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PubMed1976

The direct relationship of proinsulin-insulin hypersecretion to basal serum levels of cholesterol and triglyceride in myotonic dystrophy.

Excessive pancreatic insulin secretory responses to a variety of beta-cytotropic agents have been observed in 40 to 60 per cent of subjects with myotonic dystrophy; in addition, 25 to 30 per cent of affected persons manifest mild glucose intolerance, suggesting that circulating insulin may be biologically ineffective. To test this hypothesis, 8 men with myotonic dystrophy were challenged with a 100 gm. oral glucose load; responses were compared to an age, sex, weight-matched control group. Fasting serum immunoreactive insulin (IRI), cholesterol, and triglyceride levels in the myotonic group did not differ significantly from the controls. In contrast, fasting blood glucose and serum free fatty acid (FFA) levels in the myotonic group were significantly elevated above control, although still within the accepted normal range. Following oral glucose challenge, myotonic subjects exhibited mild glucose intolerance and excessive IRI response, but the FFA and serum alpha-amino nitrogen responses were comparable to control responses. Serum proinsulin was separated from insulin by gel filtration and quantitated by immunoassay. Overall, the proinsulin level in myotonic serum was not greater than the accepted normal level. The mean proinsulin level at the peak serum IRI response during the test was 18.6 +/- 4.1 per cent of the total IRI; 3 myotonic subjects responded with greater than 20 per cent proinsulin. The proinsulin secretory response correlated significantly with basal triglyceride (r = 0.972) and cholesterol (r = 0.794) levels but not with fasting glucose or FFA levels. Peak insulin response was also significantly correlated with triglyceride but not with cholesterol levels. Serum insulin-like activity (ILA) from myotonic dystrophic patients was assessed in vitro employing rat adipose tissue and skeletal muscle in the presence and absence of excess guinea pig anti-insulin serum. Comparison of suppressible insulin-like activity to immunoreactive insulin revealed that the mean biological recovery of serum insulin in these assay systems was 85 to 90 per cent, indicating that endogenous insulin was biologically active on both adipose tissue and skeletal muscle in vitro. We conclude that a biologically ineffective form of circulating insulin does not exist in myotonic dystrophy and that the pancreatic insulin response mechanism may be excessively sensitive, resulting in balanced hypersecretion of proinsulin and insulin. The highly significant correlation between proinsulin and serum triglyceride or cholesterol levels suggests that, in addition to insulin, proinsulin may also exert an important influence on lipid metabolism.

Adult↗
PubMed1994

Transcriptional regulation of the apoC-III gene by insulin in diabetic mice: correlation with changes in plasma triglyceride levels.

Insulin-dependent diabetes mellitus (IDDM) is associated with elevated plasma triglyceride levels that normalize after insulin administration. The observation that overexpression of the apoC-III gene in transgenic mice can cause hypertriglyceridemia and other evidence implicating apoC-III in the regulation of triglyceride levels prompted us to examine whether apoC-III might be involved in the hypertriglyceridemia associated with IDDM. To this end, the regulation of apoC-III gene expression was studied in the streptozotocin-treated mouse model of IDDM. In the insulin-deficient diabetic state, these mice have elevated glucose and triglyceride levels and a 1.4- to 1.5-fold increase in hepatic apoC-III mRNA levels, by Northern analysis as well as quantitative solution hybridization RNase protection assay. Insulin treatment normalized the glucose and triglyceride levels and diminished hepatic apoC-III mRNA levels by 59%. Analysis of transcription rates using the nuclear run-on technique demonstrated that the changes in hepatic apoC-III mRNA levels were the results of changes in the transcriptional activity of the gene. To determine the role of insulin in the regulation of apoC-III transcription, HepG2 cells were transfected with an apoC-III reporter construct, and treated with different insulin concentrations. The results demonstrated that insulin treatment induced a dose-dependent down-regulation of apoC-III transcriptional activity. These data suggest that the apoC-III transcriptional changes seen in animals are caused by differences in insulin concentrations. Assuming that apoC-III mRNA levels reflect the synthesis and secretion of the protein, these results present the possibility that overexpression of the apoC-III gene could contribute to the hypertriglyceridemia observed in IDDM.

Animals↗
PubMed1994

Pancreatic lipase assays with triglycerides as substrate: contribution of each sequential reaction to product formation.

Human pancreatic lipase assays are usually performed in the presence of either emulsified triglycerides or diglycerides within the limits of their solubility. Two reactions are catalyzed in the presence of triglycerides: hydrolysis of triglycerides to diglycerides, and diglycerides to monoglycerides. The contribution of each reaction to the final result was determined after extensive kinetic studies on the appearance and/(or) accumulation of intermediates and/(or) products. Acylated glycerides were analyzed after extraction from the reaction mixture, separation of lipid classes by thin-layer chromatography, and quantification by capillary gas chromatography. The results show that after 10 min of reaction in the presence of high concentrations of triolein, 75% of the released fatty acids arise from the first reaction. Relative merits and disadvantages of each substrate (triglyceride or diglyceride) are discussed in terms of practicability.

Acylation↗
PubMed1994

Synthesis and lymphatic transport of intestinal apolipoprotein A-IV in response to graded doses of triglyceride.

Factors regulating the intestinal synthesis and secretion of apoA-IV are incompletely understood. Although it is known that apoA-IV is stimulated by dietary lipid, it is not known whether graded doses of triglyceride elicit graded responses in apoA-IV synthesis and secretion. We used the chronic intestinal lymph-fistula rat to examine the effect of graded levels of intestinal triglyceride transport on secretion of apoA-IV into lymph and synthesis of apoA-IV in various regions of intestine. Rats were implanted with chronic duodenal and intestinal lymph duct cannulas and infused with lipid emulsions containing 5, 10, 20, 40, 80 mumol triolein (including [3H]triolein, 1.2 microCi), 8.7 mumol phosphatidylcholine, and 57 mumol sodium taurocholate in 3 ml phosphate-buffered saline (pH 6.4) at ml/h for 8 h. Lymph samples were collected for 1 h prior to and at 2, 4, 5, 6, 7, and 8 h after the start of lipid infusion. Lymphatic output of triglyceride, phospholipid, and apoA-IV was measured. Steady-state (8 h) content of radioactive lipid was also measured in the lumen and the wall of the gut. In separate studies rats were given infusions of either 5% glucose in saline ("fasting") or triolein emulsion (10, 20, 40, 80 mumol/h) for 8 h after which incorporation of [3H]leucine into apoA-IV in isolated, in situ loops of duodenum, proximal jejunum, mid-distal jejunum, and terminal ileum was measured. Lipid output increased dose-dependently in response to triolein infusion, with steady-state lipid transport achieved by 5 h after start of lipid infusion. Total recovery of 3H-labeled lipid was similar for all triolein doses. Increase in lymphatic apoA-IV output lagged that of triglyceride by 3-4 h, but by 8 h showed graded increases with triolein dose. ApoA-IV synthesis (apoA-IV radioactivity immunoprecipitated by an apoA-IV monospecific antibody and expressed as % of trichloroacetic acid-precipitable [3H]leucine radioactivity) in the duodenum and proximal jejunum showed a 2-fold increase (compared with fasting) in response to 10 mumol triolein/h, but no further increase at higher doses. However, apoA-IV synthesis in mid to distal jejunum increased dose-dependently.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Detergent extraction and enzymatic analysis for fecal long-chain fatty acids, triglycerides, and cholesterol.

We report a procedure for determining fecal long-chain fatty acids (LCFA), triglycerides, and cholesterol after detergent extraction with 10 mL/L Triton X-100, 6 mL/L Brij 30, and 0.1 mol/L HCl in isotonic saline by enzymatic analysis of the extraction supernates. Mean recoveries of calibrators ranged from 105% to 117%. Assays of fecal extracts were linear with concentration from 0 to 1000 mumol/L for LCFA, from 10 to 90 mumol/L for triglycerides, and from 0 to 300 mumol/L for cholesterol. Within-run CVs were < 3% for medium and high concentrations, and 3%, 14%, and 28% for low concentrations of LCFA, cholesterol, and triglycerides, respectively. Correlation with gravimetric determination resulted in coefficients (r2) of 0.72 for total fat, 0.63 for neutral fat, and 0.66 for nonesterified fat. Assays of extracts and residues prepared for gravimetric determination indicated that approximately 90% of triglycerides, cholesterol, and LCFA were extracted by organic solvents and that the extracts contain a significant amount of other fats. The proposed method appears accurate, precise, specific, and suitable for routine analysis.

Cholesterol↗
PubMed1994

Microsomal triglyceride transfer protein, the abetalipoproteinemia gene product, mediates the secretion of apolipoprotein B-containing lipoproteins from heterologous cells.

Apolipoprotein (apo) B is an obligatory component of triglyceride-rich lipoproteins. In the rare autosomal recessive disorder abetalipoproteinemia (ABL), no triglyceride-rich lipoproteins are secreted. Mutations in the gene encoding the 97-kDa subunit of a microsomal triglyceride transfer protein (MTP) cause ABL (Sharp, D., Blinderman, L., Combs, K. A., Klenzle, B., Ricci, B., Wager-Smith, K., Gil, C. M., Turck, C. W., Bouma, M. E., Rader, D. J., Aggerbeck, L. P., Gregg, R. E., Gordon, D. A., and Wetterau, J. R. (1993) Nature 365, 65-69; Shoulders, C. C., Brett, D. J., Bayliss, J. D., Narcisi, T. M., Jarmuz, A., Grantham, T. T., Leoni, P. R. D., Bhattacharya, S., Pease, R. J., Cullen, P. M., Levi, S., Byfield, P. G. H., Purkiss, P., and Scott, J. (1993) Hum. Mol. Genet. 2, 2109-2116). Here we have examined whether MTP is both necessary and sufficient to mediate the secretion of apoB-containing lipoproteins from cells that do not normally express either of these proteins. Carboxyl-terminal truncated forms of apoB, apoB17, and apoB41 on the centile system were expressed in COS-1 cells. ApoB17 was secreted whereas apoB41 was unable to traverse the secretory pathway. Cotransfection of apoB41 and MTP promoted the secretion of apoB41 as a buoyant lipoprotein particle with a modal density of 1.15 g/ml. When cotransfected COS-1 cells were cultured under conditions that increase the secretion of apoB100 from HepG2 cells, secretion of apoB41 was similarly increased. N-Acetyl-leucyl-leucyl-norleucinal (ALLN), a calpain I inhibitor, abolished intracellular degradation of apoB41 and increased secretion 2.5-fold. Oleate, a substrate for triglyceride synthesis, reduced degradation from 50 to 19% and increased secretion by 2.5-fold. The effects of ALLN and oleate were additive. We conclude that the secretion of apoB from COS-1 cells cotransfected with apoB and MTP is determined by the competitive processes of lipoprotein assembly and intracellular degradation in the endoplasmic reticulum and that MTP is the only tissue-specific component, other than apoB, required for the secretion of apoB-containing lipoproteins.

Abetalipoproteinemia↗
PubMed1975

The effect of tobacco smoke and some of its constitutents on triglyceride secretion in the squirrel monkey.

The acute effects of tobacco smoke and some of its constituents on plasma free fatty acid levels and on triglyceride secretion were studied in anaesthetized squirrel monkeys given Triton WR-1339. All the treatments raised plasma free fatty acids in the order high tar smoke greater than medium tar vapour phase = air:CO greater than medium tar smoke. Plasma triglyceride secretion in animals inhaling high tar smoke did not differ from controls. There was a transient rise in triglyceride secretion in animals inhaling vapour phase but the largest increase (after a significant delay) was in monkeys breathing air:CO. Maximal concentrations of blood carboxyhaemoglobin did not differ between the experimental groups. It is suggested that, under these experimental conditions, there are present in the particulate phase of tobacco smoke factors which inhibit hepatic triglyceride secretion.

Animals↗
PubMed1993

Effect of estradiol administration and subsequent nonfeeding on liver estrogen receptor, serum apolipoprotein B-100, and serum triglycerides concentrations in steers.

Estradiol was administered to 3 steers (0.12 mg/kg of body weight/d for 14 consecutive days), followed by 2 days of nonfeeding (starvation). During estradiol administration, liver nuclear estrogen receptor and serum apolipoprotein B-100 (apoB-100), as well as serum triglycerides concentrations were increased, compared with values before administration. Starvation, together with interruption of estradiol administration, resulted in rapid decreases of the receptor, serum apoB-100, and serum triglycerides concentrations, and increase of nonesterified fatty acids concentration. Of the 3 steers, 2 had higher liver triglyceride content, compared with values before treatment. In the control group (3 steers that received vehicle alone, then starved similarly), these concentrations, except for serum nonesterified fatty acids and triglycerides concentrations after starvation, were not changed. In another experiment, serum apoB-100 concentration in dairy cows was significantly (P < 0.05) lower at parturition than values before and after parturition. These results indicate that estradiol may be involved in development of fatty liver in cattle.

Animals↗
PubMed1994

Apolipoprotein E polymorphism influences postprandial retinyl palmitate but not triglyceride concentrations.

To quantify the effect of the apolipoprotein (apo) E polymorphism on the magnitude of postprandial lipemia, we have defined its role in determining the response to a single high-fat meal in a large sample of (N = 474) individuals taking part in the biethnic Atherosclerosis Risk in Communities Study. The profile of postprandial response in plasma was monitored over 8 h by triglyceride, triglyceride-rich lipoprotein (TGRL)-triglyceride, apo B-48/apo B-100 ratio, and retinyl palmitate concentrations, and the apo E polymorphism was determined by DNA amplification and digestion. The frequency of the apo E alleles and their effects on fasting lipid levels in this sample were similar to those reported elsewhere. Postprandial plasma retinyl palmitate response to a high-fat meal with vitamin A was significantly different among apo E genotypes, with delayed clearance in individuals with an epsilon 2 allele, compared with epsilon 3/3 and epsilon 3/4 individuals. In the sample of 397 Caucasians, average retinyl palmitate response was 1,489 micrograms/dl in epsilon 2/3 individuals, compared with 1,037 micrograms/dl in epsilon 3/3 individuals and 1,108 micrograms/dl in epsilon 3/4 individuals. The apo E polymorphism accounted for 7.1% of the interindividual variation in postprandial retinyl palmitate response, a contribution proportionally greater than its well-known effect on fasting LDL-cholesterol. However, despite this effect on postprandial retinyl palmitate, the profile of postprandial triglyceride response was not significantly different among apo E genotypes. The profile of postprandial response was consistent between the sample of Caucasians and a smaller sample of black subjects. While these data indicate that the removal of remnant particles from circulation is delayed in subjects with the epsilon 2/3 genotype, there is no reported evidence that the epsilon 2 allele predisposes to coronary artery disease (CAD). The results of this study provide not only a reliable estimate of the magnitude of the effect of the apo E polymorphism on various measurements commonly used to characterize postprandial lipemia, but also provide mechanistic insight into the effects of the apo E gene polymorphism on postprandial lipemia and CAD.

Apolipoproteins B↗
PubMed1994

Effects of specimen turbidity and glycerol concentration on nine enzymatic methods for triglyceride determination.

We compared the effects of specimen turbidity and glycerol concentration on nine enzymatic methods for triglyceride measurement. We assayed 51 specimens with triglyceride concentrations of 0.85-8.21 mmol/L (75-727 mg/dL) and turbidity at 420 nm equivalent to > or = 0.1 mmol/L (8.8 mg/dL) triglyceride (measured as part of our comparison method). The data were analyzed by multiple regression, which gave coefficients for the effects of glycerol concentration and the change in turbidity during the reaction. The effects of specimen turbidity and glycerol concentration were method-dependent and ranged from 6.20% to -15.67% of the measured result. The magnitude of the turbidity effect (in assays with a significant turbidity interference) was similar to that for glycerol (in assays with a significant glycerol interference). A triglyceride assay with a bichromatic measurement was less subject to interference from turbidity.

Autoanalysis↗
PubMed1993

[Laboratory findings in the medical examination of chronic "Yusho" (PCB poisoning) patients: with special reference to blood PCB and serum triglyceride].

Associations of blood PCB concentration with serum levels of triglyceride, gamma-GTP, total-, and conjugated-bilirubin were investigated in "Yusho" patients twenty years after outbreak, using the information obtained from the medical examinations in 1988 and 1989. Study subjects were 259 patients in 1988, and 268 patients in 1989, including 190 patients who consecutively received both examinations. Blood PCB concentrations (mean +/- SE) were 4.78 +/- 0.22 ppb in 1988, and 4.47 +/- 0.17 ppb in 1989. The results of blood-chemical analysis were compared among four categorized concentrations of blood PCB, using the analysis of variance. Significant difference was observed for triglyceride (1988: p < 0.025, 1989: p < 0.005), but not for gamma-GTP, total-, and conjugated-bilirubin. In 1988, the mean triglyceride levels were 108, 137, 145, and 166 mg/dl at < 2.7, > or = 2.7, > or = 4.1, and > or = 6.1 ppb of blood of PCB, respectively. Corresponding figures in 1989 were 106, 129, 154, and 156 mg/dl at < 2.7, > or = 2.7, > or = 4.0, and > or = 5.7 ppb of blood PCB, respectively. Thus, clear positive association between blood PCB and serum triglyceride was observed in the patients twenty years after exposure.

Aged↗
PubMed1993

Comparison of taurine, alpha-tocopherol, retinol, selenium, and total triglycerides and cholesterol concentrations in cats with cardiac disease and in healthy cats.

Epidemiologic relations were evaluated between plasma concentrations of nutrients and cardiovascular diseases. A total of 220 cats were assessed: 144 cats with noninduced acquired heart disease and 76 clinically normal cats. Plasma was assayed for taurine, alpha-tocopherol, selenium, retinol, and total cholesterol and triglycerides concentrations. Cardiovascular disease groups included dilated cardiomyopathy (n = 53), left ventricular hypertrophy (n = 28), hyperthyroidism (n = 11), and uncertain classification (n = 52). In cats with dilated cardiomyopathy, mean plasma taurine concentration was the lowest of that in cats of any group, being only 38% of the value in healthy cats; females had less than half the mean value of males. Tocopherol concentration was 20% lower than normal, and retinol concentration was 40% higher than normal. Total cholesterol concentration was 36% lower than normal. Triglycerides concentration was higher in these cats than in any other group--twice the value recorded in healthy cats and 67% higher than that in hyperthyroid cats. In cats with hypertrophic cardiomyopathy, almost 15% had mean plasma taurine concentration < 30 mumol/L. Retinol concentration was 15% higher, and triglycerides concentration was 54% higher than normal. Approximately 27% of hyperthyroid cats had mildly decreased plasma taurine concentration. Hyperthyroid cats had the lowest tocopherol and cholesterol values; both were at least 30% lower than normal. Retinol concentration was 30% higher than normal. Approximately 14% of cats with uncertain classification had mildly decreased plasma taurine concentration. Plasma retinol and triglycerides concentrations were higher than normal in 25 and 38% of these cats, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

[Effect of pancreas transplantation on triglyceride metabolism].

Transplantation of pancreatic gland with systemic venous drainage of the graft causes elevated plasma levels of insulin. To examine lipid metabolism triglyceride clearance capacity, lipolytic enzymes, plasma lipids and lipoproteins were quantified in pancreas-kidney transplant recipients and compared them to lipid parameters of healthy controls and those of patients who had received only kidney transplants. Eleven pancreas-kidney transplant recipients with type I diabetes, 9 non-diabetic kidney transplant recipients as controls for the effects of immunosuppressive medication, and 11 healthy controls were studied. In pancreas-kidney transplant recipients fasting cholesterol, non-HDL cholesterol, triglyceride levels were found 5.5 (+/- 1.0), 3.4 (+/- 0.78) and 1.06 (+/- 0.29) respectively and expressed in mmol/L (mean +/- SE). The results were statistically not different from those of healthy controls. In contrast, non-diabetic kidney transplant recipients cholesterol, non-HDL cholesterol and triglyceride levels were increased to 6.1 (+/- 0.81) (p < 0.05), 4.6 (+/- 1.1) (p < 0.05) and 2.34 (+/- 1.53) mmol/L (p < 0.05). HDL cholesterol averaged 2.08 (+/- 0.36) in pancreas-kidney transplant recipients, clearly higher than that of kidney transplant recipients 1.53 (+/- 0.39) mmol/L (p > 0.01), or of controls 1.61 (+/- 0.37) mmol/L (p < 0.05). In pancreas-kidney transplant recipients postprandial lipaemia was the lowest and lipase activity was the highest compared both to kidney transplant recipients (p < 0.001, p < 0.05) and controls (p < 0.01, p < 0.05). This excellent triglyceride clearing capacity appears to be the result of a high activity of lipoprotein lipase, which, can be explained by the peripheral hyperinsulinaemia.

Endopeptidases↗
PubMedDate not supplied

Metabolic effects of infusion of a structured-triglyceride emulsion in healthy subjects.

Structured-triglyceride (STG) emulsions may have beneficial effects compared with traditional emulsions. We infused equimolar doses of STG and long-chain fatty acid triglyceride (LCT; Intralipid 20%) emulsions for 6 h into eight healthy subjects. Six subjects were also infused with either a low or a high dose of the STG emulsion. Blood concentrations of triglycerides and glycerol increased dose-dependently. In seven of the eight subjects the increase in serum triglyceride concentrations was greater during LCT infusion than during STG infusion. The molar ratio of medium- to long-chain fatty acids in the plasma after infusions of STG at medium and high rates was close to the compositional molar ratio of this emulsion (1:1), indicating that medium- and long-chain fatty acids were released at similar rates. During fat infusion there was a small but significant decrease in plasma glucose and a modest increase in serum beta-hydroxybutyrate concentrations but no hypoglycemia. Serum phospholipids increased significantly in all groups except the one receiving the low dose of STG. Plasma insulin, serum lactate, and serum cholesterol concentrations did not change. In conclusion, the capacity of healthy subjects to hydrolyze STG was at least as high as that to hydrolyze LCT. Plasma fatty acid profiles during fat infusions were similar to the fatty acid compositions of the infused emulsions.

3-Hydroxybutyric Acid↗
PubMed1995

Lipoteichoic acid stimulates lipolysis and hepatic triglyceride secretion in rats in vivo.

The host response to infection is frequently accompanied by changes in lipid metabolism. Previous studies have shown that endotoxin (LPS), a component of the cell wall of gram-negative bacteria, increases serum lipid levels. In this study, we demonstrate that lipoteichoic acid (LTA), a component of the cell membrane of gram-positive bacteria, also increases serum lipid levels in rats in a dose-dependent manner (0.1-300 micrograms/200 g body weight). Serum triglyceride levels increased within 2 h after LTA administration with peak values at 4 h (2-fold increase). Serum cholesterol levels also increased but the effect was delayed occurring at 16 h and was relatively small (1.2-fold increase). LTA (10 micrograms/200 g BW) did not decrease adipose tissue lipoprotein lipase activity or the clearance of triglyceride-rich lipoproteins. Rather, the LTA-induced hypertriglyceridemia is due to an increase in hepatic triglyceride secretion. LTA stimulates both hepatic de novo fatty acid synthesis and lipolysis. The increased delivery of free fatty acids to the liver plays a major role in the LTA-induced hypertriglyceridemia. Pretreatment with phentolamine, an alpha-adrenergic receptor antagonist, and alprenolol, a beta-adrenergic receptor antagonist, or phentolamine alone significantly suppressed the hypertriglyceridemia induced by LTA. These adrenergic inhibitors had no significant effect on the increase in lipolysis. These results indicate that catecholamines are involved in mediating the LTA-induced increase in hepatic triglyceride secretion via alpha-adrenergic receptors. These changes in lipid metabolism may play an important role in the organism's response to gram-positive infection.

Adipose Tissue↗
PubMed1996

The effect of reduced extrinsic sucrose intake on plasma triglyceride levels.

OBJECTIVE: To examine the effect on plasma triglycerides of removing most of the extrinsic sugar from the diet of free living hypertriglyceridaemic individuals while controlling weight loss. DESIGN: Free living subjects were randomly assigned to intervention and control groups. The intervention group undertook to consume a "sugar free' diet for six months after a three month baseline period. The control group maintained their usual diets for the nine month period. The results from the two groups were compared using repeated measures ANOVA. SUBJECTS: Thirty two hypertriglyceridaemic individuals, selected from members of the public in Dunedin, New Zealand. RESULTS: Subjects in the intervention group were able to achieve a mean reduction in sucrose intake of > 70%, largely extrinsic sucrose, resulting in a group mean reduction in plasma triglyceride levels of > 20% and a mean weight loss over the six month period of about 2%. Repeated measures ANOVA on the mean triglyceride figures after the individual figures had been adjusted for this small weight loss, showed that there was a significant fall in triglyceride levels over the study period compared with the baseline. CONCLUSIONS: Hypertriglyceridaemia can be reduced in some individuals by the reduction of extrinsic sucrose in the diet. When allowance is made for weight loss the reduction is still significant.

Adult↗
PubMed1995

Liver fat, serum triglycerides and visceral adipose tissue in insulin-sensitive and insulin-resistant black men with NIDDM.

OBJECTIVE: We investigated the relationship of liver fat to visceral adipose tissue, serum triglyceride levels and glucose disposal. DESIGN: Cross-sectional, prospective. SUBJECTS: 21 lean to moderately obese black NIDDM men (mean +/- s.d. age 48.9 +/- 9.4 years, body mass index 26.3 +/- 2.4, fasting plasma glucose 104 +/- 10 mg/dl, HBA1C 4.6 +/- 0.8% and body fat 26 +/- 6%) with no evidence of liver disease or alcohol abuse. Eleven were insulin-sensitive (glucose disposal > 5.5 mg/kg/min) and ten were insulin-resistant subjects during euglycemic insulin clamps. MEASUREMENTS: Body composition and liver density were determined by whole body computed tomography using 22 scans. Liver fat score was defined as 100 minus the absolute liver density. Glucose disposal was measured during 1 mU/kg/min euglycemic insulin clamp with 3-3H glucose. RESULTS: Visceral adipose tissue volume was 3.54 +/- 1.87 litres. The liver fat score was 48.8 +/- 5.0 (not in the range of clinical hepatic steatosis). Glucose disposal ranged from 2.5 to 8.1 mg/kg/min. The liver fat score was correlated with visceral/total adipose tissue ratio (r = 0.65, P = 0.001) and to fasting serum triglyceride levels (r = 0.47, P = 0.032). Fasting serum triglyceride levels were related to visceral adipose tissue (r = 0.52, P = 0.016). Liver fat was inversely related to glucose disposal (r = -0.42, 1 tail P = 0.036). CONCLUSIONS: In non-insulin-dependent diabetes mellitus, liver fat may contribute to insulin resistance and be a link between visceral adipose tissue mass and serum triglyceride levels.

Adipose Tissue↗
PubMed1997

Mitochondrion is the principal target for nutritional and pharmacological control of triglyceride metabolism.

Fish oil polyunsaturated fatty acids and fibrate hypolipidemic drugs are potent hypotriglyceridemic agents that act by increasing fatty acid catabolism and decreasing triglyceride synthesis and secretion by the liver. A major unresolved issue is whether this hypotriglyceridemic effect can occur independent of induction of peroxisomal beta-oxidation, a predisposing factor for hepatocarcinogenesis. The present study was undertaken to determine which component of fish oil, eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA), is responsible for its triglyceride-lowering effect. We demonstrate that EPA and not DHA is the hypotriglyceridemic component of fish oil and that mitochondria and not peroxisomes are the principal target. Results obtained by fenofibrate feeding support the hypothesis that the mitochondrion is the primary site for the hypotriglyceridemic effect. In contrast to fibrates, EPA did not affect hepatic apolipoprotein C-III gene expression. Therefore, increased mitochondrial beta-oxidation with a concomitant decrease in triglyceride synthesis and secretion seems to be the primary mechanism underlying the hypotriglyceridemic effect of EPA and fibrates in rats, rabbits and possibly also in humans. In addition, these data show that lowering of plasma triglycerides can occur independently of any deleterious peroxisome proliferation.

Animals↗