Lipid-rich Meal Research Articles

Sucrose in a lipid-rich meal amplifies the postprandial excursion of serum and lipoprotein triglyceride and cholesterol concentrations by decreasing triglyceride clearance

Nineteen young male normolipidemic volunteers sequentially consumed three test meals consisting of cream only, sucrose only, or cream with sucrose. These oral fat-tolerance tests showed an amplification of the postprandial excursion of serum triglyceride and cholesterol concentrations when sucrose was included in a lipid-rich meal compared with both the cream-only meal and the sucrose-only meal. The triglyceride concentration increase occurred only in the late postprandial phase whereas the cholesterol concentration was increased for the entire 8 h studied. The increased triglyceride and cholesterol concentrations in the triglyceride-rich lipoprotein (TRL) fraction accounted for most of the increase. The clearance of an intravenous lipid emulsion was measured before and 2 and 4 h after a sucrose meal. The two postprandial clearance rates were 34% slower than the fasting value. These data indicate that sucrose-induced postprandial hypertriglyceridemia may be induced by an inhibition of the clearance of triglyceride. The slower rate of lipolysis may cause the accumulation of cholesterol in TRL.

Effect of coenzyme a infusions on postprandial triglyceride metabolism and PAI-1 levels in patients with moderate hypertriglyceridemia

A controlled, double-blind study was conducted to evaluate the metabolic effects of coenzyme A (CoA) on postprandial hyperlipidemia, by monitoring changes in plasma triglyceride levels and levels of PAI-1, the circulating inhibitor of fibrinolysis. Twenty patients of both sexes with moderate hypertriglyceridemia (>250 mg/dl), some with adult-onset diabetes, participated. The subjects were randomly assigned to receive 2 weeks of treatment with CoA 4000 IU IM or a corresponding placebo. At the beginning and end of treatment, the patients were challenged with a lipid-rich meal eliciting, in our experience, a close to doubling of baseline triglyceridemia. Treatment with CoA significantly inhibited postprandial hypertriglyceridemia; the increase in plasma triglyceride levels was 90% to 97% before and after placebo treatment, whereas it was less than half that after CoA. Although only modest changes were noted in high-density lipoprotein cholesterol levels, high-density lipoprotein triglyceride levels were somewhat elevated after CoA treatment. The reduction in PAI-1 levels noted after the fatty meal was more consistent in the CoA group. These results demonstrate that parenteral CoA can effectively prevent postprandial hypertrigly ceridemia and may also have some effects on the fibrinolytic system.

Functional differences in human neutrophils isolated pre- and post-prandially

Activated polymorphonuclear leukocytes have been associated with neoplasia, atherogenesis and reperfusion injury. Since some of these conditions are also correlated with dietary fat, we examined the functional characteristics of leukocytes isolated from subjects before and after consumption of a lipid-rich meal. There was up to 2-fold greater superoxide generation in response to agonists in leukocytes obtained post-prandially; the maximum increase was observed about 4 h after eating and followed the peak (2–4 h) in serum triglycerides. Neutrophils isolated post-prandially also exhibited impaired chemotaxis and defective bacterial killing, but normal phagocytosis. These findings provide a new variable that should be considered in studies of leukocytes.

Interaction between orally administered tyramine and moclobemide

This article describes a standardized oral tyramine pressor test designed to give information on safety aspects in the real everyday life situation where tyramine is ingested only with food. Results showed that significantly higher doses of tyramine were required to raise standing blood pressure by at least 30 mmHg (TYR 30) when it was taken with food than when subjects fasted. The same test was then conducted in 8 healthy volunteers during treatment with moclobemide 200 mg 3 times daily and tranylcypromine 10 mg 3 times daily. With moclobemide the mean TYR 30 dose was 306 mg, and the ratio of this to baseline was 5.0. With tranylcypromine, however, the mean TYR 30 dose was only 35 mg and the TSF ratio 38.2. The potentiation by tranylcypromine was thus 7.6 times greater than that of moclobemide. When tyramine was given in the food under treatment with MAO inhibitors, the TYR 30 doses were larger than those obtained under fasting conditions, but the TSF ratios were not altered. When the tyramine was given in a protein-rich or a lipid-rich meal, the previously established TYR 30 had significantly less effect on the blood pressure. The lowest TYR 30 dose during moclobemide treatment is at least 150 mg tyramine, an amount contained in about 300 g strong cheese or 100 g of yeast extract. These quantities are unlikely to be consumed in a normal meal. The corresponding TYR 30 dose for tranylcypromine, however, is only 20 mg tyramine, which can easily be contained in a fairly normal portion of strong cheese (40 g).(ABSTRACT TRUNCATED AT 250 WORDS)

Lipoproteins, diet and atherosclerosis

A controlled, double-blind study was conducted to evaluate the metabolic effects of coenzyme A (CoA) on postprandial hyperlipidemia, by monitoring changes in plasma triglyceride levels and levels of PAI-1, the circulating inhibitor of fibrinolysis. Twenty patients of both sexes with moderate hypertriglyceridemia (>250 mg/dl), some with adult-onset diabetes, participated. The subjects were randomly assigned to receive 2 weeks of treatment with CoA 4000 IU IM or a corresponding placebo. At the beginning and end of treatment, the patients were challenged with a lipid-rich meal eliciting, in our experience, a close to doubling of baseline triglyceridemia. Treatment with CoA significantly inhibited postprandial hypertriglyceridemia; the increase in plasma triglyceride levels was 90% to 97% before and after placebo treatment, whereas it was less than half that after CoA. Although only modest changes were noted in high-density lipoprotein cholesterol levels, high-density lipoprotein triglyceride levels were somewhat elevated after CoA treatment. The reduction in PAI-1 levels noted after the fatty meal was more consistent in the CoA group. These results demonstrate that parenteral CoA can effectively prevent postprandial hypertrigly ceridemia and may also have some effects on the fibrinolytic system.

The effect of age on the relationship between plasma elastase and ingested lipid.

In human subjects ranging in age from 57 to 99 years the elastase content of the plasma increased following the ingestion of a lipid-rich meal. Animal experiments have shown that peak elastase levels are attained after 3 to 4 hours, which are similar to the appearance of peak levels of triglyceride. The difference between the postprandial and fasting levels of elastase is age-dependent, being greatest among the lowest ages studied and falling exponentially at ages above 65-70. Since it has already been shown that individuals aged 65-75 with high fasting levels of plasma elastase are less likely to survive into their ninth or tenth decades it is suggested that the measurement of the increase in elastase associated with the intake of a lipid-rich meal can provide an acceptable indication of survival potential.