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Fractional fatty acid incorporation into human adipose tissue (FIAT) in hypertriglyceridemia.

Two processes regulate the removal of lipoprotein triglycerides from plasma: (1) hydrolysis of triglycerides by lipoprotein lipase to fatty acids in the capillaries; (2) local uptake and esterification of fatty acids by adipose tissue, muscle and other tissues. This second process has been studied on needle biopsy specimens of adipose tissue from normotriglyceridemic and hypertriglyceridemic subjects. Hypertriglyceridemie was found to be associated to low fatty acid incorporation into adipose tissue.

Adipose Tissue↗

The fibrinolytic system and coagulation during bezafibrate treatment of hypertriglyceridemia.

Bezafibrate was given to 23 hypertriglyceridemic but otherwise healthy middle-aged men in a double-blind, cross-over study to evaluate its effect on the components of the fibrinolytic system as well as on ATIII, FVIIIR: Ag, FVIII: C and platelet aggregation. Fibrinogen dropped markedly (P less than 0.05) and there was a small but significant fall of ATIII. The second wave of platelet aggregation was found much less frequently than in controls (P less than 0.001). Bezafibrate seemed to decrease the rate of formation of the first wave platelet aggregation.

Adult↗

Effect of clofibrate on postheparin plasma triglyceride lipase activities in patients with hypertriglyceridemia.

The lipoprotein lipase (LPL) and hepatic triglyceride lipase (HL) activities of postheparin plasma were determined by a specific immunochemical method in 17 patients with primary hyperlipoproteinemia before and during treatment with clofibrate. The drug caused a significant reduction of serum cholesterol (11%) and triglyceride (45%) levels. Postheparin plasma LPL activity rose in all subjects, the average change being 46% (p less than 0.001). The increase of LPL was positively correlated to the pretreatment LPL activity. There was no correlation between the serum triglyceride concentration and postheparin LPL activity either before or during clofibrate administration. On the other hand, in the clofibrate responders there was a weak correlation between the relative changes of triglyceride concentration and LPL activity (r = 0.43, p less than 0.05). During clofibrate treatment the LPL activity of the hypertriglyceridemic patients was significantly higher than the corresponding value of untreated healthy normoglyceridemic subjects of similar age. The postheparin plasma HL activity was not influenced by clofibrate.

Adult↗

Dietary omega-3 fatty acids prevent carbohydrate-induced hypertriglyceridemia.

Dietary fish oils rich in omega-3 fatty acids are remarkably hypotriglyceridemic in both normal and hypertriglyceridemic subjects. This present study was designed to examine the hypothesis that dietary fish oils could prevent the usual sharp increase in plasma triglyceride and very low-density lipoprotein (VLDL) levels that occur physiologically after the induction by a high-carbohydrate diet. Seven healthy volunteers consumed three experimental liquid formula diets: the baseline diet (45% fat, 10% protein, 45% carbohydrate) and two high-carbohydrate diets (15% fat, 10% protein, 75% carbohydrate), one as a control diet and the other containing fish oil. The baseline and control dietary fats were a mixture of peanut oil and cocoa butter, whereas the fish oil diet contained high levels of omega-3 fatty acids. The plasma triglyceride levels rose from 105 mg/dL during baseline diet to 194 mg/dL during the high-CHO control diet (P less than 0.005). VLDL triglyceride levels increased from 69 to 156 mg/dL (P less than 0.005) and VLDL cholesterol from 18 to 34 mg/dL (P less than 0.005). When fish oil was substituted for the control fats, plasma triglyceride levels fell from 194 to 75 mg/dL (P less than 0.005), VLDL triglyceride and cholesterol levels were reduced from 156 to 34 mg/dL (P less than 0.005) and from 34 to 12 mg/dL (P less than 0.005), respectively. These effects were noted by two to three days after beginning the fish oil diet. Thus, dietary omega-3 fatty acids from fish oil rapidly and markedly reduced VLDL triglyceride levels even in the face of a high-carbohydrate diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Pharmacologic action of L-carnitine on hypertriglyceridemia in obese Zucker rats.

Administration of pharmacologic amounts of L-carnitine was studied in the hypertriglyceridemic Zucker rat. When administered subcutaneously, doses from 250 to 2,000 mg/kg/d significantly decreased plasma triglycerides in obese rats over eight to 12 weeks, with no effect on plasma triglycerides in lean rats. Oral doses at the same high levels were not effective in decreasing plasma triglycerides. Triglyceride secretion rate was reduced from 367 micrograms/min to 168 micrograms/min in treated obese rats. Concurrently, liver lipid was increased twofold in obese treated rats, and the livers of these rats showed significant fatty infiltration. The mechanism of action of carnitine in decreasing plasma triglycerides appeared to be via decreased secretion of triglycerides by the liver of obese rats. There was no effect of L-carnitine in lean or obese rats on the following variables: carnitine palmitoyltransferase-A kinetics or malonyl CoA inhibition, mitochondrial or peroxisomal oxidative capacity, lipoprotein lipase in heart, muscle, and adipose, or fecal lipids. The effect of pharmacologic L-carnitine thus appears to be an inhibition of triglyceride synthesis and/or secretion by the liver.

Animals↗

Long-term hypertriglyceridemia and glucose intolerance in rats fed chronically an isocaloric sucrose-rich diet.

We have previously shown that short-term feeding [20 to 25 day induction period (IP)] normal rats a sucrose-rich diet (SRD) results in an increase of plasma (P), liver (L), and heart (H) triacylglycerol (TG) levels, accompanied by a drop in plasma postheparin total (T-TGL) and hepatic (H-TGL) triglyceride lipases activities, IV glucose intolerance (low Kg) and hyperinsulin responses both in vivo and in vitro, suggesting that a state of insulin resistance had developed. Since normalization of P-TG ensued in the medium term [40 to 55 day adaptation period (AP)] we decided to carry out a longitudinal, long-term (90 to 120 day) follow-up study to observe the dynamic behavior of the above metabolic and hormonal parameters as compared to the appropriate time course control rats were fed the standard chow (STD).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Decreased removal of triglycerides from the blood--a mechanism for the hypertriglyceridemia in male patients with coronary artery disease.

We determined serum apolipoprotein A I and A II concentrations and triglyceride and cholesterol concentrations in serum lipoprotein density classes in 28 male patients with severe ischaemic heart disease (IHD) and with angiographically verified coronary artery disease (CAD) and in age-matched controls. Both triglyceride and cholesterol concentrations in very low density lipoproteins and in low density lipoproteins were higher in IHD-patients than in the controls. The triglyceride but not the cholesterol concentration in serum was higher in IHD-patients than in the controls. The cholesterol in high density lipoproteins and the serum apolipoprotein A I concentration were lower in IHD-patients than in the controls. At least in part the higher triglyceride concentration in very low density lipoproteins could be attributed to a decreased removal of triglycerides from the blood since the fractional removal rate of an i.v. injected artificial triglyceride emulsion (Intralipid) was slower in IHD-patients than in the controls.

Adult↗