Long-chain Fat Research Articles

Treatment of carnitine deficiency.

Carnitine deficiency is a secondary complication of many inborn errors of metabolism. Pharmacological treatment with carnitine not only corrects the deficiency, it facilitates removal of accumulating toxic acyl intermediates and the generation of mitochondrial free coenzyme A (CoA). The United States Food and Drug Administration (US FDA) approved the use of carnitine for the treatment of inborn errors of metabolism in 1992. This approval was based on retrospective chart analysis of 90 patients, with 18 in the untreated cohort and 72 in the treated cohort. Efficacy was evaluated on the basis of clinical and biochemical findings. Compelling data included increased excretion of disease-specific acylcarnitine derivatives in a dose-response relationship, decreased levels of metabolites in the blood, and improved clinical status with decreased hospitalization frequency, improved growth and significantly lower mortality rates as compared to historical controls. Complications of carnitine treatment were few, with gastrointestinal disturbances and odour being the most frequent. No laboratory or clinical safety issues were identified. Intravenous carnitine preparations were also approved for treatment of secondary carnitine deficiency. Since only 25% of enteral carnitine is absorbed and gastrointestinal tolerance of high doses is poor, parenteral carnitine treatment is an appealing alternative therapeutic approach. In 7 patients treated long term with high-dose weekly to daily venous boluses of parenteral carnitine through a subcutaneous venous port, benefits included decreased frequency of decompensations, improved growth, improved muscle strength and decreased reliance on medical foods with liberalization of protein intake. Port infections were the most troubling complication. Theoretical concerns continue to be voiced that carnitine might result in fatal arrhythmias in patients with long-chain fat metabolism defects. No published clinical studies substantiate these concerns. Carnitine treatment of inborn errors of metabolism is a safe and integral part of the treatment regime for these disorders.

More Evidence that Fish is Brain Food

Barberger-Gateau and colleagues investigated whether consumption of fish (rich in long-chain polyunsaturated fats [PUFAs]) or consumption of meat (rich

Introduction of a ketogenic diet in young infants.

The ketogenic diet is a rational treatment for pyruvate dehydrogenase complex deficiency (McKusick 312170) and GLUT1 deficiency syndrome (McKusick 138140). An increasing number of patients are diagnosed in early infancy, but few data are available on the introduction of a ketogenic diet in this age group. GLUT1 deficiency syndrome was suspected in four infants presenting with seizures and unexplained hypoglycorrhachia. A ketogenic diet was introduced at 6-28 weeks of age. Ketosis was initiated by fasting, monitored by bedside blood glucose and 3-hydroxybutyrate determinations, and was maintained successfully using supplemented carbohydrate-free infant formula and emulgated triglycerides. All patients developed ketosis within 24 h. 3-Hydroxybutyrate concentrations available at the bedside correlated inversely with the base excess. At glucose levels < or = 40 mg/dl patients remained asymptomatic in the presence of ketones. The ketogenic formula was tolerated well, parental compliance was good, and all patients remained seizure-free on the diet. GLUT1 deficiency was confirmed in two patients; the diet was discontinued in the other two patients. In one infant, failure to thrive on medium-chain triglycerides was effectively reversed using long-chain triglycerides. Urine dipstick analyses failed to detect ketosis in another infant. Adverse effects of the diet were limited to renal stones in one patient. The ketogenic diet can be introduced and maintained successfully in young infants using long-chain fat emulsion. Monitoring 3-hydroxybutyrate at the bedside was useful for metabolic control and superior to urine dipstick analysis. Seizure control was effective and adverse effects were limited, but evaluation of the long-term effects of the ketogenic diet in this age group must await ongoing studies.

Treatment of cardiomyopathy and rhabdomyolysis in long-chain fat oxidation disorders using an anaplerotic odd-chain triglyceride

The current dietary treatment of long-chain fatty acid oxidation defects (high carbohydrate with medium-even-chain triglycerides and reduced amounts of long-chain fats) fails, in many cases, to prevent cardiomyopathy, rhabdomyolysis, and muscle weakness. We hypothesized that the apparent defect in energy production results from a depletion of the catalytic intermediates of the citric acid cycle via leakage through cell membranes (cataplerosis). We further hypothesized that replacing dietary medium-even-chain fatty acids (precursors of acetyl-CoA) by medium-odd-chain fatty acids (precursors of acetyl-CoA and anaplerotic propionyl-CoA) would restore energy production and improve cardiac and skeletal muscle function. We fed subjects with long-chain defects a controlled diet in which the fat component was switched from medium-even-chain triglycerides to triheptanoin. In three patients with very-long-chain acyl-CoA dehydrogenase deficiency, this treatment led rapidly to clinical improvement that included the permanent disappearance of chronic cardiomyopathy, rhabdomyolysis, and muscle weakness (for more than 2 years in one child), and of rhabdomyolysis and weakness in the others. There was no evidence of propionyl overload in these patients. The treatment has been well tolerated for up to 26 months and opens new avenues for the management of patients with mitochondrial fat oxidation disorders.

Treatment of cardiomyopathy and rhabdomyolysis in long-chain fat oxidation disorders using an anaplerotic odd-chain triglyceride

Treatment of cardiomyopathy and rhabdomyolysis in long-chain fat oxidation disorders using an anaplerotic odd-chain triglyceride

The absorption of stearic acid from triacylglycerols: an inquiry and analysis

Although stearic acid is a saturated fatty acid, its influence on plasma cholesterol acid other health variables is neutral; possibly owing in part to poor absorption. Reduced absorption of stearic acid from particular triacylglycerols, cocoa butter and novel fats formulated with short- and long-chain acid triacylglycerol molecules (Salatrims) has been attributed to high intakes. However, the circumstances and causes of poor stearic acid digestion from triacylglycerols are unclear; published data were therefore collected and analysed, with emphasis on human studies. Of twenty-eight studies conducted in adults, most are in men (>90%). The assertion that reduced absorption is due to a high intake of stearoyl groups is not supported: dietary intakes of stearoyl of 0.05-0.65 g stearic acid equivalent/kg body weight (cf typical intake of 0.2 g stearic acid equivalent/kg body weight in the Western diet) indicate that the 'true' digestibility of stearoyl is 0.98 (SE 0.01) g/g, with apparent digestibility less than this value at low intakes owing to endogenous stearic acid excretion and to inter-publication variation of unidentified cause. The neutral health impact of stearic acid must be due to factors other than availability. Exceptions include cocoa butter, Salatrims and tristearin, for which digestibility is an additional factor. The efficiency with which human subjects digest stearoyl from cocoa butter still remains uncertain, while the digestion of total long-chain fat from this source is 0.89-0.95 g/g, high in comparison with 0.33 g/g for Salatrim 23CA and 0.15 g/g for tristearin in their prepared states. Salatrims contain the highest proportion of long-chain fatty acids that are stearic acid-rich other than tristearin, which is the main component of fully-hydrogenated soyabean and rapeseed oil. Analysis shows that apparent digestibility of stearic acid is associated with stearoyl density within the triacylglycerol molecule and that, in Salatrims, the occurrence of short-chain fatty acids in place of long-chain fatty acids increases this density. Soap formation appears not to be a major factor in the reduced digestion of stearic acid from tristearin under regular dietary circumstances, but both microcrystallinity and reduced digestibility of tri-, di- and monostearoylglycerols appears to be important. Solubilisation of high-melting-point tristearin in low-melting-point oils improves the digestibility of its stearic acid, particularly when emulsified or liquidized at above melting point. However, without such artificial aids, the digestive tracts of the rat, dog and man have a low capacity for emulsifying and digesting stearic acid from tristearin. Reduced digestibility of stearic acid from Salatrim 23CA also appears to be attributable to reduced digestibility of di- and monostearoylglycerols and is particularly due to remnants with the 1- or 3-stearoylglycerol intact after initial hydrolytic cleavage. Short-chain organic acid in Salatrim 23CA, which is readily hydrolysed, leaves such remnants. Unlike tristearin, Salatrim 23CA melts at body temperature and mixing it with low-melting-point oils is not expected to cause further disruption of microcrystalline structures to aid digestibility of its stearoyl groups. The low digestibility of stearoyl in Salatrim 23CA, together with the occurrence of short-chain organic acids in this product, account for its relatively low nutritional energy value (about 20 kJ (5 kcal)/g) compared with traditional fats (37 kJ (9 kcal)/g) and low fat value (<20:37 kJ/kJ; <5:9 kcal/kcal) relative to traditional fats. In part these differences are because of minor effects of Salatrim 23CA on the excretion of other fat and protein, due to the bulking properties of this poorly-digestible fat.

Colonic digestion and absorption of energy from carbohydrates and medium-chain fat in small bowel failure.

Gut function and the degree of intestinal insufficiency or failure in short bowel patients can be quantified with respect to wet weight and energy absorption by the use of balance studies. This enables the physician to distinguish patients with extreme intestinal failure inconsistent with the restoration of intestinal autonomy by dietary manipulation from short bowel patients with borderline gut failure in whom dietary manipulations may result in the weaning from parenteral support. A high-carbohydrate, low long-chain fat diet and a diet where long-chain fat has been replaced by medium-chain triglycerides increase absorption of energy in patients with small bowel failure, provided that they have a preserved colon in continuity. This is due to the ability of the colonic flora to ferment carbohydrates malabsorbed in the small bowel to the short-chain fatty acids (SCFAs). These SCFAs are easily absorbed across the colonic mucosa resulting in a salvage of carbohydrate energy that otherwise would have been lost in feces. In contrast, long-chain fatty acids are not absorbed by the colon, and long-chain fat malabsorbed in the small bowel of short bowel patients are not retained in the large bowel. Recent work has indicated that the water soluble medium-chain fatty acids are effectively absorbed in the large bowel similar to the SCFAs. This may explain an almost complete absorption of medium-chain triglycerides in short bowel patients, even in patients with virtually no absorption of long-chain fat, and why this only occurs in patients with a colon in continuity. Manipulation of the dietary fat:carbohydrate ratio is much less efficacious in short bowel patients with no colonic function, and the use of medium-chain triglycerides has no proven effect on overall energy absorption from short bowel patients without a large bowel in continuity. Hence, the colon has increasingly important digestive functions as small bowel failure proceeds, not only when it comes to absorption of water and sodium, but also of energy from carbohydrates and medium-chain fat.

Feeding the child with chronic liver disease.

Protein energy malnutrition leading to growth failure is an inevitable consequence of chronic liver disease in 60% of children. Malnutrition should be anticipated by serial anthropometric assessment and prevented by early intervention with nutritional support. Both morbidity and mortality postliver transplantation have been related to the degree of pretransplant malnutrition, and thus nutritional status is an important risk factor for survival postliver transplantation. As survival following pediatric liver transplantation improves, with most centers reporting 1 y survival rates of 90-95% and 5 y survival rates of 80-85%, attention has focused on achieving nutritional rehabilitation, normal psychosocial development, and normal quality of life. An understanding of the etiology of protein malnutrition in liver disease is essential when planning therapeutic strategies. Considerable research progress has been made exploring the pathophysiology of malnutrition, including long-chain fat malabsorption with essential fatty acid deficiency, abnormal energy metabolism, substrate utilization, and nitrogen metabolism in liver disease. Effective strategies are emerging and future advances include docosahexaenioc acid, branched chain amino acids, and structured lipids. The key to success is a multidisciplinary approach to nutritional intervention, including pediatric dietitian, liaison nurse, feeding psychologist, and clinician.

A medium chain triglyceride-based diet in patients with HIV and chronic diarrhea reduces diarrhea and malabsorption: A prospective, controlled trial

Our objective was to determine whether a medium-chained triglyceride (MCT)-based diet, compared to a long-chain triglyceride (LCT)-based diet, conveys a beneficial effect on diarrhea and fat malabsorption in human immunodeficiency virus (HIV)-infected individuals with chronic diarrhea and weight loss. A secondary objective was to evaluate the pathogens associated with the diarrhea and to evaluate whether the etiologic agent was a determinant of response to the nutritional intervention. Prospective, randomized double-blind comparative trial was conducted in 24 adult patients with HIV, diarrhea of greater than 4-wk duration, fat malabsorption, and loss of 10–20% of ideal body weight, these patients were recruited from our outpatient infectious disease clinic. Evaluations of diarrheal pathogens were made by complete stool examination, upper and lower endoscopy with quantitative culture, and biopsy. Body composition determinations, and measurements of fat, carbohydrate, and vitamin absorption pre- and postinervention. Patients were randomly assigned to one of two complete nutritional products with either medium- or long-chain triglyceride fat exclusively for 12 d followed by treatment of infectious pathogens. Ten patients were found to have Microsporidium and 9 patients had no identifiable pathogen. All patients responded to intervention with both nutritional products overall with 45% fewer stools, decreased stool fat and weight, and a significant increase in urine nitrogen. The group that received the MCT product demonstrated significantly decreased stool number (mean 4 to 2.5), stool fat (mean 14 to 5.4 g), and stool weight (mean 428 to 262 g) compared with baseline ( P < 0.01 for all). Patients with both species of microsporidia and with pathogen negative diarrhea had good response. We found that HIV patients with diarrhea, regardless of etiology, and documented fat malabsorption may benefit symptomatically from a diet composed of an MCT-based liquid supplement.

Filamentous growth in activated sludge.

Bulking and foaming in activated sludge have been associated with filamentous overgrowth. Filamentous Nocardia amarae and nonfilamentous Pseudomonas auruginosa were cultured using fatty acids (C2-C24) as the sole carbon. N. amarae could utilize all acids tested for growth, whereas P. auruginosa hardly grew on acids with 12 or more carbons. Maximum specific growth rate and saturation constant of N. amarae on C24, at 0.048 h-1 and 1.520 g COD/L, respectively, were much lower than that of P. auruginosa, showing that N. amarae had a relatively stronger affinity for long-chain fatty acids. N. amarae was competitive in activated sludge processes that receive sewage containing a high proportion of long-chain fatty acids, oils, and fats.

New developments in the diagnosis and investigation of mitochondrial fatty acid oxidation disorders.

Since the discovery of muscle carnitine palmitoyltransferase deficiency in 1973, a dozen separate defects of mitochondrial fatty acid beta-oxidation in man have been identified. With the exception of medium-chain acyl-CoA dehydrogenase (MCAD) deficiency, which occurs with a frequency approaching 1:10,000 among Caucasians of Northern European origin, the other defects are quite rare. Collectively, however, they are common causes of disease resembling Reye syndrome in early life, and some have a later and more chronic presentation with cardiomyopathy and skeletal muscle weakness. They also represent a small, but significant, proportion of cases of sudden and unexplained death within the first 2 years of life. Diagnosis of these disorders has become increasingly sophisticated, with the advent of new analytical technologies and an increased awareness of the appropriate clinical and laboratory investigations needed in order to evaluate potential defects of this pathway. The combination of provocative testing (e.g., carnitine loading, phenylpropionic acid loading, long-chain fat loading) and advanced analytical techniques for the measurement of blood and urinary metabolites (e.g., tandem fast atom bombardment-mass spectrometry, stable isotope dilution gas chromatography-mass spectrometry) permits a specific diagnosis in the case of several, although not all, of the disorders of this pathway. Methods for the measurement of all of the enzymes of beta-oxidation are now available to enhance this diagnostic capability. There remain, however, many patients in whom clinical and laboratory signs point to a defect in beta-oxidation, but in whom no specific diagnosis has yet been made.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of dietary menhaden oil on mucosal adaptation after small bowel resection in rats

Adaptive hyperplasia of the small intestine is important in the outcome of short bowel syndrome. Previous studies have shown that long-chain fats stimulate this process. In the present study, the trophic effects of dietary menhaden oil, a highly unsaturated fat source, on mucosal adaptation following small bowel resection in rats was evaluated. Thirty weanling Sprague-Dawley rats and their controls were fed diets containing fats provided primarily as menhaden oil, safflower oil, or beef tallow. After 4 weeks, animals underwent a 70% jejunoileal resection. Mucosal mass, DNA, protein, and sucrase levels were assessed 14 days after a 70% jejunoileal resection or control feeding. Serum fatty acid composition and several gastrointestinal hormone levels were measured. Resected animals fed menhaden oil showed a marked increase in mucosal weight, DNA, and protein levels compared with rats fed the other fat sources. Enteroglucagon level was increased in all resected groups, but least increased in the menhaden-fed animals. In contrast, peptide YY concentrations were most increased in animals fed menhaden oil. Menhaden oil appears more effective in inducing intestinal adaptation than less highly unsaturated fats. Analysis of gastrointestinal hormones revealed no clear-cut explanation for this finding, other than a modest but associated increase in peptide YY levels.

Successful treatment of long-chain 3-hydroxyacyl-coenzyme a dehydrogenase deficiency with an elemental formula preparation

Tolerex™ supplemented with medium-chain triglyceride (MCT) was used to treat an infant with a rare inborn error of long-chain fatty acid metabolism. A 3 month old infant was admitted to the Medical University of South Carolina with dehydration, diarrhea, vomiting, lethargy, failure to thrive, and hepatitis of unknown etiology. During the course of her hospitalization she received Pregestimil concentrated to 24 Calories (Cals) per ounce. Pregestimil has 36 grams of fat per liter with 60% as MCT and 40% as long-chain triglyceride (LCT). She failed to gain weight after five weeks, so LCT was added to increase caloric density to 28 Cals per ounce. Due to increased stooling on this formulation, the LCT supplementation was discontinued. During her hospitalization, she was subjected to a fasting study. This was terminated at 19 hours when her blood sugar fell to 36 mg/dl. Serum free fatty acid levels rose but β-hydroxybutyrate failed to rise above 10% of expected. In addition, a serum acyl carnitine profile showed dramatic elevations of long-chain species including 3-hydroxy compounds. A diagnosis of long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency was made based on these findings. Since this condition is characterized by an inability to break down long-chain fatty acids, it was deemed appropriate to use a formula that is low in LCT. Tolerex, a low fat formula, was supplemented with MCT oil as the primary fat source and enough safflower oil to meet essential fatty acid needs. By contrast, this formulation contains 40 Cals per ounce and provides 150 Cals/kg and 2.3 grams protein/kg. The RDA for all nutrients was satisfied by the addition of appropriate vitamins and minerals. Frequent feedings were provided to allow a constant supply of energy and prevent the mobilization of stored long-chain fats. Over a two month period on this formula, the patient experienced dramatic catch-up growth. Weight increased from below the first percentile(%) to the 10%, head circumference increased from the 10% to the 25%, and weight for height ratio increased from <5% to the 25% on the National Center for Health Statistic Growth Charts. Average weight gain increased from 7.6 grams to 28.5 grams per day when the Tolerex formulation was used. Liver function tests also normalized. This patient's successful recovery with the use of a diet very low in long-chain fatty acids validates the diagnosis and confirms the mode of dietary treatment.

Effects of dietary behenate and a caprenin-like fat on lipids in the hamster

To study the effects of dietary behenic acid on cholesterol metabolism, we fed hamsters four synthetic, randomly arranged triglycerides that were formulated to allow the comparison of the effects of a single dietary fatty acid. The dietary triglycerides (including that from chow) fed to the linoleate group contained approximately 55% linoleic acid. The palmitate, oleate, and behenate groups received fats similar in composition to the linoleate fat, but approximately half of the linoleic acid of the triglyceride was replaced with either palmitic, oleic, or behenic acid. In addition to this long-chain behenate fat (BLCT), behenic acid was also fed as a triglyceride made from medium-chain fatty acids and behenic acid (BMCT). This BMCT fat was similar in composition to caprenin, a reduced-calorie alternative to cocoa butter. A group that received medium-chain triglycerides (MCT) was included for comparison with the BMCT group. The synthetic fats were all fed at a level of 15% by weight, along with 84.8% chow and 0.2% cholesterol. After 4 weeks the animals were sacrificed and LDL cholesterol levels were measured. Measurements are mmol/L, common superscripts indicate no difference, P < 0.05. Chow, 0.78 ± 0.05∗; Linoleate, 4.73 ± 0.23†, Palmitate, 5.07 ± 0.31†; Oleate, 2.79 ± 0.10‡,§; BLCT, 2.53 ± 0.13‡; BMCT, 3.26 ± 0.28 ± §; MCT, 4.16 ± 0.34¶. Behenic acid in feces was measured after methylation and extraction with ether. Behenic acid absorption ranged from 19–29%. The presence of unhydrolyzed triglyceride in the feces of the BLCT group suggested that BLCT might alter the absorption of dietary cholesterol. In a second study, fecal cholesterol and its metabolites were measured after feeding BLCT. The fecal choleterol was nearly three times that from a safflower oil-fed control group.

The Regulation of Mitochondrial Fatty Acid Oxidation and Hepatic Gene Expression by Catecholamine

We hypothesized that dopamine or dobutamine may alter hepatic mitochondrial fatty acid oxidation secondary to an effect on hepatic gene expression. We investigated the effect of dopamine or dobutamine on hepatic fat oxidation and gene transcription by studying the enzyme carnitine palmitoyltransferase (CPT), the rate-limiting step in hepatic mitochondrial long-chain fat oxidation. We incubated either H4IIE rat hepatoma cells or rat hepatocytes in primary cell culture with either dopamine (1,0.1, 0.01 μg/ml), dobutamine (1,0.1, 0.01 μg/ml), or vehicle control for 1, 2, 3, or 4 hr. We investigated the effect on (1) CPT mRNA (Northern or dot blotting) and the possible regulatory mechanism by incubating dopamine (0.1 μg/ml) or dobutamine (0.1 μg/ml) with propranolol or phentolamine, (2) CPT translation (CPT [ 35S]methionine incorporation), and (3) hepatic mitochondrial fatty acid oxidation ([1- 14C]palmitate oxidation to acid-soluble products). We conclude that (1) dopamine or dobutamine increases both hepatic CPT mRNA and CPT protein translation, (2) the effect on CPT mRNA is mediated by the β-receptor, (3) the increase in hepatic mitochondrial fat oxidation induced by dopamine or dobutamine may be, in part, secondary to increased CPT transcription and translation, and (4) the significant difference in hepatic fat oxidation induced by dopamine as compared with that by dobutamine is secondary to factors other than transcriptional or translational mechanisms. We speculate that dopamine treatment in the critically ill may increase hepatic mitochondrial fatty acid oxidation and ketogenesis and that this increase in β-oxidation may be, in part, secondary to increased CPT gene expression.

Factors affecting food efficiency and body composition of growing ruminants offered straw-based diets: supplementation with lipids with and without protein meal

ABSTRACTGrowing heifers (experiment 1) and wether lambs (experiments 2 and 3) were offered ammoniated cereal straw with or without a protein meal. The effects of supplementation with long-chain fatty acids (LCFA; as calcium salts of LCFA (CaLCFA) or fat prills) on nutrient utilization were studied.Intake of the basal diet (g/kg live weight) was unaffected by the protein meal, but was often reduced by supplementation with LCFA, especially fat prills. Live-weight gain was increased both by supplementation with protein meal and CaLCFA. Fat prills only increased live-weight gain in the presence of protein meal and depressed live-weight gain in the absence of protein meal. There were small differences between the two sources of LCFA in their apparent effects on rumen fermentation.Supplementation with protein meal increased relative protein content (P &lt; 0·05) and tended to increase water content (P &gt; 0·05) in the wethers in experiment 3 (corrected to equal empty-body weight at slaughter). Of the LCFA, only CaLCFA tended to increase relative body fat content (by proportionately 0·23; (P &gt; 0·05) but decreased relative protein and water content by 0·05 and 0·06 (P &lt; 0·05).Supplementation of straw-based diets with as little as 20 g CaLCFA per kg food dry matter improved live-weight gain and efficiency of nutrient utilization of ruminants, particularly when offered in combination with a protein meal. There appeared to be marked differences in the effects of CaLCFA and fat prills on food intake, productivity and to some extent body composition.

Long-Chain versus Medium and Long-Chain Triglyceride-based Fat Emulsion in Parenteral Nutrition of Severe Head Trauma Patients

In order to assess the metabolic value of medium-chain triglycerides (MCT) in severely stressed intensive care unit patients, two fat emulsions containing either long-chain triglycerides (LCT), or a mixture of 50% MCT and 50% LCT were compared in 24 head trauma patients over a 10 day period. Variations of serum triglyceride, non-esterified fatty acid, glycerol and phospholipid concentrations remained comparable after both lipid infusions. Bilirubin, alkaline phosphatase and transaminase plasma levels were altered in both groups without any significant differences or clinical consequences. Cumulative nitrogen balance remained negative (-10 g N. day-1 i.e. -100 g N. 10 days-1) and comparable in both groups. However, thyroxin-binding prealbumin concentrations increased significantly in patients receiving the MCT/LCT mixture. It is concluded that MCT might have a beneficial effect on visceral protein metabolism after trauma.

Gastric Lipolysis and Fat Absorption in Preterm Infants: Effect of Medium-Chain Triglyceride or Long-Chain Triglyceride-Containing Formulas

The extent of gastric lipolysis, fat absorption, and infant weight gain was studied in 12 preterm infants (gestational age 28.75 +/- 0.50 weeks, postnatal age 6.08 +/- 0.81 weeks) fed medium-chain triglyceride or long-chain triglyceride formula for 1 week in a crossover design. The former formula contained 42% of 8:0 and 10:0 and 19% of 12:0, 14:0, and 16:0; the latter formula contained only 7% of 8:0 and 10:0 and 46% of 12:0, 14:0, and 16:0. Gastric aspirates were obtained on the second and third day of formula feeding for quantitation of lipase activity and of the extent of gastric lipolysis. Fat balance studies were conducted during the last three days of each feeding regimen. The study showed that (1) there was marked hydrolysis of formula fat in the stomach during feeding of either medium-chain triglyceride formula or long-chain triglyceride formula (20% and 16%, respectively); (2) lipase activity in the gastric aspirates was less during feeding of medium-chain triglyceride formula than before the meal, which suggested stimulation of lipase secretion by long-chain fatty acid released from long-chain triglyceride formula fat or more rapid binding of lipase to ingested lipid in the medium-chain triglyceride formula; (3) fatty acid distribution in glycerides and free fatty acids showed preferential release of medium-chain (8:0, 10:0) and long-chain unsaturated (18:1, 18:2) fatty acids in the stomach. The low content of 8:0 and 10:0 in gastric triglyceride and free fatty acids suggested that medium-chain fatty acids were absorbed directly in the stomach.(ABSTRACT TRUNCATED AT 250 WORDS)

Macronutrient selection in an animal model of cholestatic liver disease

Diet selection was investigated in an animal model of cholestatic liver disease produced by bile duct ligation. Animals self-selected diets from separate sources of macronutrients (protein, fat, carbohydrate). Diet selection was evaluated when the fat source was comprised of either a primarily medium-chain fat (coconut oil) or a primarily long-chain fat (Crisco vegetable shortening). Relative to intakes of control animals, bile duct ligated (BDL) animals consuming the long-chain fat decreased fat intake, decreased protein intake, and increased carbohydrate intake. Consumption of the fat source was decreased in BDL rats fed the medium-chain fat relative to intakes of control animals, however carbohydrate and protein intakes were not affected. Total caloric intake was comparable to control intakes by day 16 post-ligation in BDL rats fed the long-chain fat and by day 11 in BDL rats fed the medium-chain fat. Body weight gain was significantly greater in BDL rats fed the medium-chain fat than in those fed the long-chain fat. Mortality was 44% in BDL animals fed the long-chain fat, and 0% in those fed the medium-chain fat. The results suggest that BDL animals make dietary selections which may decrease the severity of liver disease. Differences between ligated animals consuming either medium- or long-chain fats suggest that some fat sources may be more beneficial during cholestasis.

Environmental factors in coronary heart disease: diet.

The customary diet of a population is the essential factor determining susceptibility to atherosclerosis and coronary heart disease (CHD), and it does so through its effects on lipoproteins, blood pressure and the coagulation system. The simplest and possibly strongest measure of this dietary effect is the serum total cholesterol concentration in the population. Within populations on high-risk diets [high saturated fat intakes and low ratio of polyunsaturated to saturated fatty acids (P/S ratio)], hypertension and cigarette smoking are potent secondary factors. Adipose tissue fatty acid studies support this concept of a dietary basis to CHD; low levels of linoleic acid and high P/S ratios are associated with a higher risk of CHD. Marine long-chain polyunsaturated fats may play a protective role in the CHD story. Monounsaturated fats are as effective in lowering serum total cholesterol as low fat-high carbohydrate diets. Coagulation factors of possible importance to CHD risks can be affected by dietary fat intake. Dietary fats affect blood pressure levels and may initiate hypertension. Coffee and alcohol consumption do not appear to effect the risk of CHD, although coffee may raise the blood cholesterol and alcohol raise the blood pressure. Diet is probably the central environmental factor in the development of CHD.