chronic exercise decreases postprandial lipemia by reducing chylomicron-TG's half-life. This effect is due partly to reduced fasting serum TG pool size and partly to a direct effect of exercise on the serum TG removal system.

The role of insulin in triglyceride turnover in rats

Exogenously induced hyperinsulinemia can increase in vivo triglyceride production in rats receiving dietary fructose, either as monosaccharide or as sucrose, but not in those receiving only glucose. Thus, in the presence of fructose, but not glucose, insulin stimulates triglyceride production. Dietary fructose can also impair the removal of circulating triglyceride. Exogenous insulin overcomes this fructose-associated impairment of triglyceride removal. On the other hand, streptozotocin-diabetic rats showed a suppressed triglyceride secretion rate (TgSR) but their plasma triglyceride level was unchanged. Therefore, insulin deficiency may result in not only decreased production of triglyceride but also impaired triglyceride removal from the circulation. Fructose-fed diabetic rats showed higher plasma triglyceride levels than chow-fed diabetic rats without a concomitant increase in TgSR, suggesting impaired triglyceride removal from the circulation induced by fructose in diabetic rats. Glucose-fed diabetic rats did not differ in TgSR or plasma triglyceride level from chow-fed diabetic rats. These observations indicate that circulating insulin and dietary fructose, but not glucose, have a key role in very-low-density lipoprotein triglyceride turnover in rats.

Removal of triglycerides from polymer surfaces in relation to surfactant packing. Ellipsometry studies

La performance de l'agent de surface depend des autres composants dans la solution de purification et depend du type d'agent de surface

Very low density lipoprotein triglyceride metabolism in relatives of hypertriglyceridemic probands. Evidence for genetic control of triglyceride removal.

The production and catabolism of very low density lipoprotein triglycerides (VLDL-TG) were determined in 11 index patients with primary hypertriglyceridemia and in their 70 first-degree relatives. In the probands the mean value for VLDL-TG production rate was twice normal, and the mean fractional catabolic rate (FCR) was reduced to 50% from normal. A similar kinetic pattern was also observed in most hypertriglyceridemic relatives. In the normotriglyceridemic relatives the mean values of both kinetic parameters were comparable to those of controls. No kinetic differences were observed between families with familial hypertriglyceridemia, familial combined hyperlipidemia, or genetically unclassified hypertriglyceridemia (all diagnosed by lipoprotein phenotypes). Thus, no explanation for the phenotypic differences between the two forms of familial hyperlipoproteinemia was found in plasma VLDL-TG metabolism. When the families were grouped according to the VLDL-TG production rate of the proband, there was no significant difference between the VLDL-TG production rates of relatives of "overproducer" probands and relatives of the probands with normal VLDL-TG production rate. In contrast, relatives of low FCR probands had significantly lower mean FCR than the relatives of probands with a normal FCR. This difference in FCR was present both in hypertriglyceridemic and normotriglyceridemic relatives. These results suggest that the catabolism (lipolysis) of VLDL-TG is under genetic control, whereas the VLDL-TG production rate is mainly related to obesity. It is likely that hypertriglyceridemia often develops on the basis of VLDL overproduction in individuals who have a genetically low VLDL triglyceride removal (lipolytic) capacity.

Removal of triglycerides from hard surfaces by surfactants: An ellipsometry study

AbstractThe removal of triglycerides from hard surfaces by surfactants was studied by means of ellipsometry. Various surfactants were examined, and as the nonionic surfactants of the alkyl polyoxyethylene type proved to be most efficient, they were studied in particular detail. The influence of factors such as surfactant critical micelle concentration, the length of the polyoxyethylene chain in the nonionic surfactants, the pH, the temperature, and the agitation were investigated. The cleaning process involves many consecutive steps on the molecular level, and the measurements provide interesting information about the cleaning mechanism.

Acute and Chronic Effects of Dihydropyridines on Triglycerides in Humans

Several drugs used in the treatment of hypertension have been shown to affect lipid metabolism. A few studies have examined in detail the effects of calcium antagonists on blood lipids. We investigated the effects of nifedipine and nitrendipine on blood lipids using two experimental protocols. The first study was a double-blind, randomized, placebo-controlled trial to assess the effects of acute oral administration of nifedipine 10 mg on blood lipids in 10 patients (9 males, 1 female; age range 26-50 years) with mild hypertriglyceridemia. Serum triglycerides were not significantly affected (from 310 +/- 120 to 280 +/- 110 mg/dl 2 h after nifedipine) but a slight decrease was observed in patients with higher baseline levels. In the second study, an intravenous fat tolerance test (ivFTT, Intralipid 10%, 1 ml/kg body weight, as a bolus) was performed before and after chronic oral administration of nitrendipine 10 mg b.i.d. in 10 mild to moderate hypertensive patients (7 males, 3 females; age range 40-60 years). After nitrendipine treatment, the fractional removal rate (K2) of the lipid emulsion was significantly increased from 3.1 +/- 0.9 to 3.8 +/- 0.9% min (p less than 0.05). The main findings of these studies suggest that the secretion of lipoprotein lipase might be stimulated by calcium antagonists. Alternatively, the vasodilation produced by these compounds may influence triglyceride removal by expanding the capillary bed where the enzyme exerts its activity. In conclusion, calcium antagonists do not seem to cause unwanted side effects on blood lipids and apparently enhance triglyceride removal.