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PubMed2003

Apolipoprotein CIII deficiency prevents the development of hypertriglyceridemia in streptozotocin-induced diabetic mice.

To explore the role of apolipoprotein (apo) CIII in the development of hypertriglyceridemia associated with diabetes mellitus, we examined triglyceride (TG) kinetics in apo CIII - deficient mice (apo CIII - null) and wild-type (WT) (C57BL/6J) mice with diabetes induced by the injection of streptozotocin (STZ). Plasma TG levels increased significantly in WT mice after diabetes was induced (102 +/- 29 v 65 +/- 33 mg/dL, P <.01). Apo CIII-null mice had a significantly lower TG level (35 +/- 9 mg/dL) that remained unchanged even when diabetes was induced (35 +/- 8 mg/dL). The TG secretion rate (TGSR) measured by the Triton WR1339 method tended to decrease in diabetic WT, indicating that catabolism of TG was impaired. Apo CIII-null mice showed 2-fold higher TG production than WT mice, indicating markedly faster clearance of TG. The high TGSR was halved when diabetes was induced in apo CIII-null mice, and the fractional catabolic rate (FCR) of TG was also halved, although it was still significantly higher than in WT mice. Lipoprotein lipase (LPL) activity in postheparin plasma was not significantly altered in WT or apo CIII-null mice regardless of the presence or absence of diabetes. [(3)H] very-low-density lipoprotein (VLDL)-TG from WT or apo CIII-null mice showed similar clearance by WT recipients, and this was also observed when VLDL was obtained from diabetic counterparts. In contrast, VLDL-TG was cleared faster by apo CIII-null recipients compared with WT recipients, regardless of the VLDL donors. These results suggest that apo CIII deficiency prevents the development of hypertriglyceridemia associated with diabetes by stimulating TG removal, possibly by promoting the interaction of VLDL with the TG removal system.

Animals↗
PubMed1998

Impaired myocardial vasodilation during hyperemic stress with dipyridamole in hypertriglyceridemia.

OBJECTIVES: This study sought to investigate the specific role of hypertriglyceridemia in the myocardial hyperemic stress with dipyridamole/rest flow ratio (MDR). BACKGROUND: Reduced MDR has been reported in hypercholesterolemic patients without evidence of ischemia. However, the specific role of hypertriglyceridemia in MDR has not been studied. METHODS: Fifteen nondiabetic normocholesterolemic hypertriglyceridemic patients and 13 age-matched control subjects were studied. Myocardial blood flow (MBF) during dipyridamole administration and baseline MBF in hypertriglyceridemic patients and control subjects were measured using positron emission tomography and nitrogen-13 ammonia, after which the MDR was calculated. RESULTS: Baseline MBF (ml/min per 100 g heart weight) in hypertriglyceridemic patients (mean +/- SD 73.6 +/- 24.1) did not differ significantly from that in control subjects (81.6 +/- 37.2). MBF during dipyridamole loading in hypertriglyceridemic patients (198 +/- 106) was significantly reduced compared with that in control subjects (313 +/- 176, p < 0.05), as was the MDR (2.71 +/- 1.07 vs. 3.73 +/- 1.14, respectively, p < 0.05). Spearman rank-order correlation analysis showed a significant relation between plasma triglyceride concentration and MDR (r = -0.466, asymptotic SE 0.157, p = 0.0125); however, no such significant relation was seen between total plasma cholesterol concentration and MDR (r = -0.369, asymptotic SE 0.130, p = 0.059). CONCLUSIONS: Impaired myocardial vasodilation was suggested in hypertriglyceridemic patients without symptoms and signs of ischemia.

Adult↗
PubMed1998

Partial replacement of dietary casein with soy protein isolate can reduce the severity of retinoid-induced hypertriglyceridemia.

Previous research carried out in an animal model of retinoid-induced hypertriglyceridemia - rats fet a 13-cis retinoic acid (13cRA)-containing diet having casein as the protein source - has demonstrated that the complete replacement of dietary casein with soy protein isolate (SPI) can decrease the severity of this condition. In this study, the effect of partially replacing dietary casein with SPI was investigated. Five groups of male Fischer 344 rats were used in a 14-day study, with two groups being fed diets having casein as the protein source, without or with 13cRA (groups A and B, respectively), and three groups being fed 13cRA-containing diets in which SPI was used to bring about the isonitrogenous replacement of 25, 50, or 100% of the casein in the formula for the diet used for group B (groups C-E, respectively). Serum triglyceride concentration for group B was significantly different (p < 0.05) from that of groups A, D, and E (5.41 vs 2.62, 4.04, and 2.66 mmol/l, respectively). Serum cholesterol concentrations for groups D and E were significantly lower (p < 0.05) than for groups A and B (1.63 and 1.60 vs 2.00 and 2.14 mmol/l, respectively). Thus, the isonitrogenous replacement of 50% of dietary casein with SPI can reduce the severity of retinoid-induced hypertriglyceridemia while decreasing the serum concentration of cholesterol.

Animals↗
PubMed2000

Tamoxifen-induced severe hypertriglyceridemia and pancreatitis.

Tamoxifen exhibits favorable effects on the lipid and lipoprotein profile since it decreases the total and LDL cholesterol levels as well as the Lp(a) levels. Additionally, a small increase in serum triglycerides is commonly found after tamoxifen administration. However, severe hypertriglyceridemia which can sometimes be associated with life-threatening complications is occasionally noticed. Herein, we describe a patient who developed tamoxifen-induced severe hypertriglyceridemia and pancreatitis. An analysis of the underlying pathogenetic mechanisms as well as a review of the relevant literature is also provided.

Antineoplastic Agents, Hormonal↗
PubMed2005

Severe hypertriglyceridemia with a history of treatment failure.

Background A 53-year-old man with a history of hypertension and gout was referred to our clinic for severe hypertriglyceridemia, diagnosed 3 years previously. He was asymptomatic and had no history of abdominal pain, pancreatitis or diabetes, but consumed six cans of beer per night. Over the previous 2 years, he had been treated unsuccessfully with multiple medications; during this period his fasting triglycerides ranged from 5.41 mM to 55.04 mM (479 to 4,871 mg/dl). Investigations Physical examination including fundoscopy, medication review, and laboratory tests.Diagnosis Severe hypertriglyceridemia due to a genetic combined hyperlipidemia, exacerbated by persistent excessive alcohol intake and metabolic syndrome. Management Cessation of alcohol intake, initiation of a fat-restricted diet, and fibrate therapy, with close follow-up. Once serum triglycerides were controlled, attention was turned to lowering LDL-cholesterol concentration according to The National Cholesterol Education Program, Adult Treatment Panel III guidelines.

Alcohol Drinking↗
PubMed2000

Compound heterozygosity of Leu252Val and Leu252Arg causing lipoprotein lipase deficiency in a chinese patient with hypertriglyceridemia.

BACKGROUND: We investigated lipoprotein lipase (LPL) gene mutations in a Chinese male with severe hypertriglyceridemia and recurrent pancreatitis. METHODS: We screened for LPL sequence mutation in the LPL gene in this patient, his relatives and 160 unrelated hypertriglyceridaemic subjects. We determined the postheparin plasma LPL activity of subjects carrying a LPL mutation and studied the in vitro expression of mutant LPL in COS-1 cells. RESULTS: The proband was found to be a compound heterozygote for a novel Leu252Val and a reported Leu252Arg mutation in the LPL gene. He had low plasma levels of postheparin LPL activity and mass. The two mutations segregated independently in his family. In vitro expression analysis showed that Leu252Arg abolished both the catalytic function and secretion of LPL, while Leu252Val abolished the catalytic function but only reduced secretion by about half. We have also detected heterozygous Leu252Val and Leu252Arg mutations each in one hypertriglyceridaemic individual. CONCLUSION: These results indicated that the leucine 252 is critical for the catalytic activity and secretion of LPL. Why the substitution by valine instead of arginine resulted only in a partial suppression of LPL secretion, remains to be investigated. Leu252Val and Leu252Arg are the likely cause of hypertriglyceridemia in these subjects because of their deleterious effects on LPL activity or secretion. Leu252Val/Leu252Arg is the first compound heterozygous mutation known to occur in the same codon of the LPL gene. So far they are found only in Chinese.

Adolescent↗
PubMed1998

The use of soy protein isolate to reduce the severity of 13-cis retinoic acid-induced hypertriglyceridemia.

The ability of soy protein isolate to reduce the severity of 13-cis retinoic acid (13cRA)-induced hypertriglyceridemia was assessed in an animal model of this condition (rats fed a 13cRA-containing, casein-based diet). Male Fischer 344 rats (N = 7/group) were fed purified diets containing either casein or soy protein isolate and having either no 13cRA or retinoid at a level of 100 mg/kg diet-designated as Groups C, S, C + R, and S + R, respectively. Diet had no effect on either food intake or final body weight, and the serum levels of 13cRA were not significantly different for Groups C + R and S + R. Groups fed diets having 13cRA had significantly (p < 0.05) higher serum triglyceride levels than ones fed the corresponding retinoid-free diets, but the serum triglyceride level for Group S + R was significantly lower than for Group C + R, being 2.99 vs. 6.97 mM (265 vs. 617 mg/dl). Thus, soy protein isolate can reduce the severity of 13cRA-induced hypertriglyceridemia without affecting serum retinoid level.

Animals↗
PubMed2000

Contribution of fibrinogen and lipoproteins to plasma viscosity in hypercholesterolemia and hypertriglyceridemia: evaluation by selective depletion of low-density lipoproteins or fibrinogen.

Epidemiological studies suggest that the plasma fibrinogen concentration is the main determinant of plasma viscosity (PV), but the concentration of other macromolecules (eg, immunoglobulins) and low-density lipoprotein (LDL) cholesterol and triglycerides are also correlated with PV. However, only a few data exist concerning the in vitro effects of these plasma constituents on PV. Therefore, we investigated PV before and after the specific elimination of fibrinogen and LDL in hypercholesterolemic and hypertriglyceridemic plasma. First, hypercholesterolemic samples (n = 7) were pumped simultaneously through 2 columns: a fibrinogen-depleting column containing the pentapeptide Gly-Pro-Arg-Pro-Lys (GPRPK) and a LDL-depleting column containing specific antibodies against apolipoprotein B-100. In the plasma and in each fraction from the column, the cholesterol level was measured enzymatically, fibrinogen was determined by immunonephelometry, and PV was analyzed using a low-shear rotation viscosimeter. After the fibrinogen-depleting column, the fibrinogen concentration decreased from 3.21 +/- 0.20 to 0.94 +/- 0.16 g/L (P < .005), inducing a decrease in PV from 1.27 +/- 0.02 to 1.17 +/- 0.01 mPas (milliPascal seconds) (P < .005). Despite a marked reduction of the LDL cholesterol after the LDL-depleting column (from 6.40 +/- 0.23 to 4.08 +/- 0.32 mmol/L, P < .005), PV remained unchanged. Second, hypertriglyceridemic samples (n = 7) were pumped through the fibrinogen-depleting column, which reduced the fibrinogen concentration from 4.29 +/- 0.79 to 1.62 +/- 0.69 g/L (P < .001) and PV from 1.42 +/- 0.06 to 1.03 +/- 0.05 mPas (P < .01) while the triglyceride concentration remained unchanged. Our results confirm the epidemiological correlation between the fibrinogen concentration and PV in patients with hypercholesterolemia and hypertriglyceridemia. The influence of fibrinogen on PV seems much more pronounced than the direct effect of lipoprotein concentrations. Therefore, the elevated PV in patients with hypercholesterolemia and especially with hypertriglyceridemia seems mainly due to elevated fibrinogen levels.

Antibodies↗
PubMed2001

Triglyceride-rich lipoprotein cholesterol exceeds low-density lipoprotein cholesterol in hypertriglyceridemia patients.

The atherogenicity of triglyceride-rich lipoprotein has been revealed. This study was performed to explore the clinical importance of triglyceride-rich lipoprotein by measuring its cholesterol content and comparing it with other lipoprotein fractions. Blood samples were obtained from 103 patients whose fasting plasma triglyceride concentration exceeded 300 mg/dl. The cholesterol monitor using the technique of high-performance liquid chromatography was used for the measurement of their plasma cholesterol concentrations and the determination of cholesterol distribution among lipoprotein fractions. This monitor showed 4 peaks: large-triglyceride-rich lipoprotein, small-triglyceride-rich lipoprotein, low-density lipoprotein, and high-density lipoprotein. Total cholesterol increased with increasing triglyceride. The increment of total cholesterol was nearly equal to that of small-triglyceride-rich lipoprotein cholesterol. Small-triglyceride-rich lipoprotein cholesterol exceeded low-density lipoprotein cholesterol where plasma triglyceride concentration was over 500 mg/dl. In conclusion, triglyceride-rich lipoprotein may be clinically important for hypertriglyceridemic patients as a source of cholesteryl ester in arteriosclerotic plaques, and increased triglyceride-rich lipoprotein cholesterol may be used as a basis for hypertriglyceridemia atherogenicity. Our study suggests that hypertriglyceridemia should be treated to prevent arteriosclerotic disease.

Apolipoproteins E↗
PubMed1999

Overexpression of human apolipoprotein A-II in mice induces hypertriglyceridemia due to defective very low density lipoprotein hydrolysis.

Two lines of transgenic mice, hAIItg-delta and hAIItg-lambda, expressing human apolipoprotein (apo)A-II at 2 and 4 times the normal concentration, respectively, displayed on standard chow postprandial chylomicronemia, large quantities of very low density lipoprotein (VLDL) and low density lipoprotein (LDL) but greatly reduced high density lipoprotein (HDL). Hypertriglyceridemia may result from increased VLDL production, decreased VLDL catabolism, or both. Post-Triton VLDL production was comparable in transgenic and control mice. Postheparin lipoprotein lipase (LPL) and hepatic lipase activities decreased at most by 30% in transgenic mice, whereas adipose tissue and muscle LPL activities were unaffected, indicating normal LPL synthesis. However, VLDL-triglyceride hydrolysis by exogenous LPL was considerably slower in transgenic compared with control mice, with the apparent Vmax of the reaction decreasing proportionately to human apoA-II expression. Human apoA-II was present in appreciable amounts in the VLDL of transgenic mice, which also carried apoC-II. The addition of purified apoA-II in postheparin plasma from control mice induced a dose-dependent decrease in LPL and hepatic lipase activities. In conclusion, overexpression of human apoA-II in transgenic mice induced the proatherogenic lipoprotein profile of low plasma HDL and postprandial hypertriglyceridemia because of decreased VLDL catabolism by LPL.

Animals↗
PubMed2000

Disruption of the sterol 27-hydroxylase gene in mice results in hepatomegaly and hypertriglyceridemia. Reversal by cholic acid feeding.

Sterol 27-hydroxylase (CYP27) participates in the conversion of cholesterol to bile acids. We examined lipid metabolism in mice lacking the Cyp27 gene. On normal rodent chow, Cyp27(-/-) mice have 40% larger livers, 45% larger adrenals, 2-fold higher hepatic and plasma triacylglycerol concentrations, a 70% higher rate of hepatic fatty acid synthesis, and a 70% increase in the ratio of oleic to stearic acid in the liver versus Cyp27(+/+) controls. In Cyp27(-/-) mice, cholesterol 7alpha-hydroxylase activity is increased 5-fold, but bile acid synthesis and pool size are 47 and 27%, respectively, of those in Cyp27(+/+) mice. Intestinal cholesterol absorption decreases from 54 to 4% in knockout mice, while fecal neutral sterol excretion increases 2.5-fold. A compensatory 2.5-fold increase in whole body cholesterol synthesis occurs in Cyp27(-/-) mice, principally in liver, adrenal, small intestine, lung, and spleen. The mRNA for the cholesterogenic transcription factor sterol regulatory element-binding protein-2 (SREBP-2) and mRNAs for SREBP-2-regulated cholesterol biosynthetic genes are elevated in livers of mutant mice. In addition, the mRNAs encoding the lipogenic transcription factor SREBP-1 and SREBP-1-regulated monounsaturated fatty acid biosynthetic enzymes are also increased. Hepatic synthesis of fatty acids and accumulation of triacylglycerols increases in Cyp27(-/-) mice and is associated with hypertriglyceridemia. Cholic acid feeding reverses hepatomegaly and hypertriglyceridemia but not adrenomegaly in Cyp27(-/-) mice. These studies confirm the importance of CYP27 in bile acid synthesis and they reveal an unexpected function of the enzyme in triacylglycerol metabolism.

Adrenal Glands↗
PubMed2003

Angiopoietin-like protein 3 mediates hypertriglyceridemia induced by the liver X receptor.

The KK/San obese and diabetic mouse, a mutant strain from KK obese mice, exhibits significantly low plasma triglyceride levels. In KK/San mice, genetic analysis identified a mutation in the gene encoding angiopoietinlike protein 3 (Angptl3), a liver-specific secretory protein, which had suppressive effect on lipoprotein lipase activity. In the current study, LXR ligands augmented Angptl3 mRNA expression and protein production in hepatoma cells. LXR ligands and LXR.retinoid X receptor (RXR) complex increased the promoter activity of Angptl3 gene. Serial deletion and point mutation of Angptl3 promoter identified an LXR response element (LXRE). Gel mobility shift assay showed the direct binding of LXR.RXR complex to the LXRE of the Angptl3 promoter. Furthermore, treatment of mice with synthetic LXR ligand caused triglyceride accumulation in the liver and plasma, which was accompanied by induction of hepatic mRNAs of several LXR target genes, including sterol regulatory element binding protein-1c (SREBP-1c), fatty acid synthase (FAS), and Angptl3. In Angptl3-deficient C57BL/6J mice, LXR ligand did not cause hypertriglyceridemia but accumulation of triglyceride in the liver. Our results demonstrate that Angptl3 is a direct target of LXR and that induction of hepatic Angptl3 accounts for hypertriglyceridemia associated with the treatment of LXR ligand.

Angiopoietin-Like Protein 3↗
PubMed1991

Hypertriglyceridemia. Examining its role in coronary heart disease.

If triglyceride-rich very-low-density lipoproteins (VLDLs) are a vehicle for transporting cholesterol into the arterial wall, they can be equated to low-density lipoproteins (LDLs) in estimating CHD risk and setting targets for therapy. Furthermore, the fate of cholesterol-rich VLDL (VLDL remnants) is similar to that of LDL; that is, both are removed from the circulation via LDL receptors. Thus, combining VLDL and LDL into a common category of atherogenic lipoproteins provides a rational framework for treatment of hypercholesterolemic patients with hypertriglyceridemia. A hydroxymethylglutaryl coenzyme A reductase inhibitor may be the best choice for treatment when both triglyceride and cholesterol levels are elevated, because these agents cause the greatest reduction in VLDL and LDL cholesterol levels. When hypertriglyceridemia is severe, a fibric acid or nicotinic acid is preferable, because these agents are more effective for lowering triglyceride levels and hence for reducing risk for acute pancreatitis.

Cholesterol, HDL↗
PubMed2005

Randomized study of the safety and efficacy of fish oil (omega-3 fatty acid) supplementation with dietary and exercise counseling for the treatment of antiretroviral therapy-associated hypertriglyceridemia.

BACKGROUND: Omega-3 fatty acids (fish oils) reduce fasting serum triglyceride levels and cardiovascular disease risk in individuals without HIV infection. Whether omega-3 fatty acid supplementation can reduce hypertriglyceridemia associated with antiretroviral therapy is not known. METHODS: We conducted an open-label, randomized trial that enrolled 52 patients receiving > or =3 active antiretrovirals who had fasting triglyceride levels of >200 mg/dL and were randomized to receive nutritionist-administered dietary and exercise counseling with or without fish oil supplementation for 16 weeks. RESULTS: Patients assigned to receive fish oil experienced a 25% mean decline in fasting triglyceride levels at week 4 (95% CI, -34.6% to -15.7% change), compared with a 2.8% mean increase among patients assigned to receive counseling alone (95% CI, -17.5% to +23.1% change) (P=.007). By week 16, the mean reduction in triglyceride levels in the fish oil arm remained significant, at 19.5% (95% CI, -34.9% to -4.0% change), whereas the mean decrease in the diet and exercise only arm was 5.7% (95% CI, -24.6% to +13.2% change); however, the difference between study arms was no longer statistically significant (P=.12). Low-density lipoprotein cholesterol levels had increased by 15.6% (95% CI, +4.8% to +26.4% change) at week 4 and by 22.4% (95% CI, +7.91% to +36.8% change) at week 16 in the fish oil arm but did not change in the diet and exercise only group. Fish oil was well tolerated; only 1 patient experienced treatment-limiting toxicity. Patients assigned to receive fish oil experienced a 25% mean decline in fasting triglyceride levels at week 4 (95% CI, -34.6% to -15.7% change), compared with a 2.8% mean increase in patients assigned to receive counseling alone (95% CI, -17.5% to 23.1% change) (P=.007). By week 16, the mean reduction in triglyceride levels in the fish oil arm remained significant, at 19.5% (95% CI, -34.9% to -4.0% change), whereas the mean decrease in the diet and exercise only arm was 5.7% (95% CI, -24.6% to 13.2% change); however, the difference between study arms was no longer statistically significant (P=.12). Low-density lipoprotein cholesterol levels had increased by 15.6% (95% CI, 4.8%-26.4% change) at week 4 and by 22.4% (95% CI, 7.91%-36.8% change) at week 16 in the fish oil arm but did not change in the diet and exercise only group. Fish oil was well tolerated; only 1 patient experienced treatment-limiting toxicity. CONCLUSIONS: Supplementation with omega-3 fatty acids in combination with dietary and exercise counseling was well tolerated and reduced fasting triglyceride levels in patients receiving antiretrovirals. To what extent the increase in low-density lipoprotein cholesterol levels observed in patients assigned this intervention is attributable to omega-3 fatty acid supplementation and whether this increase attenuates any benefit in lowering triglyceride levels is unclear. Given these results, further investigation of omega-3 fatty acid supplementation for the treatment of hypertriglyceridemia in HIV-infected patients is warranted.

Adult↗
PubMed2001

Hyperglycemia and hypertriglyceridemia secondary to olanzapine.

Olanzapine is an atypical antipsychotic that is becoming more widely used in children and adolescents. There have been reports of olanzapine-induced hyperglycemia and hypertriglyceridemia in adults. This case report describes the development of both hyperglycemia and hypertriglyceridemia in a male adolescent that resolved with discontinuation of olanzapine and without dietary changes or the use of insulin or oral hypoglycemics.

Adolescent↗
PubMed1991

Postheparin lipolytic activity and plasma lipoprotein response to omega-3 polyunsaturated fatty acids in patients with primary hypertriglyceridemia.

The hypotriglyceridemic action of omega-3 (n-3) fatty acids is attributed primarily to reduction in hepatic triglyceride synthesis and reduced secretion of very-low-density lipoproteins (VLDLs). However, increased catabolism of triglyceride-rich lipoproteins was reported and could be due to increased availability of peripheral lipoprotein lipase (LPL) or hepatic lipase (HL). In this study plasma lipoproteins and postheparin activities of LPL and HL were determined in 12 patients with primary hypertriglyceridemia before and during isocaloric substitution of omega-3 fatty acids (10 g/d) for 4 wk. Omega-3 polyunsaturates resulted in 53% and 61% reductions in plasma triglyceride and VLDL-cholesterol concentrations, respectively (P less than 0.0001). However, low-density-lipoprotein (LDL)-cholesterol concentrations increased by 26% (P less than 0.001). Activities of postheparin LPL and HL essentially remained the same. Thus, in patients with primary hypertriglyceridemia, reduction in plasma triglyceride concentrations and increase in LDL-cholesterol concentrations mediated by omega-3 polyunsaturates seem to occur without an increase in LPL or HL activities.

Aged↗
PubMed2003

Sugars, hypertriglyceridemia, and cardiovascular disease.

Short-term studies consistently show that raising the carbohydrate content of the diet increases serum triacylglycerol concentrations. As compared with starches, sugars (particularly sucrose and fructose) tend to increase serum triacylglycerol concentrations by approximately 60%. The magnitude of the effect depends on other aspects of the diet, including the total amount of carbohydrate and the types of fat, carbohydrate, and fiber, but definitive studies to describe the dose-response relations are not available. Longer-term studies show that some high-carbohydrate diets are not associated with increased fasting serum triacylgycerol concentrations. However, sedentary subjects with upper-body and visceral obesity who have the metabolic syndrome tend to be at higher risk for hypertriglyceridemia in response to high-sucrose and high-carbohydrate diets; moderate weight loss mitigates the effect. Hyperinsulinemia or insulin resistance may play a role in promoting higher rates of VLDL synthesis and hypertriglyceridemia in obesity, but the mechanisms remain unclear. The effect of fructose in promoting triacylglycerol synthesis is independent of insulinemia, however. In terms of the long-term effects of diets high in sugars on the risk of cardiovascular disease, available epidemiologic evidence indicates no association of sugars or total carbohydrate intake per se, but high dietary glycemic load is associated with higher serum triacylglycerol concentrations and greater risk of coronary heart disease in women. Studies are needed to delineate the independent effects of dietary sugars and glycemic load on serum triacylglycerol concentrations in lean and obese men and women and to determine whether the elevations in fasting and fed concentrations of serum triacylglycerol with high-carbohydrate and high-sugars diets are associated with increased risk of cardiovascular disease.

Adult↗
PubMed2004

Plasmapheresis as an adjuvant therapy for hypertriglyceridemia-induced pancreatitis.

Hypertriglyceridemia is an uncommon cause of pancreatitis. A serum triglyceride level of more then 1000 to 2000 mg/dL is an identifiable risk factor. Interestingly, serum pancreatic enzyme levels may be normal or only minimally elevated in such cases. The reduction of triglyceride level to below 1000 mg/dL effectively prevents further episodes of pancreatitis. The mainstay of treatment for the hypertriglyceridemia associated with pancreatitis includes dietary restriction of fat and administration of lipid-lowering agents. It is thought that within 24 to 48 hours of the onset of pancreatitis, in the majority of patients, triglyceride levels fall rapidly as a result of fasting status, as the absorption of chylomicrons to the blood is cut off. Experiences with plasmapheresis are limited. We report a case of hypertriglyceridemic necrotizing pancreatitis with mildly elevated amylase and lipase, treated successfully with plasmapheresis.

Combined Modality Therapy↗