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PubMed1977

Reduction of plasma triglycerides by diet in subjects with chronic renal failure.

The response of plasma triglyceride levels to changes in the composition of meal formula diets was studied in 12 subjects who had moderate to severe chronic renal failure. Fasting hypertriglyceridemia (greater than 150 mg/100 ml) was present in seven of 12 subjects. Fasting plasma triglyceride levels decreased in all subjects in response to a reduction in the proportion of carbohydrate (from 50 to 35% of total daily calories) and an increase in the poly-unsaturated to saturated fat ratio (from 0.2 to 2.0) in an isocaloric diet. Fasting plasma cholesterol and postprandial triglyceride levels were unchanged. Both the triglyceride production rate and the insulin response were significantly lower on a diet in carbohydrate and higher in polyunsaturated fat. These data indicate that hypertriglyceridemia occurs in subjects with moderate to severe chronic renal failure, and that dietary modification promptly reduces triglycerides levels over an 11 day period. A long term study on a dietary program incorporating these changes is indicated to determine whether this effect is sustained.

Adult↗
PubMed1998

Overfeeding fat as monoglyceride or triglyceride: effect on appetite, nutrient balance and the subsequent day's energy intake.

OBJECTIVE: To examine the effect of overfeeding isoenergetic diets enriched in 1-monoglyceride or triglyceride on nutrient oxidation and appetite throughout the day that it was given and the subsequent day's food and energy intake. DESIGN: Six men [mean (s.d.) weight; 76.89 (7.00) kg, height; 1.77 (0.05) m, age; 26.4 (6.0) y], were each studied twice in a 3 d protocol. On day 1 (maintenance day) they were fed a medium fat (MF) maintenance diet (MF: 40% fat, 47% carbohydrate and 13% protein by energy) calculated at 1.6 x resting metabolic rate (RMR). Subjects entered the calorimeter at 06.30 on day 2 for 49.5 h. On day 2 (manipulation day) subjects consumed a MF diet at 1.6 x RMR with an additional 0.45 x RMR as either 1-monoglyceride or triglyceride. On day 3 (outcome day), subjects had ad libitum access to isoenergetic, isoenergetically dense MF (40 :47: 13, 550 kJ/ 100 g) foods. Subjective hunger and satiety were tracked hourly, during waking hours throughout days 1-3. RESULTS: There was no significant effect of diet on nutrient oxidation or balance either during day 2 (manipulation day) or day 3 (outcome day), fat oxidation was similar on both diets. Subjective hunger was not affected by diet on either day with mean values of 34.3 and 35.0 mm (SED 5.2) on manipulation day (day 2) and outcome day (day 3), 35.3 and 40.8 mm (SED 5.2) on the 1 -monoglyceride or triglyceride diets respectively. Day 3 food and energy intake were unaffected by the previous day's dietary treatment, with mean intakes of 15.9 and 15.6 MJ (SED 1.07) on the 1-monoglyceride or triglyceride treatments, respectively. CONCLUSIONS: This study suggests that when 1-monoglyceride is covertly incorporated into a diet at unusually high levels, it behaves in a manner that is very similar to triglyceride, in its effects on appetite, feeding behaviour and net nutrient balance.

Adult↗
PubMed2000

Cholesterol and triglyceride concentrations, birthweight and central obesity in pre-school children. ALSPAC Study Team. Avon Longitudinal Study of Pregnancy and Childhood.

OBJECTIVE: To investigate the relationship between blood cholesterol and triglyceride, birthweight and central obesity in pre-school children, after controlling for height and body mass index. METHODS: This was a longitudinal population-based study in south-west England. Research clinics were held when the children were 31 and 43 months of age, where anthropometric measurements were made and a non-fasting blood sample was taken and analysed for triglyceride, total cholesterol and high-density lipoprotein (HDL) cholesterol. Low-density lipoprotein (LDL) cholesterol values were calculated using the Friedewald equation. Central obesity was estimated using the ratio of waist circumference:arm circumference (WC:AC). RESULTS: Complete blood lipid and anthropometric data were available for 385 children at 31 months and 470 children at 43 months. Height was negatively associated with the concentration of triglyceride, and total and LDL cholesterol. There was little evidence for a relationship between body mass index (BMI) and blood lipids at either 31 or 43 months. The only significant relationship between birthweight and blood lipids was a negative association with HDL (and consequently a positive association with the ratio of total:HDL cholesterol) in boys at 43 months. Adjustment for current height and BMI had little effect on the associations between birthweight and blood lipid concentrations. WC:AC was positively associated with triglycerides and negatively associated with HDL values in boys, and had a quadratic relationship with LDL concentrations among girls. These relationships were unchanged or became stronger on adjustment for current height and body mass index. CONCLUSION: In the pre-school child, central obesity has a relationship with triglyceride and HDL concentrations that is independent of current height and BMI. We have found no evidence that increasing birthweight is associated with a more favourable blood lipid profile at 31 and 43 months.

Anthropometry↗
PubMed1968

The control of fatty acid and triglyceride synthesis in rat epididymal adipose tissue. Roles of coenzyme A derivatives, citrate and L-glycerol 3-phosphate.

1. Methods are described for the extraction and assay of acetyl-CoA and of total acid-soluble and total acid-insoluble CoA derivatives in rat epididymal adipose tissue. 2. The concentration ranges of the CoA derivatives in fat pads incubated in vitro under various conditions were: total acid-soluble CoA, 0.20-0.59mm; total acid-insoluble CoA, 0.08-0.23mm; acetyl-CoA, 0.03-0.14mm. 3. An investigation was made of some postulated mechanisms of control of fatty acid and triglyceride synthesis in rat epididymal fat pads incubated in vitro. The concentrations of intermediates of possible regulatory significance were measured at various rates of fatty acid and triglyceride synthesis produced by the addition to the incubation medium (Krebs bicarbonate buffer containing glucose) of insulin, adrenaline, albumin, palmitate or acetate. 4. The whole-tissue concentrations of glucose 6-phosphate, l-glycerol 3-phosphate, citrate, acetyl-CoA, total acid-soluble CoA and total acid-insoluble CoA were assayed after 30 or 60min. incubation. The rates of fatty acid and triglyceride synthesis, calculated from the incorporation of [U-(14)C]glucose into fatty acids and glyceride glycerol respectively, and the rates of glucose uptake, lactate plus pyruvate output and glycerol output were measured over a 60min. incubation. 5. The rate of triglyceride synthesis could not be correlated with the concentrations of either l-glycerol 3-phosphate or long-chain fatty acyl-CoA (measured as total acid-insoluble CoA). Factor(s) other than the whole-tissue concentrations of these recognized precursors appear to be involved in the determination of the rate of triglyceride synthesis. 6. No relationship was found between the rate of fatty acid synthesis and the whole-tissue concentrations of the intermediates, citrate or acetyl-CoA, or with the two proposed effectors of acetyl-CoA carboxylase, citrate (as activator) or long-chain fatty acyl-CoA (as inhibitor). The control of fatty acid synthesis appears to reside in additional or alternative factors.

Acetates↗
PubMed1975

Triglyceride, free fatty acid and carbohydrate metabolism in hyperlipaemic (type IV) and normolipaemic subjects on carbohydrate- of fat-rich diets.

1. Five patients with hyperlipoproteinaemia type IV and five normolipaemic controls were maintained on diets containing either a fat or a carbohydrate content of approximately 60%. Leg exchanges of triglycerides, free fatty acid (NEFA), glucose and other metabolites were measured in the basal state. The metabolic response to an intravenous glucose load and the turnover of intravenously infused (14C)oleic acid were determined. Individual fatty acids were analysed in plasma NEFA and very-low-density lipoprotein triglyceride. 2. No differences were detected between patients and controls with regard to leg uptake of triglyceride or NEFA on either diet. On shifting from a fat-rich to a carbohydrate-rich diet, the control subjects showed reduced values for arterial NEFA and for NEFA turnover, accompanied by a lowered release of NEFA and glycerol from the leg. In patients, on the other hand, the arterial concentration and turnover of NEFA remained unchanged and the release of glycerol from the leg increased. Glucose administration gave a less-pronounced fall of arterial NEFA on either diet in the patients and the incorporation of (14C)oleic acid into triglycerides after glucose administration was more marked than in the controls. 3. No difference in net uptake of triglyceride by the leg was demonstrable between patients and controls. 4. it is concluded that hyperlipaemic patients show an altered metabolic response to a carbohydrate-rich diet, possibly contributing to the development of a hyperlipaemic state, and that acute glucose loading results in a greater incorporation of circulating NEFA into very-low-density lipoproteins in these patients.

Adult↗
PubMed2002

Triglyceride, but not total cholesterol or low-density lipoprotein cholesterol levels, predict development of proteinuria.

BACKGROUND: Epidemiological data about the relationship between dyslipidemia and proteinuria are sparse. We conducted a retrospective and longitudinal study in a large screened cohort to evaluate whether triglyceride, high-density lipoprotein (HDL) cholesterol, total cholesterol, and low-density lipoprotein (LDL) cholesterol levels increase the risk of development of proteinuria and loss of renal function. METHODS: Post hoc analysis was performed for 4326 subjects who were free from proteinuria (dipstick 1+ or higher) at baseline (1997) with a follow-up period through 2000. Outcome measures were the development of proteinuria (1+ or higher) and change in glomerular filtration rate (GFR). Multiple logistic analysis and multiple regression analysis were used to analyze baseline characteristics related to the outcome measures. RESULTS: During the observational period, 505 (11.7%) of subjects had one or more episodes of proteinuria (>/=1+). Adjusted relative risk of triglycerides for one or more incidences of proteinuria was 1.007 (95% CI 1.000 to 1.105, P = 0.04) in men and 1.032 (95% CI 1.004 to 1.061, P = 0.02) in women. Total cholesterol, HDL cholesterol, and LDL cholesterol were not significant predictors of proteinuria. The mean change in GFR between 1997 and 2000 was -6.3 (SD = 9.0) mL/min/1.73 m2 in men, and -7.8 (SD = 10.7) mL/min/1.73 m2 in women. HDL cholesterol (beta = 0.04, t = 3.7, P = 0.0002) in men and triglycerides (per 10 mg/dL, beta = -0.09, t = -2.2, P = 0.02) in women were correlated with the change in GFR. CONCLUSIONS: High triglyceride levels predicted a risk of developing proteinuria in both men and women, but not total cholesterol nor LDL cholesterol. High triglyceride in women and low HDL cholesterol in men predicted the decline of renal function. It remains to be determined whether prospective treatment of dyslipidemia will protect against renal injury.

Adult↗
PubMed2000

Postprandial apolipoprotein B48-and B100-containing lipoproteins in type 2 diabetes: do statins have a specific effect on triglyceride metabolism?

There is little information about the effect of an alteration of low-density lipoprotein (LDL) turnover on chylomicron and very-low-density lipoprotein (VLDL) metabolism, yet chylomicron remnant particles are thought to be particularly atherogenic. This study examined the effect of inhibition of cholesterol synthesis on postprandial lipoproteins. Eight type 2 diabetic patients were examined before treatment with the 3-hydroxy-3-methyl glutaryl coenzyme A (HMGCoA) reductase inhibitor cerivastatin, after 4 weeks on active treatment, and 4 weeks after stopping treatment. On each occasion, blood was collected fasting and at 2-hour intervals for up to 8 hours after a high-fat meal. Chylomicrons and VLDLs were isolated by sequential ultracentrifugation. Compositional analysis was performed including the measurement of apolipoprotein B48 (apo B48) and apo B100 using polyacrylamide gradient gel electrophoresis. During statin treatment, there was a significant reduction in the postprandial chylomicron apo B48 area under the curve (AUC) from 23 +/- 16 to 17 +/- 10 (P < .01) and apo B100 in the chylomicron fraction from 166 +/- 148 to 70 +/- 70 (P < .05). Postprandial cholesterol (362 +/- 193 to 74 +/- 39, P < .005), triglyceride (2,222 +/- 1,440 to 746 +/- 329), and phospholipid (518 +/- 267 to 205 +/- 94) also decreased (P < .005). In the VLDL fraction, the postprandial cholesterol and triglyceride AUC were significantly reduced by statin (316 +/- 228 to 171 +/- 78, P < .05, and 1,733 +/- 833 to 857 +/- 468, P < .02, respectively). Four weeks after cessation of treatment, the chylomicron fraction triglyceride AUC had returned to the pretreatment level, but postprandial chylomicron cholesterol and VLDL cholesterol, triglyceride, and phospholipid were significantly lower than baseline (P < .05). Plasma total cholesterol and LDL cholesterol were significantly reduced with treatment (6.2 +/- 0.5 to 4.3 +/- 1.0 mmol/L, P < .001, and 4.5 +/- 0.4 to 2.8 +/- 1.0 mmol/L, P < .01, respectively) and returned to baseline following cessation of treatment. Fasting plasma triglycerides decreased significantly on treatment (2.4 +/- 1.0 to 1.7 +/- 0.2 mmol/L, P < .05) but remained significantly lower than baseline 4 weeks later (1.8 +/- 0.3 mmol/L, P < .05). This study suggests major postprandial lipoprotein changes on statin therapy which may account, in part, for the beneficial effects of statins in the prevention of myocardial infarction.

Adult↗
PubMed2002

Interaction of endothelial cells and triglyceride-rich lipoproteins with apolipoprotein E (Arg-->Cys) from a patient with lipoprotein glomerulopathy.

We saw a patient with proteinuria and characteristics of lipoprotein glomerulopathy (LPG). Histologic analysis of renal biopsy showed a thrombus-like substance in the markedly dilated glomerular capillaries, which stained positive with oil red O. Increased concentration of plasma apolipoprotein E (apoE) was also noted. Those findings are consistent with the diagnostic criteria of LPG, as reported by Oikawa et al. In isoelectric focusing gel electrophoresis of apoE, a band (apoE3') between apoE3 and E2 was observed. The patient's DNA sequence exhibited a C to G substitution in exon 3 of the apoE gene at the position of the 25th amino acid, resulting in an amino acid substitution of the arginine residue for cysteine residue. To clarify the pathophysiologic role of this mutation, we investigated the binding and the uptake of apoE3' triglyceride-rich lipoproteins to human umbilical vein endothelial cells (HUVEC). The binding of apoE3'-triglyceride-rich lipoproteins to the cell-surface of HUVEC increased up to 30% to 50%, compared with apoE3-triglyceride-rich lipoproteins. But the uptake of apoE3'-triglyceride-rich lipoproteins into the cells was not different between them. These findings are consistent with the idea that an increase in binding of triglyceride-rich lipoproteins possessing apoE (Arg(25)-->Cys) to endothelial cells may promote deposition of lipid in the glomerular capillaries.

Adult↗
PubMed1997

The role of insulin and proinsulin in the regulation of triglyceride metabolism.

The mechanisms underlying the associations between abnormal glucose tolerance and myocardial infarction are poorly understood. It has often been suggested that an increased plasma insulin concentration is causally linked to many of the metabolic abnormalities that are associated with abnormal glucose tolerance, although this suggestion remains controversial. Recently it has been proposed that proinsulin and proinsulin-like molecules may also be involved in the atherogenic process. Both hyperinsulinaemia and insulin resistance are associated with fasting hypertriglyceridaemia and both increased VLDL production and increased plasma triglyceride concentrations commonly occur in association with abnormal glucose tolerance and atheromatous vascular disease. In order to study the effects of insulin, proinsulin and proinsulin-like molecules on hepatic triglyceride secretion we have undertaken experiments in vitro using the liver cell line HepG2. In conjunction with these in vitro experiments we have also studied, in vivo, the associations between insulin, proinsulin, proinsulin-like molecules and plasma triglyceride concentrations in subjects with both normal and abnormal glucose tolerance. Our results in vitro show that proinsulin and proinsulin-like molecules have similar and not different effects to insulin but are less biologically active. In vivo, our results show that concentrations of insulin, proinsulin and proinsulin-like molecules per se are not an important determinant of plasma triglyceride concentrations. Both abnormal NEFA suppression during an oral glucose tolerance test and increased central adiposity are closely linked to poor glucose tolerance and are the most important determinants of plasma triglyceride concentrations. Taken together these results suggest that it is not insulin nor proinsulin concentrations per se that are causally linked to hypertriglyceridaemia. We suggest that abnormal NEFA suppression plays an important part in the increase in risk of vascular disease associated with insulin resistance.

Adult↗
PubMed1988

Influence of fast, body weight and diet on serum cholesterol, triglycerides, and phospholipids concentrations in the aging rat.

The present study was performed to document factors playing a role in the age-related increase of serum total cholesterol, triglycerides, and phospholipids in male WISTAR rats. In 59 and 122 week old rats, serum concentrations of all three parameters were significantly higher than those determined in younger rats (15-17 weeks of age). Serum triglycerides and cholesterol concentrations were higher in post absorptive than in fasting state. In mature rats of same age (59 weeks), mean concentrations of cholesterol, triglycerides, and phospholipids were significantly higher in the heavier animals than in the others. A strong correlation could be established between body weight and serum cholesterol or triglycerides of these animals. The composition of diet appears to play a role in serum cholesterol concentration but not in serum triglycerides concentration in old rats (59-65 weeks of age). This effect is demonstrated even if daily caloric intake and daily body weight gain of old rats (40-50 weeks of age) were not significantly different with both diets tested (2900 and 3250 cal/kg). In conclusion old Wistar rats develop increased concentrations of serum lipids parameters.

Aging↗
PubMed1998

Body fat distribution, insulin mediated suppression of non-esterified fatty acids and plasma triglycerides in obese subjects.

Triglyceride levels and free fatty acid metabolism are influenced by body fat distribution. To test whether the pattern of fat distribution in obese subjects results in distinct insulin mediated suppression of non-esterified fatty acids which could account for differences in plasma triglycerides, we studied 59 obese subjects who were classified according to waist-to-hip ratio. Non-esterified fatty acids and insulin response to a 75 g oral glucose tolerance test were higher in abdominal obesity. Total non-esterified fatty acids response, after adjustment for sex, showed a positive association with waist-to hip ratio (r = 0.292; p < 0.05). The abdominal obese group had higher fasting triglycerides (1.74+/-0.83 versus 1.11+/-0.71 mmol/L; p = 0.003) and lower glucose/insulin ratio (5.2+/-2.3 versus 7.1+/-2.4; p = 0.003). Stepwise multiple regression analysis showed that triglyceride levels are explained by fasting and 120 min non-esterified fatty acids and by glucose/insulin ratio. We conclude that abdominal obesity is associated with a higher resistance to insulin mediated suppression of non-esterified fatty acids in obese subjects. Variation of triglyceride concentrations in obesity is dependent on both fasting and 120 min non-esterified fatty acids as well as on insulin sensitivity to glucose utilization.

Adolescent↗
PubMed2003

Triglyceride accumulation protects against fatty acid-induced lipotoxicity.

Excess lipid accumulation in non-adipose tissues is associated with insulin resistance, pancreatic beta-cell apoptosis and heart failure. Here, we demonstrate in cultured cells that the relative toxicity of two common dietary long chain fatty acids is related to channeling of these lipids to distinct cellular metabolic fates. Oleic acid supplementation leads to triglyceride accumulation and is well tolerated, whereas excess palmitic acid is poorly incorporated into triglyceride and causes apoptosis. Unsaturated fatty acids rescue palmitate-induced apoptosis by channeling palmitate into triglyceride pools and away from pathways leading to apoptosis. Moreover, in the setting of impaired triglyceride synthesis, oleate induces lipotoxicity. Our findings support a model of cellular lipid metabolism in which unsaturated fatty acids serve a protective function against lipotoxicity though promotion of triglyceride accumulation.

Animals↗
PubMed2000

Genomic interval engineering of mice identifies a novel modulator of triglyceride production.

To accelerate the biological annotation of novel genes discovered in sequenced regions of mammalian genomes, we are creating large deletions in the mouse genome targeted to include clusters of such genes. Here we describe the targeted deletion of a 450-kb region on mouse chromosome 11, which, based on computational analysis of the deleted murine sequences and human 5q orthologous sequences, codes for nine putative genes. Mice homozygous for the deletion had a variety of abnormalities, including severe hypertriglyceridemia, hepatic and cardiac enlargement, growth retardation, and premature mortality. Analysis of triglyceride metabolism in these animals demonstrated a several-fold increase in hepatic very-low density lipoprotein triglyceride secretion, the most prevalent mechanism responsible for hypertriglyceridemia in humans. A series of mouse BAC and human YAC transgenes covering different intervals of the 450-kb deleted region were assessed for their ability to complement the deletion induced abnormalities. These studies revealed that OCTN2, a gene recently shown to play a role in carnitine transport, was able to correct the triglyceride abnormalities. The discovery of this previously unappreciated relationship between OCTN2, carnitine, and hepatic triglyceride production is of particular importance because of the clinical consequence of hypertriglyceridemia and the paucity of genes known to modulate triglyceride secretion.

Animals↗
PubMed2002

ANGPTL3 decreases very low density lipoprotein triglyceride clearance by inhibition of lipoprotein lipase.

KK/San is a mutant mouse strain established in our laboratory from KK obese mice. KK/San mice show low plasma lipid levels compared with wild-type KK mice despite showing signs of hyperglycemia and hyperinsulinemia. Recently, we identified a mutation in the gene encoding angiopoietin-like protein 3 (Angptl3) in KK/San mice, and injection of adenoviruses encoding Angptl3 or recombinant ANGPTL3 protein to mutant KK/San mice raised plasma lipid levels. To elucidate the regulatory mechanism of ANGPTL3 on lipid metabolism, we focused on the metabolic pathways of triglyceride in the present study. Overexpression of Angptl3 in KK/San mice resulted in a marked increase of triglyceride-enriched very low density lipoprotein (VLDL). In vivo studies using Triton WR1339 revealed that there is no significant difference between mutant and wild-type KK mice in the hepatic VLDL triglyceride secretion rate. However, turnover studies using radiolabeled VLDL revealed that the clearance of (3)H-triglyceride-labeled VLDL was significantly enhanced in KK/San mice, whereas the clearance of (125)I-labeled VLDL was only slightly enhanced. In vitro analysis of recombinant protein revealed that ANGPTL3 directly inhibits LPL activity. These data strongly support the hypothesis that ANGPTL3 is a new class of lipid metabolism modulator, which regulates VLDL triglyceride levels through the inhibition of LPL activity.

Angiopoietin-Like Protein 3↗
PubMed2002

Overexpression of apolipoprotein B in the heart impedes cardiac triglyceride accumulation and development of cardiac dysfunction in diabetic mice.

The heart secretes apolipoprotein B (apoB) containing lipoproteins. Herein, we examined whether the overexpression of a human apoB transgene in the heart affects triglyceride accumulation and development of cardiac dysfunction in streptozotocin-treated diabetic mice. Blood glucose, plasma free fatty acids, and plasma triglycerides were similarly affected in diabetic wild type mice and diabetic apoB transgenic mice as compared with non-diabetic mice of the same genotype. After 12 weeks, heart triglycerides were increased by 48% in diabetic wild type mice. These mice displayed an increased expression of brain natriuretic peptide and deterioration of heart function on echocardiography. In diabetic apoB transgenic mice, heart triglyceride levels were identical to those in non-diabetic wild type and apoB transgenic mice, and brain natriuretic peptide expression as well as echocardiographic indexes of heart function were only marginally affected or unaffected. The findings suggest that triglyceride accumulation in the heart is important for development of diabetic cardiomyopathy in mice, and that lipoprotein formation by cardiomyocytes plays an integrated role in cardiac lipid metabolism.

Animals↗
PubMed2003

Apolipoprotein A5, a crucial determinant of plasma triglyceride levels, is highly responsive to peroxisome proliferator-activated receptor alpha activators.

The recently discovered APOA5 gene has been shown in humans and mice to be important in determining plasma triglyceride levels, a major cardiovascular disease risk factor. apoAV represents the first described apolipoprotein where overexpression lowers triglyceride levels. Since fibrates represent a commonly used therapy for lowering plasma triglycerides in humans, we investigated their ability to modulate APOA5 gene expression and consequently influence plasma triglyceride levels. Human primary hepatocytes treated with Wy 14,643 or fenofibrate displayed a strong induction of APOA5 mRNA. Deletion and mutagenesis analyses of the proximal APOA5 promoter firmly demonstrate the presence of a functional peroxisome proliferator-activated receptor response element. These findings demonstrate that APOA5 is a highly responsive peroxisome proliferator-activated receptor alpha target gene and support its role as a major mediator for how fibrates reduce plasma triglycerides in humans.

Apolipoprotein A-V↗
PubMed1979

Selective deficiency of hepatic triglyceride lipase and hypertriglyceridaemia in kwashiorkor.

1. Serum postheparin lipolytic activities (PHLA), triglyceride and free fatty acid concentrations were determined in children with kwashiorkor before and after treatment and also in normal control children. 2. Using the range (571-1650 mumol/l) of serum triglyceride of the control children as normal, five (20%) of the twenty-five children with kwashiorkor had low (less than 570 mumol/l), thirteen (52%) had normal (571-1650 mumol/l) and seven (28%) had high (more than 1650 mumol/l) serum triglyceride levels. 3. The serum PHLA did not show any definite correlation with the level of circulating triglycerides, although the lowest levels of PHLA were found in the malnourished children with highest triglyceride level. 4. While the hepatic PHLA in the malnourished children was significantly less than control value, the extrahepatic PHLA did not differ significantly. 5. After treatment, serum PHLA rose significantly and the mean levels were within normal range. 6. Our findings suggest that a defect in catabolism of very-low-density lipoprotein caused by a low hepatic PHLA may cause hypertriglyceridaemia in children with kwashiorkor.

Body Weight↗
PubMed1988

Effects of treadmill exercise on the transfer of plasma triglyceride into the ovary of the laying fowl.

1. The effects of 90 min continuous treadmill exercise on the plasma-to-ovary transfer of 14C-labelled triglycerides in laying hens were examined. 2. Exercised birds showed a 4-fold increase in plasma free fatty acid concentration, a 15% decrease in plasma glucose concentration and unchanged plasma triglyceride concentration compared with resting controls. The mean plasma-to-ovary triglyceride transfer rate was approximately halved by exercise. 3. The surface area-specific triglyceride transfer rate was greatest for oocytes weighing 0.25-1.5 g and decreased with increasing oocyte size. The lowest rates were in the small (less than 0.25 g) white oocytes. This pattern was largely unaffected by exercise. 4. Factors that might be responsible for the reduction in triglyceride transfer into the oocytes during exercise include hormonal effects on the permeability of the oocyte envelope, increased competition for plasma lipids by the working muscles and reduced blood flow to the ovary, as a result of the release of vasoconstrictors.

Animals↗