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PubMed2001

Analysis of the ileal bile acid transporter gene, SLC10A2, in subjects with familial hypertriglyceridemia.

Familial hypertriglyceridemia (FHTG), a disease characterized by elevated plasma very low density lipoprotein triglyceride levels, has been associated with impaired intestinal absorption of bile acids. The aim of this study was to test the hypothesis that defects in the active ileal absorption of bile acids are a primary cause of FHTG. Single-stranded conformation polymorphism analysis was used to screen the ileal Na(+)/bile acid cotransporter gene (SLC10A2) for FHTG-associated mutations. Analysis of 20 hypertriglyceridemic patients with abnormal bile acid metabolism revealed 3 missense mutations (V98I, V159I, and A171S), a frame-shift mutation (646insG) at codon 216, and 4 polymorphisms in the 5' flanking sequence of SLC10A2. The SLC10A2 missense mutations and 5' flanking sequence polymorphisms were not correlated with bile acid production or turnover in the hypertriglyceridemic patients and were equally prevalent in the unaffected control subjects. In transfected COS cells, the V98I, V159I, and A171S isoforms all transported bile acids similar to the wild-type SLC10A2. The 646insG frame-shift mutation abolished bile acid transport activity in transfected COS cells but was found in only a single FHTG patient. These findings indicate that the decreased intestinal bile acid absorption in FHTG patients is not commonly associated with inherited defects in SLC10A2.

Adult↗
PubMed1973

Abnormal lipoprotein lipase in familial exogenous hypertriglyceridemia.

A 5-yr old male proband and his sister have had hypertriglyceridemia and hepatosplenomegaly since birth. When studied on a metabolic ward, they demonstrated rapid decreases in serum triglycerides on 3 g fat/day diets. Oral glucose tolerance tests were normal. Postheparin lipolytic activity (PHLA) against chylomicrons was virtually absent in both children whereas the mother and a normolipemic sister had levels approximately 50% normal. However, all four had a normal PHLA against commercial triglyceride emulsion (Intralipid). Two unrelated children from different kindreds of typical type 1 hyperlipoproteinemia and two patients with acquired type V hyperlipoproteinemia had deficient PHLA against both substrates. No inhibitors of PHLA could be demonstrated in the proband's plasma, and his own PHLA could not be enhanced by either normal concentrated plasma or pooled d > 1.063 lipoprotein fraction. The proband's postheparin plasma required almost 20 times the normal chylomicron-triglyceride concentration to reach one-half maximal lipase velocity. Both affected siblings showed heavy pre-beta lipoprotein electrophoretic bands plus chylomicrons in their fasting plasmas while ingesting a 33% carbohydrate, 30% fat diet. Incubation of their postheparin plasma with S(f) > 400 chylomicrons in vitro produced a smaller S(f) 20-400 "remnant" with pre-beta electrophoretic mobility that was not seen under the same conditions when normal postheparin plasma was used. Postheparin monoglyceridase and phospholipase activities were either normal or only moderately decreased when determined with appropriate artificial substrates. These data are consistent with either (a) a mutant gene producing a lipoprotein lipase with unusual substrate specificities or (b) an absolute deficiency of normal lipoprotein lipase with a compensatory increase in some other postheparin triglyceridase.

Blood Protein Disorders↗
PubMed1975

Effects of polyunsaturated fats on lipid metabolism in patients with hypertriglyceridemia.

Studies were carried out on the effects of polyunsaturated fats on lipid metabolism in 11 patients with hypertriglyceridemia. During cholesterol balance studies performed in eight patients, the feeding of polyunsaturated fats, as compared with saturated fats, caused an increased excretion of endogenous neutral steroids, acidic steroids, or both in most patients. Increases in steroid excretions were marked in some patients and generally exceeded the decrement of cholesterol in the plasma compartment. The finding of a greater excretion of fecal steroids on polyunsaturated fats in hypertriglyceridemic patients contrasts to the lack of change in sterol balance previously reported for patients with familial hypercholesterolemia; however, other workers have found that polyunsaturated fats also enhance steroid excretion in normal subjects. In most of the patients, simultaneous studies were carried out on biliary lipid composition, hourly outputs of biliary lipids, and pool sizes of bile acids. In several but not all patients, fasting gallbladder bile became more lithogenic after institution of polyunsaturated fats. This increased lithogenicity was not due to a decrease in bile acid pools; in no case was the pool decreased by polyunsaturated fats. On the other hand, two patients showed an increased output of biliary cholesterol, and frequently there was an increase in fecal neutral steroids that were derived from cholesterol; thus, polyunsaturated fats may increase bile lithogenicity in some patients through mobilization of cholesterol into bile. Reductions in plasma cholesterol during the feeding of polyunsaturated fats was seen in most patients, and these changes were usually associated with a decrease in concentration of plasma triglycerides. In fact, the degree of cholesterol lowering was closely correlated with the extent of triglyceride reduction. Therefore, in hypertriglyceridimec patients polyunsaturated fats may contribute to cholesterol reduction by changing the metabolism of triglycerides or very low density lipoproteins. The findings of changes in the metabolism of cholesterol, bile acids, and triglycerides in the patients of this study suggests that polyunsaturated fats may cause a lowering of cholesterol through multiple mechanisms, and it seems unlikely that a single action can explain all the effects of these fats on the plasma lipids.

Adult↗
PubMed1982

Effect of somatostatin-induced suppression of postprandial insulin response upon the hypertriglyceridemia associated with a high carbohydrate diet.

In an attempt to define the relationship between plasma insulin and triglyceride concentrations, we have studied the effect of suppression of the postprandial insulin response upon the secretion and plasma concentration of very low density lipoprotein (VLDL)-triglycerides. Eight nondiabetic subjects with a wide range of fasting plasma triglyceride levels (100-358 mg/dl) were studied during three dietary periods: base line, high carbohydrate (80% calories), and high carbohydrate (80% calories) with a daily intravenous infusion of somatostatin (SRIF) (1.3 micrograms/min) between 800 and 2,100 h. The significant increase in postprandial insulin response observed during high carbohydrate vs. base line was completely abolished during high carbohydrate-SRIF. However, plasma triglyceride levels rose in all subjects during each high carbohydrate period (with/without SRIF) vs. base line and the mean values reached during each period were the same (476 +/- 165 vs. 482 +/- 152 mg/dl, respectively). The secretion of VLDL-triglyceride into plasma was higher in four subjects, the same in two subjects, and lower in one subject during high carbohydrate-SRIF vs. high carbohydrate alone. The mean production rate of VLDL-triglyceride (mg/kg per h) was 25.6 +/- 4.9 during the high carbohydrate and 40.9 +/- 28.1 during the high carbohydrate-SRIF periods. These values were not significantly different. Postprandial glucose levels were slightly increased during high carbohydrate-SRIF, but overnight glucose concentrations were not affected. Plasma FFA levels were not different during the two high carbohydrate periods. Plasma glucagon levels did not appear to affect the results either. This study indicates that postprandial hyperinsulinemia during a high carbohydrate diet is not necessary for induction of hypertriglyceridemia.

Adult↗
PubMed1976

Induction of hypertriglyceridemia by a low-fat diet.

We have studied the effects of moderate dietary fat restriction on plasma triglyceride, cholesterol, glucose, and insulin response in 27 subjects. Compared with a control diet (45% fat, 40% carbohydrate [CHO], 15% protein) the low fat (higher CHO) diet (30% fat, 55% CHO, 15% protein) produced a 41% increase in fasting triglyceride level (155 +/- 17 to 219 +/- 23 mg%) with no change in fasting plasma cholesterol level. Furthermore, this increase in triglyceride levels; induced by the higher CHO content of the low fat diet, was seen in 26 out of 27 subjects. Postprandial triglyceride, glucose, and insulin levels were also higher on the low fat (higher CHO) diet. Since hypertriglyceridemia is a significant risk factor for the development of coronary heart disease, and since our data indicate that the moderate increase in dietary CHO associated with a low fat diet will elevate plasma triglyceride levels, we believe that more caution is necessary before recommending the wide-spread use of low fat diets for heart disease prevention.

Adult↗
PubMed1976

Reversal of decreased human adipose tissue lipoprotein lipase and hypertriglyceridemia after treatment of hypothyroidism.

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.

Adipose Tissue↗
PubMed1987

Relationship of organ lipoprotein lipase activity and ketonuria to hypertriglyceridemia in starved and streptozocin-induced diabetic rats.

Although lipoprotein lipase (LPL) is believed to be rate limiting in the catabolism of triglyceride-rich lipoproteins, LPL activity has not correlated with plasma triglyceride concentrations in experimental rat diabetes. To gather more information about this enzyme system in diabetes, LPL activities were measured in representative tissues from control and streptozocin-induced diabetic rats fed fat-free chow and in 48-h-starved animals. The DNA content of each tissue was determined so that LPL activity could be expressed in a way that was unaffected by tissue wasting. Diabetic animals lost approximately 20% of their body mass. Adipose tissue and soleus muscle cell masses were reduced, and there was marked fat atrophy at necropsy. Adipose tissue LPL was decreased in both starved and diabetic animals, whereas skeletal muscle activities were variably affected. Lipase content and distribution among the individual organs were calculated with published data for rat carcass composition. In diabetic rats, total LPL (adipose tissue, muscle, and parenchymal organs) was reduced by nearly two-thirds so that skeletal muscle became the predominant source of LPL. Ketonuria was less frequent in diabetic than in starved rats (P less than .018) despite their severe wasting. Serum triglyceride concentrations were higher in ketonuric than nonketonuric diabetic animals, and severe hypertriglyceridemia was seen exclusively in heavily ketonuric animals. These observations together with published information suggest that plasma triglyceride concentrations in the rat model are determined by a complex interplay between very-low-density lipoprotein synthesis, the capacity of the LPL removal system, properties of the lipoprotein substrate, and other unidentified factors.

Adipose Tissue↗
PubMed1996

Diabetic dyslipidemia: basic mechanisms underlying the common hypertriglyceridemia and low HDL cholesterol levels.

Elevated levels of plasma triglycerides (TG) and reduced concentrations of HDL cholesterol are very common in patients with diabetes, particularly NIDDM. Although regulation of the plasma concentrations of VLDL, the major TG-rich lipoprotein is extremely complex, it is clear from in vivo kinetic studies that increased rates of secretion of VLDL into plasma is almost uniformly present in patients with NIDDM and hypertriglyceridemia. Recent studies at the cellular level indicate that increased fatty acid flux to the liver, also common in NIDDM (and other insulin-resistant states associated with elevated plasma TG levels), will stimulate the assembly and secretion of apoprotein (apo) B-containing lipoproteins by targeting apoB for secretion rather than intracellular degradation. Increased rates of secretion of VLDL into plasma appears to drive the exchange of TG from these lipoproteins for HDL cholesteryl ester. This exchange, which occurs in plasma, is facilitated by cholesteryl ester transfer protein, and generates a TG-enriched HDL that is a substrate for either hepatic lipase or lipoprotein lipase. When the TG in HDL is hydrolyzed, the resultant particle is smaller, and this appears to affect the binding of the major HDL protein, apoA-I. ApoA-I dissociates from the smaller, lipid-poor HDL, and the free apoA-I (molecular weight 28,000) can be filtered by the glomerulus in the kidney and most likely is degraded in renal tubular cells after reabsorption. Thus, increased free fatty acid transport in plasma, a common abnormality in insulin-resistant states, may be the underlying driving force for the two common lipid abnormalities seen in diabetes.

Apolipoprotein A-I↗
PubMed1986

Increased risk for vitamin A toxicity in severe hypertriglyceridemia.

A 48-year-old woman with malabsorption and type V hyperlipoproteinemia developed hypervitaminosis A with a total plasma vitamin A level of 871 micrograms/dL during therapy with an oral dosage of 18,000 retinol equivalents (60,000 IU) daily. Twelve percent of the total plasma retinol was found to be transported in the chylomicron-very low density lipoprotein (VLDL) fraction, which does not contain retinol-binding protein. For comparison, concentrations of retinyl esters and retinol were determined in nine patients with type V hyperlipoproteinemia and nine control subjects, none of whom were using vitamin A supplements. Both retinyl esters and retinol were significantly elevated in the group with hyperlipoproteinemia (p less than 0.0005 in both cases). Eight of these nine patients had retinol present in the chylomicron-VLDL fraction, whereas retinol was not detectable in this fraction in any of the nine normal controls. The data suggest that patients with severe hypertriglyceridemia associated with type V hyperlipoproteinemia are at increased risk for hypervitaminosis A.

Female↗
PubMed1982

Association of hyperapobetalipoproteinemia with endogenous hypertriglyceridemia and atherosclerosis.

Researchers disagree on whether plasma triglyceride levels are an independent risk factor for atherosclerotic coronary artery disease. We hypothesized that patients with endogenous hypertriglyceridemia would differ: Some would have normal values of plasma low-density lipoprotein (LDL) B protein; others, despite their normal level of LDL cholesterol, would have increased levels of LDL B protein. We believe the latter patients--those with hyperapobetalipoproteinemia--would be the ones at risk for atherosclerosis. We studied two populations. Group 1, consisting of 162 patients with type IV lipoprotein patterns, was divided into two groups. One subgroup (A), which included 38 patients with elevated plasma LDL B atherosclerotic disease than the other subgroup (B) of 36 patients with normal levels of plasma LDL B protein (10 patients versus two, p less than 0.02). Group 2 consisted of 100 patients who had had myocardial infarction. Eighty-one percent of the 47 hypertriglyceridemic and 70% of the 53 normotriglyceridemic patients had elevated plasma LDL B protein levels (129 mg/dL or greater)--a proportion significantly higher than that in Group 1 (p less than 0.001). Thus, an elevated plasma level of LDL B protein not only identifies subgroups of patients with type IV lipoprotein patterns, but also may be an important marker for atherosclerotic disease.

Adult↗
PubMed1976

Effect of 1,5-dicaffeoylquinic acid on ethanol-induced hypertriglyceridemia. Short communication.

Male Wistar rats were administered acutely and chronically ethyl alcohol. The effect of 1,5-dicaffeoylquinic acid (cynarine) on ethanol induced hypertriglyceridemia and on hepatic concentration of triglyceride was investigated. In rats treated acutely with ethanol the serum and hepatic triglycerides showed significant rise by 216 and 111%, resp. The prolonged administration of ethanol caused insignificant increase of the serum triglyceride concentration by 40%, while its hepatic content was significantly increased by 100%. In rats receiving ethanol and cynarine simultaneously, distinct reduction of the serum and hepatic triglyceride concentration was observed.

Alcoholism↗
PubMed2001

[Apolipoprotein C III gene Sst I polymorphism in patients with endogenous hypertriglyceridemia in Chinese population].

OBJECTIVE: To investigate the apoC III gene Sst I polymorphism and its relationship with serum lipids and apolipoproteins (apo) levels in patients with endogenous hypertriglyceridemia in Chinese population. METHODS: The genotype and allele frequency of apoC III gene Sst I polymorphism was assayed by polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP). Serum lipids were measured by enzymatic kits and apolipoproteins A I, A II, B100, C II, C III and E were measured by RID kits developed by Apolipoprotein Research Unit of WCUMS in 176 HTG patients whose fasting serum TG levels were > or = 2.26 mmol/L and in 199 healthy subjects whose fasting serum TG levels were < 1.82 mmol/L and TC levels < 6.2 mmol/L from a population of Chinese Han nationality in Chengdu area. RESULTS: In both HTG group and control group, S1 allele was the major allele and homozygous S1S1 genotype was the most frequent one. The frequency of S2 allele was significantly higher than that reported in Caucasians (0.289 vs 0.06-0.16, P < 0.05). No differences were found in apoC III gene Sst I polymophism in the HTG group when compared with the control group (0.287 vs 0.289, P > 0.05). The genotype of S2S2 was not associated with higher TG and apolipoproteins levels when compared with the genotypes of S1S1 and S1S2 (P > 0.05). CONCLUSION: These results suggest that the Sst I polymorphism of the apoC III gene was not associated with endogenoushypertriglyceridemica in Chinese population.

Adult↗
PubMed1975

Mechanism of avian estrogen-induced hypertriglyceridemia: evidence for overproduction of triglyceride.

Relying on methods other than the determination of turnover rate of triglyceride from the curve of plasma triglyceride radioactivity after administration of labeled precursor, we have confirmed that the endogenous hypertriglyceridemia induced by estrogenization of the chick is accompanied by increased production of triglyceride. Chicks estrogenized with diethylstilbestrol became grossly hypertriglyceridemic and had elevated levels of plasma free fatty acid. Within 5 min of administration of labeled palmitate, estrogenized hypertriglyceridemic birds converted approximately 10 times more plasma free fatty acid to hepatic triglyceride than did controls. In addition, 2 hr after intraperitoneal injection of [14-C]acetate or [U-14-C]glucose, the specific activity of very low density lipoprotein triglyceride (VLDL-TG) of estrogenized birds reached or exceeded that of the untreated controls, and the rapid enrichment of the vastly expanded plasma VLDL-TG pool with labeled triglyceride further indicated that increased production of triglyceride occurs with estrogenization. Furthermore, [14-C]acetate incorporation into VLDL-TG was calculated to be 1.6 and 6.6% of the injected dose in estrogenized birds compared with 0.1 and 0.2% in untreated birds. Increased production of plasma VLDL-TG was confirmed by a kinetic study of VLDL-TG metabolism, employing reinjected, endogenously prepared [14-C]triglyceride-labeled VLDL. The fractional turnover rate of VLDL-TG in estrogenized hypertriglyceridemic birds was substantially less than that in untreated controls (0.32 plus or minus 0.03 vs 0.71 plus or minus 0.03/hr), but the total turnover rate was nearly 50 times greater (244 plus or minus 52 vs. 5 plus or minus 1 mg/hr).

Acetates↗
PubMed1976

Measurement of two plasma triglyceride lipases by an immunochemical method: studies in patients with hypertriglyceridemia.

Postheparin plasma lipolytic activity consists of two hydrolytic activities, hepatic triglyceride lipase and lipoprotein lipase. These two enzymes were separated and partially purified by means of ammonium sulfate precipitation and affinity chromatography using Sepharose with covalently linked heparin and concanavalin A, respectively. Antibodies were produced against hepatic triglyceride lipase and they did not cross react with lipoprotein lipase. Optimal conditions for selective precipitation of hepatic lipase and specific measurement of these two lipases were investigated. This method was applied to the study of 15 patients with hypertriglyceridemia and 8 patients with familial lecithin-cholesterol-acyltransferase deficiency of whom 6 also had a marked elevated plasma triglyceride concentration. All patients had normal values of hepatic plasma lipase. All 8 patients with Type I and 2 of 4 patients with Type V hyperlipoproteinemia had lipoprotein lipase activities that were markedly reduced. The patients with Type III hyperlipoproteinemia and all 8 patients with lecithin-cholesterol-acyltransferase deficiency also had normal lipoprotein lipase values. These studies emphasize the necessity for differentiating between triglyceride lipase activity of hepatic and extrahepatic origin in evaluating patients with impaired triglyceride metabolism.

Acyltransferases↗
PubMed1990

[Two cases of brain infarction associated with hypertriglyceridemia].

We reported two cases of brain infarction. They were cousins. Case 1 was a 12-year-old girl, who complained of aphasia, dyscalculia, right-left disorientation and right homonymous hemianopsia. CT showed low density areas in left superior and middle temporal gyri. Case 2 was a 15-year-old boy, who had left hemiplegia and hypesthesia to pain, temperature and touch on the left side of the body. CT showed low density areas from the genu of the internal capsule to the corona radiata, and from the posterior portion of putamen to the posterior limb of the internal capsule on the right side. Both cases had hypertriglyceridemia which might be associated with the etiology of infarction.

Adolescent↗
PubMedDate not supplied

[Change in the apoproteins of very low density lipoproteins in the blood in hypertriglyceridemia].

Some properties of very low density lipoproteins were studied under conditions causing an increase of their concentration in blood plasma. Content of high molecular apolipoprotein B and low molecular lipoproteins were estimated after fractionation using column chromatography and selective precipitation with tetramethylurea. In 216 men (40-59 years old) with hypertriglyceridemia the increase in content of particles of very low density lipoproteins was accompanied by simultaneous alteration in their composition in blood plasma: content of low molecular polypeptides, triglycerides and cholesterol was increased per a weight unit of apoprotein B. At the same time, the absolute concent of apoprotein B and of low molecular apoproteins of very low density lipoproteins was increased in blood plasma. The most distinct alteration in the ratio of apolipoproteins to very low density lipoproteins was observed, if content of testosterone--activator of lipoprotein lipase--was decreased in blood plasma.

Adult↗
PubMed1979

Secondary hypertriglyceridemia and hyperlipoproteinemia in patients with primary asymptomatic gout.

We carefully selected 30 men with primary gout, rendered asymptomatic by therapy, to examine the frequency and type of hyperlipidemia and hyperlipoproteinemia, with the objective of determining whether serum uric acid, alcohol intake, liver function, kidney function, and (or) drugs were participating in the secondary lipid disorder. Sixty-one age- and sex-matched men were used as controls. About 73% of the gout patients had hypertriglyceridemia, 1.6-fold the frequency found in the control group. Types IV and IIb lipoprotein electrophoretic patterns were most prevalent in the gout group. Neither alcohol intake nor hyperuricemia, per se, seems to be the cause of the lipid and lipoprotein disorder and cannot be related to liver or kidney dysfunctions. Obesity was the major underlying factor associated with the lipidemia. The study suggests that diet and, possibly, defective clearance of triglycerides may be etiologic factors associated with the abnormal serum triacylglycerol (triglyceride) and lipoprotein concentrations in these individuals.

Blood Chemical Analysis↗