Triglyceride Infusion Research Articles

Effect of Increased Plasma Non-Esterified Fatty Acid Concentrations on Endurance Performance During Beta-Adrenoceptor Blockade

Inhibition of adipose tissue lipolysis, leading to a reduced availability of non-esterified fatty acids for energy production in the active skeletal muscles, may be involved in the impairment of endurance exercise capacity after administration of a beta-adrenoceptor blocking agent. The effect of increasing the availability of plasma NEFA during exercise after beta-blocker administration was studied. In a double-blind, randomized cross-over study 12 healthy volunteers were treated for 14 days with placebo, atenolol, and propranolol. On the 7th and 14th day of each treatment period an endurance exercise test at 70% of maximal aerobic power until exhaustion was performed while a continuous infusion of saline or triglycerides (Intralipid)+heparin was administered. Endurance time was reduced by 11% (n.s.) during atenolol and 40% (p < 0.01) during propranolol. Intralipid administration had no statistically significant effect on endurance in any treatment. Plasma NEFA and glycerol concentrations were elevated above control levels during Intralipid infusion, plasma glucose and lactate concentrations were unaffected. These results suggest that reduced availability of NEFA is not a major factor in the reduction of endurance performance during beta-adrenoceptor blockade, although an effect of beta-blockade on NEFA membrane transport cannot be excluded.

Effects of different lipid substrates on glucose metabolism in normal postabsorptive humans

We investigated the effects on glucose metabolism of the infusion of either long-chain triglycerides (LCT), a mixture of long-chain and medium-chain triglycerides ( MCT LCT ), d-β-hydroxybutyrate ( d-β-OHB), or saline in normal postabsorptive subjects. Plasma insulin, C-peptide, and glucagon concentrations were unchanged in all groups. LCT and MCT LCT infusions increased levels of plasma free fatty acids (FFA) compared with those of the saline group, whereas d-β-OHB decreased them. Plasma ketone body concentrations were higher during the d-β-OHB and triglyceride infusions than during the saline test. Glucose concentrations and appearance (R a) and disappearance (R d) rates were not modified during saline infusion. Glucose levels decreased only in the d-β-OHB and MCT LCT groups ( P < .05), whereas they were unchanged during LCT infusion. Glucose R a decreased slightly by 15% to 17% in LCT, MCT LCT , and d-β-OHB groups ( P < .05 v saline). Glucose R d decreased by 14% to 16% in each lipid-infusion group ( P < .05 v saline). Glucose clearance rates decreased by 14% only in the LCT group ( P < .001). Glucose oxidation rates did not change significantly during the lipid substrate infusions compared with saline infusion. In conclusion, (1) the effects of fatty acids on glucose metabolism appear to depend on the fatty acid chain length, since only LCT infusion significantly impaired glucose utilization; and (2) in subjects with normal endocrine pancreas function, we found no adverse effects of a short-term increase in lipid substrate availability on glucose production rate and concentration.

Stimulation of pyloric contractions by intraduodenal triglyceride is persistent and sensitive to atropine.

Intraduodenal lipid infusion stimulates phasic and tonic pyloric contractions and suppresses antral contractions. This study determined: (i) whether this response is sustained over 90 min; and (ii) the role of muscarinic mediation of this response. Antropyloroduodenal motility was recorded in 17 healthy volunteers with a sleeve/sidehole manometric assembly. Subjects received either a 90 min intraduodenal infusion of saline or triglyceride (20% Intralipid) at a rate of 1 mL/min; 30 min after the start of this infusion, the eight subjects who received triglyceride were given intravenous atropine 15 micrograms/kg over 30 s, followed by a maintenance infusion of 4 micrograms/kg/h until the study was completed. Intraduodenal triglyceride infusion stimulated isolated pyloric pressure waves consistently, producing a median rate of 2.4 per min after 30 min of triglyceride infusion, compared with a median rate of 0 per min pre-infusion. In intravenous saline studies, there was a reduction (P < 0.05) in the median rate of isolated pyloric pressure waves to 1.3 per min at 90 min, when compared with pyloric pressure waves at 30 min. Atropine reduced isolated pyloric pressure waves to a median rate of 0 per min, significantly different from preatropine (P < 0.01) and from intravenous saline studies (P < 0.0001). These results indicate that the phasic pyloric response to intraduodenal lipid persists during 90 min stimulation, albeit with significant attenuation. In humans, muscarinic cholinergic blockade prevents the occurrence of triglyceride stimulated localized pyloric contractions.

Adaptive changes in the pyloric motor response to intraduodenal dextrose in normal subjects

Gastric emptying of glucose is faster after dietary supplementation of glucose, suggesting specific adaptation to changes in nutrient intake. In the present study, the effects of a continuous long-term (0–120-minute) and two short-term (0–20- and 80–100-minute) intraduodenal infusions of dextrose (2.4 kcal/min) on antropyloroduodenal motility and blood glucose, plasma gastric inhibitory polypeptide, and insulin concentrations were evaluated in nine volunteers. In four volunteers, an intraduodenal infusion of triglyceride (2.4 kcal/min) was administered immediately after the long-term dextrose infusion. The long-term dextrose infusion initially increased isolated pyloric pressure waves (IPPWs) and basal pyloric pressure (P < 0.05 for both), but after about 30 minutes IPPWs and basal pyloric pressure decreased and returned to baseline within 80 minutes. Each short-term infusion increased IPPWs and basal pyloric pressure (P < 0.05 for both). Antral pressure waves remained suppressed during the long-term dextrose infusion. Intraduodenal triglyceride increased IPPWs and basal pyloric pressure (P < 0.05 for both). The long-term dextrose infusion was associated with a sustained increase, and both short-term dextrose infusions were associated with peaks in glucose, insulin, and gastric inhibitory polypeptide levels. There was no significant relationship between biochemical measurements and antropyloroduodenal motility. It is concluded that specific adaptive changes occur rapidly in the phasic and tonic pyloric motor response, but not the antral motor response, to intraduodenal dextrose.

Relation of pyloric motility to pyloric opening and closure in healthy subjects.

The relation between pyloric motor activity, opening, and closure was examined in eight healthy men. Manometry was performed with an assembly combining 13 side holes and a sleeve sensor positioned astride the pylorus. Simultaneous with manometry, pyloric opening and closure and antroduodenal contractions were observed fluoroscopically with the antrum filled with barium. During intraduodenal normal saline infusion, coordinated antral pressure waves swept over the pylorus and ejected barium into the duodenum. No localised pyloric motor pattern was observed under these conditions. In contrast, the intraduodenal triglyceride infusion was associated with the absence of antral pressure waves and virtual absence of antral wall movement. At the pylorus, there was a zone of luminal occlusion less than 1 cm long that persisted for the period of observation. This zone of luminal occlusion corresponded precisely with manometric recordings of a narrow zone of pyloric phasic and tonic activity. During the duodenal triglyceride infusion, the pylorus was closed for 98.5% of the measurement period when basal pyloric pressure was 4 mm Hg or more, and during this motor pattern, barium did not traverse the pylorus. Localised pyloric contractions cause sustained pyloric closure, whether these contractions are phasic or tonic. These contractions occur independently of antral or duodenal contractions and may interrupt gastric emptying.

Lack of accumulation of midazolam in plasma and lipoprotein fractions during intravenous lipid infusions in patients on artificial respiration.

Severely ill patients often require total parenteral nutrition including intravenous lipid emulsions concurrently administered with lipophilic drugs. Therefore we investigated whether therapeutic application of a mixed medium chain/long chain triglyceride infusion affects the disposition of midazolam necessary for sedation in patients on artificial respiration. The concentrations of midazolam were measured in unfractionated plasma, and in lipoprotein fractions isolated from ex vivo blood samples, including determination of triglycerides and cholesterol; the albumin level was also analysed. Midazolam in the VLDL fraction was only 0.246 microgram.ml-1, whereas the total plasma concentration averaged 1.101 micrograms.ml-1, and the midazolam content of the LDL plus HDL fractions amounted to 1.771 micrograms.ml-1. Albumin in these lipoprotein fractions was just as unequally distributed. A lipid infusion resulted in a significant elevation of total triglycerides from 157 to 221 mg.dl-1 and VLDL-triglycerides from 77 to 155 mg.dl-1. The triglyceride content of the LDL plus HDL fraction rose from 102 to 139 mg.dl-1. At the same time the midazolam concentration in unfractionated plasma and in the VLDL and the LDL + HDL fractions decreased to 0.899 microgram.ml-1, 0.130 micrograms.ml-1, and 1.265 micrograms.ml-1, respectively. Cholesterol and albumin concentrations were not affected. The data show for the first time that a significant increase in plasma triglycerides during an intravenous lipid infusion does not result in accumulation of midazolam in lipoproteins, probably because albumin binding of the drug is very strong. The lack of midazolam trapping is important with respect to the safety of concurrent use of lipophilic drugs and intravenous lipid infusions.

Effect of medium- and long-chain triglyceride infusion on lipoprotein and hepatic lipase in healthy subjects

Plasma lipolytic activity and hydrolysis of intravenous fat were studied in six healthy subjects during infusion of a long-chain triglyceride (LCT) fat emulsion (Intralipid 20%) or of a medium-chain triglyceride (MCT)/LCT emulsion (Lipofundin MCT 20%). The fat emulsions were infused continuously at a rate of 0.17 g triglyceride kg-1 body weight (BW)h-1 for 6 h in random order at 7-day intervals. A continuous infusion of glucose (0.18 g kg-1 BW h-1) was administered for a period of 7 h and was started 1 h before the lipid infusion. Infusions of both types of fat increased plasma triglyceride (TG), free fatty acid (FFA) and lipoprotein lipase (LPL) levels and steady-state values were present during the 3rd to 5th h of infusion. MCT/LCT infusion resulted in higher plasma levels at steady-state of TG (3.63 +/- 0.45 [SEM] vs 2.73 +/- 0.45 mmol l-1; P less than 0.05), FFA (1.05 +/- 0.08 vs 0.54 +/- 0.04 mmol l-1; P less than 0.01) and LPL (4.6 +/- 0.6 vs 2.6 +/- 0.5 mU ml-1; P less than 0.05) in comparison with LCT administration. There was a positive correlation between plasma LPL activity and TG concentration (r = 0.77; P less than 0.001) when data for the two infusions were combined. Although the same amount of fat was infused on a weight basis, the molar infusion rate was 40% higher with MCT/LCT than with LCT infusion, due to differences in molecular weights (634 vs 885 Da).(ABSTRACT TRUNCATED AT 250 WORDS)

Short chain fatty acids in the terminal ileum accelerate stomach to caecum transit time in the rat.

We have previously shown that infusion of triglycerides and long chain fatty acids into the ileum of humans and rats delays small bowel transit time. The present studies have investigated the effect on the stomach to caecum transit time of a baked bean meal of the ileal infusion of 20 mM, 50 mM, and 100 mM acetic, butyric, hexenoic, and caprylic acids in rats. After an 18 hour fast either a control or a short chain fatty acid (SCFA) solution (pH 6.5) was infused into the ileum for 30 minutes (0.3 ml/hour). A test meal was given by gavage and the infusion continued for a further 150 minutes. The arrival of the meal in the colon was signalled by a rise in the exhaled hydrogen concentration. Acetic acid (20 mM, 50 mM, 100 mM), butyric acid (100 mM), and caprylic acid (100 mM) produced a significant acceleration of transit which was inversely proportional to SCFA chain length. In a separate experiment, infusion of 100 mM acetic acid, the most potent SCFA, into an isolated ileal Thirty-Vella loop failed to accelerate transit of the test meal. Our results suggest that SCFAs accelerate transit via a local enteric reflex.

Glucose-Induced Exertional Fatigue in Muscle Phosphofructokinase Deficiency

The exercise capacity of patients with muscle phosphofructokinase deficiency is low and fluctuates from day to day. The basis of this variable exercise tolerance is unknown, but our patients with this disorder report that fatigue of active muscles is more rapid after a high-carbohydrate meal. To determine the effect of carbohydrate on exercise performance, we asked four patients with muscle phosphofructokinase deficiency to perform cycle exercise under conditions of differing availability of substrate--i.e., after an overnight fast, and during an infusion of glucose or triglyceride (with 10 U of heparin per kilogram of body weight) after an overnight fast. As compared with fasting and the infusion of triglyceride with heparin, the glucose infusion lowered plasma levels of free fatty acids and ketones, reduced maximal work capacity by 60 to 70 percent, and lowered maximal oxygen consumption by 30 to 40 percent. Glucose also increased the relative intensity of submaximal exercise, as indicated by a higher heart rate at a given workload during exercise. The maximal cardiac output (i.e., oxygen delivery) was not affected by varying substrate availability, but the maximal systemic arteriovenous oxygen difference was significantly lower during glucose infusion (mean +/- SE, 5.5 +/- 0.3 ml per deciliter) than after fasting (7.6 +/- 0.4 ml per deciliter, P less than 0.05) or during the infusion of triglyceride with heparin (8.9 +/- 1.3 ml per deciliter, P less than 0.05). In muscle phosphofructokinase deficiency, the oxidative capacity of muscle and the capacity for aerobic exercise vary according to the availability of blood-borne fuels. We believe that glucose infusion lowers exercise tolerance by inhibiting lipolysis and thus depriving muscle of oxidative substrate (plasma free fatty acids and ketones); this impairs the capacity of working muscle to extract oxygen and lowers maximal oxygen consumption.

Metabolic and Neurologic Effects of an Intravenous Medium‐Chain Triglyceride Emulsion

These studies were undertaken to investigate the relationship between medium-chain fatty acid availability, medium-chain fatty acid oxidation, and central nervous system toxicity during infusion of medium-chain triglycerides in dogs. Six dogs received a sequential, stepwise infusion of trioctanoin at three different rates for 80 min each, providing calories below and equal to resting energy expenditure in the species. Ketone body production rates (using a 14C beta-hydroxybutyrate tracer) and plasma concentrations of lactate and octanoate were monitored. Three animals were infused with saline to serve as controls. Blood-brain barrier integrity was assessed with Evans blue dye, and brain samples were taken at the end of the study to quantify brain water. Three animals were studied under anesthesia to obtain good quality EEG and intracranial pressure measurements. Results were (1) plasma octanoate increased to 0.37 +/- 0.13, 0.78 +/- 0.2, and 1.44 +/- 0.41 mmol/liter during the three infusion intervals; (2) emesis, somnolence, and coma were observed at the two highest trioctanoin rates; (3) ketone body concentrations and production increased from 102 +/- 15 to 859 +/- 54 mumol/liter and 3.6 +/- 0.43 to 18.5 +/- 1.7 mumol/kg/min, respectively, at the highest trioctanoin infusion rate; and (4) plasma lactate also increased from 1.3 +/- 0.1 to 4.3 +/- 0.9 mmol/liter at the highest infusion rate. EEG changes were also observed, consisting of high amplitude slowing and reduction in amplitude of faster components. There was no extravasation of Evans blue dye, nor change in brain water or intracranial pressure. The conclusion--medium-chain triglycerides have significant dose-related central nervous system toxicity in dogs. Therefore, caution should be exercised in clinical studies with MCTs, including careful measurement of medium-chain fatty acid concentrations.

Parenteral Infusion of Long‐ and Medium‐Chain Triglycerides and Reticuloendothelial System Function in Man

Previous study demonstrated that patients who received total parenteral nutrition (TPN) with standard intermittent infusion of long chain triglyceride (LCT) at 0.13 g kg-1hr-1 over 10 hr for each of three days showed a significant decline in 99Tc-sulfur colloid (TSC) clearance rate by the reticuloendothelial system (RES). The present studies evaluated eight patients who received the same total lipid dose of LCT infused continuously as in a three-in-one admixture, and another nine patients receiving the same amount of fat as a medium chain triglyceride (MCT)/LCT (75%/25%) emulsion intermittently over 10 hr at 0.13 g kg-1hr-1 for three consecutive days. Patients were given continuous total parenteral nutrition (TPN) comprised of protein, 1.5 g kg-1day-1, and dextrose, 4.5 g kg-1day-1. RES function was examined by measuring the clearance rates of intravenously injected TSC while receiving TPN containing only protein and dextrose, and again after three days of fat infusion. Mean (+/- SEM) clearance rate constants before and after continuous LCT infusion were 0.38 +/- 0.09 and 0.41 +/- 0.08 min-1, respectively, while those before and after intermittent MCT/LCT infusion were 0.50 +/- 0.18 and 0.73 +/- 0.24 min-1, respectively. In contrast to intermittent LCT infusion, the administration of continuous LCT or an intermittent MCT/LCT mixture does not impair TSC clearance by the RES. These findings suggest that condensing the daily period of LCT infusion at standard dosage may exceed the rate of metabolic utilization, resulting in increased fat removal and diminished TSC uptake by the RES.(ABSTRACT TRUNCATED AT 250 WORDS)

Luminal CCK-releasing factors in the isolated vascularly perfused rat duodenojejunum

The factors operating at the apical side of the endocrine cell releasing cholecystokinin (CCK) were investigated using the isolated vascularly perfused rat duodenojejunum. In the protease-free intestinal segment, a 30-min infusion of glucose (280 mM), oleic acid (100 mM), or triglycerides containing short- or long-chain fatty acids did not alter significantly the basal level of portal CCK-like immunoreactivity (CCK-LI), while octanoic acid (100 mM) produced a transient rise of plasma CCK-LI to approximately 250% of basal. Infusion of proteins (5% solutions of ovalbumin or casein) or of a mixture of all amino acids brought about a modest CCK secretion. In contrast, isocaloric amounts of an ovalbumin hydrolysate produced a sharp rise of portal CCK-LI to 530% of basal followed by a well-sustained plateau secretion (420% of basal) until the end of the infusion. An acid casein hydrolysate induced a slightly less pronounced CCK-LI release and was followed in decreasing order by meat, casein, and soybean peptones. Simultaneous infusion of trypsin with ovalbumin or casein hydrolysate reduced by approximately 60% the CCK release induced by peptone alone. This effect was reversed by coinfusion of soybean trypsin inhibitor (SBTI) with the trypsin-peptone mixture. Arterial infusion of tetrodotoxin (10(-6) M) or atropine (10(-5) M) had no significant effect on the trypsin-induced inhibition of peptone-mediated CCK-LI release. Administration of SBTI or camostate alone or in combination with trypsin did not alter basal CCK. Monitor peptide produced a dose-dependent transient rise of portal CCK-LI over the range from 2 to 12 micrograms.(ABSTRACT TRUNCATED AT 250 WORDS)

Kinetics of fatty acid (FA) metabolism during infusion of long-chain triglyceride (LCT) emulsions

Kinetics of fatty acid (FA) metabolism during infusion of long-chain triglyceride (LCT) emulsions

Regulation of ketone body flux in septic patients.

To assess the effect of sepsis on ketone body (KB) kinetics in humans, we measured in normal and septic subjects KB appearance rate (Ra) before (initial state) and during a rise of free fatty acids (FFA) level (intravenous infusion of a triglycerides emulsion). We studied normal subjects in postabsorptive state and septic patients when receiving an hypocaloric intravenous infusion of glucose and amino acids or 12 h after its interruption. When receiving glucose and amino acids infusion, septic patients had higher glucose and insulin levels than normal subjects, and despite lower FFA concentrations (255 +/- 44 vs. 480 +/- 51 mumol/l, P less than 0.05) comparable initial KB Ra (2.50 +/- 0.10 vs. 2.48 +/- 0.30 mumol.kg-1.min-1). Triglyceride infusion increased FFA to comparable values (septic 780 +/- 130, normal 730 +/- 45 mumol/l), but KB Ra rose in septic patients only to 3.7 +/- 1.1 instead of 7.7 +/- 1.1 mumol.kg-1.min-1 as in normal subjects (P less than 0.05). Somatostatin infusion decreased the hyperinsulinemia of septic patients but did not restore a normal ketogenesis. After interruption of nutriment infusion, septic patients had normal FFA levels and only mild hyperglycemia and hyperinsulinemia. Their initial KB Ra was not modified. However, their response of KB Ra (increase to 6.27 +/- 2.0 mumol.kg-1.min-1) to raised FFA levels (842 +/- 170 mumol/l) was comparable to the response of normal subjects. In conclusion, although septic patients receiving an hypocaloric parenteral nutrition had a depressed ketogenesis they were able to restore a normal ketogenic capacity after a short-time caloric deprivation. Glucose and/or insulin appears to have a major role in this modulation of hepatic ketogenesis.

Impairment of glucose disposal by infusion of triglycerides in humans: role of glycemia

The present study was designed to assess the role of hyperglycemia (150 mg/dl) vs. euglycemia (90 mg/dl) on glucose metabolism in vivo during the infusion of a triglyceride emulsion (Intralipid). Seven young healthy volunteers were studied on four occasions using the hyperinsulinemic clamp technique, twice during euglycemia and twice during hyperglycemia, without or with Intralipid. Glucose oxidation (O) was calculated from continuous respiratory exchange measurements, and glucose storage (S) was obtained as the difference between total glucose disposal (M) and O. Two-way analysis of variance with interaction term demonstrated 1) a significant increase for M with hyperglycemia and a decrease with Intralipid; no interaction, and 2) in euglycemia, O/M and S/M occurred in one-to-one ratios; on the other hand, during 150-mg/dl hyperglycemia, the ratio dropped roughly to 1:2. Intralipid had no effect on the ratio, and no interaction could be observed. These results suggest the existence of physiological regulatory mechanisms by which 1) the rise in plasma free fatty acid inhibits both oxidative and nonoxidative glucose disposal, and 2) the rise in glycemia stimulates predominantly nonoxidative glucose disposal.

Infusion of medium-chain triglycerides (MCT) modifies the plasma distribution of free and acylated carnitine : [formula omitted], Y.A. Carpentier, M. Richelle, W. Dahlan, N.P. D'Attellis, P. Fürst. Clinical Nutrition Unit, Univ. Hospital St. Pierre, Brussels, Belgium (a), Institute for Biological Chemistry and Nutrition, Univ. Hohenheim, Stuttgart, FRG

Infusion of medium-chain triglycerides (MCT) modifies the plasma distribution of free and acylated carnitine : [formula omitted], Y.A. Carpentier, M. Richelle, W. Dahlan, N.P. D'Attellis, P. Fürst. Clinical Nutrition Unit, Univ. Hospital St. Pierre, Brussels, Belgium (a), Institute for Biological Chemistry and Nutrition, Univ. Hohenheim, Stuttgart, FRG

Effect of exogenous triglyceride infusion on the plasma amino-acid profile in liver cirrhosis

The influence of exogenous triglyceride infusion on plasma amino-acid levels has been evaluated in 10 patients with compensated liver cirrhosis and 7 normolopidaemic volunteers. Increasing amounts of 10% Intralipid ® were infused for 3 h and plasma amino-acid, triglyceride, free fatty acid levels measured before, during and 2 hours after triglyceride infusion. A slight decrease in the levels of almost all amino-acids was observed during Intralipid ® administration. Alanine levels significantly decreased in both groups upon maximal lipid loading. A significant increase in free tryptophan concentrations was observed after 3 hours of infusion only in cirrhotic patients. Lysine values significantly decreased in both groups 2 hours after infusion withdrawal. Total triglycerides significantly increased during the infusion. Free fatty acid level raised markedly, although not significantly in both groups. It is concluded that the decrease in all amino-acid levels is likely secondary to a protein sparing effect exerted by fat-derived calories; the decrease in alanine concentration is due to decreased peripheral synthesis of this amino-acid; the increase in free tryptophan levels is secondary to the elevation of free fatty acids; the decrease in lysine values should be ascribed to the de-novo synthesis of carnitine which is consumed for exogenous fat utilisation; considering the possible role of free tryptophan in the pathogenesis of hepatic encephalopathy, the use of large amounts of i.v. fat should be discouraged in cirrhotics at high risk of neurological derangements.

Lactation Response to Short-Term Abomasal Infusion of Choline, Inositol, and Soy Lecithin

Five lactating Holstein cows averaging 13 wk postpartum were used in a Latin square design to examine the effect of daily abomasal infusion of choline (22g), myo-inositol (37g), soy oil (325ml), or crude soy lecithin (900ml) on lactation performance. Dry matter intake was reduced by infusion of soy lecithin as compared with infusion of water (18.1 and 21.1 kg/d, respectively). Plasma β-hydroxybutyrate concentration was increased when cows received the myo-inositol or soy lecithin infusion, and plasma glucose was lower when cows received the choline or soy lecithin treatment. Infusion of soy lecithin caused approximately a twofold increase in plasma triglyceriderich lipoprotein concentration. Milk fat percentage and milk fat yield were greater during soy lecithin infusion (3.54%, 1.11 kg/d) than during water (3.09%, .98 kg/d) or soy oil (3.06%, .98 kg/d) infusion. This resulted in greater 3.5% FCM yield during soy lecithin infusion (31.6 kg/d) than during water (29.5 kg/d) or soy oil (29.6 kg/d) infusion. Infusion of phospholipid with triglyceride allowed more fatty acid to be infused without causing diarrhea. Infusion of triglyceride in the presence of phospholipid increased milk fat synthesis whereas infusion of triglyceride alone did not.

Plasma levels of free tryptophan in compensated and decompensated liver cirrhosis during exogenous triglyceride infusion : [formula omitted], A.Cascino, C.Cangiano, F.Ceci, M. Familiari and F.Rossi Fanelli. Lab. Clin. Nutr., II Dept. Internal Medicine, University ‘La Sapienza’, Rome, Italy

Plasma levels of free tryptophan in compensated and decompensated liver cirrhosis during exogenous triglyceride infusion : [formula omitted], A.Cascino, C.Cangiano, F.Ceci, M. Familiari and F.Rossi Fanelli. Lab. Clin. Nutr., II Dept. Internal Medicine, University ‘La Sapienza’, Rome, Italy

Satiety effects of intragastric meals containing triglycerides with different chain lengths.

Intragastric meals containing triglycerides with chain length of 2-18 significantly reduced intake in deprived Sprague-Dawley rats feeding 20 min after infusion. Satiety after long-chain triglyceride (LCT) infusions must have been mediated via a gastroenteric signal, since feeding was reduced prior to delivery of these fats into the bloodstream. Equicaloric infusions of triglycerides with chain length of 6 to 18 had similar inhibitory effects, indicating that the satiety effects of these triglycerides depended more on the number of calories infused than on chain length. Shorter-chain triglycerides were initially more effective in reducing feeding. Except for a poorly absorbed LCT the infusions did not result in conditioned taste aversion and thus did not appear to induce discomfort. Gastric recovery of a nonabsorbable marker at the time of the feeding test indicated that gastric emptying, like satiety, was related to the caloric properties of the infusions. These effects could be mediated through neural and/or hormonal mechanisms that are stimulated through energy-related properties of triglycerides.