Comparative bioavailability of dietary alpha-linolenic and docosahexaenoic acids in the growing rat.

Animal and human studies have indicated that developing mammals fed only alpha-linolenic acid (18:3n-3) have lower docosahexaenoic acid (22:6n-3) content in brain and tissue phospholipids when compared with mammals fed 18:3n-3 plus 22:6n-3. The aim of this study was to test the hypothesis that low bioavailability of dietary 18:3n-3 to be converted to 22:6n-3 could partly explain this difference in fatty acid accretion. For that purpose, we determined the partitioning of dietary 18:3n-3 and 22:6n-3 between total n-3 fatty acid body accumulation, excretion, and disappearance (difference between the intake and the sum of total n-3 fatty acids accumulated and excreted). This was assessed using the quantitative method of whole-body fatty acid balance in growing rats fed the same amount of a 5% fat diet supplying either 18:3n-3 or 22:6n-3 at a level of 0.45% of dietary energy (i.e., 200 mg/100 g diet). We found that 58.9% of the total amount of 18:3n-3 ingested disappeared, 0.4% was excreted in feces, 21.2% accumulated as 18:3n-3 (50% in total fats and 46% in the carcass-skin compartment), and 17.2% accumulated as long-chain derivatives (14% as 22:6n-3 and 3.2% as 20:5n-3 + 22:5n-3). Similar results were obtained from the docosahexaenoate balance (as % of the total amount ingested): disappearance, 64.5%; excretion, 0.5%; total accumulation, 35% with 30.1% as 22:6n-3. Thus, rats fed docosahexaenoate accumulated a twofold higher amount of 22:6n-3, which was mainly deposited in the carcass-skin compartment (68%). Similar proportions of disappearance of dietary 18:3n-3 and 22:6n-3 lead us to speculate that these two n-3 polyunsaturated fatty acids were beta-oxidized in the same amount.

Acute hyperinsulinism modulates plasma apolipoprotein B-48 triglyceride-rich lipoproteins in healthy subjects during the postprandial period.

The role of postprandial insulin in the regulation of postprandial lipid metabolism is still poorly understood. The roles of hyperinsulinemia and insulin resistance in the alteration of postprandial lipid metabolism are not clear either. To improve knowledge in this area, we submitted healthy men to acute hyperinsulinemia in two different ways. In the first study, we compared in 10 men the effects of four isolipidic test meals that induce different degrees of hyperinsulinemia on postprandial lipid metabolism. Three different carbohydrate sources were compared according to their glycemic indexes (GIs; 35, 75, and 100 for white kidney bean, spaghetti, and white bread test meals, respectively); the fourth test meal did not contain any carbohydrates. Postprandial plasma insulin levels were proportional to the GIs (maximal plasma insulin concentrations: 113 +/- 16 to 266 +/- 36 pmol/l). We found a strong positive correlation during the 6-h postprandial period between apolipoprotein (apo) B-48 plasma concentration and insulin plasma concentration (r2 = 0.70; P = 0.0001). In a second study, 5 of the 10 subjects again ingested the carbohydrate-free meal, but during a 3-h hyperinsulinemic- (550 +/- 145 pmol/l plasma insulin) euglycemic (5.5 +/- 0.8 mmol/l plasma glucose) clamp. A biphasic response was observed with markedly reduced levels of plasma apoB-48 during insulin infusion, followed by a late accumulation of plasma apoB-48 and triglycerides. Overall, the data obtained showed that portal and peripheral hyperinsulinism delays and exacerbates postprandial accumulation of intestinally derived chylomicrons in plasma and thus is involved in the regulation of apoB-48-triglyceride-rich lipoprotein metabolism, in the absence of insulin-resistance syndrome.

Effects of graded amounts (0-50 g) of dietary fat on postprandial lipemia and lipoproteins in normolipidemic adults.

Eight normolipidemic males ingested on separate days and in a random order five mixed meals containing 0, 15, 30, 40, or 50 g fat. Fasting and postprandial blood samples were obtained for 7 h and chylomicrons and lipoproteins were isolated. The nonfat and 15-g fat meals did not generate noticeable postprandial variations except for HDL phospholipids (P < 0.05). The serum and chylomicron triacylglycerol responses obtained after the meals correlated positively with the amount of fat ingested and peaked after 2-3 h. Serum free cholesterol and phospholipids increased and esterified cholesterol decreased postprandially in a dose-response manner. At the same time, triacylglycerol-rich-lipoprotein triacylglycerols, esterified cholesterol, LDL free cholesterol, HDL triacylglycerols, phospholipids, and free cholesterol increased whereas LDL and HDL esterified cholesterol decreased when the amount of ingested fat increased. The data showed that increasing the amount of fat in the usual range of ingestion (0-50 g) led to stepwise increases in the postprandial rise of chylomicron and serum triacylglycerols and induced marked changes in serum lipoproteins postprandially. The existence of a no-effect level of dietary fat (15 g) on postprandial lipemia and lipoproteins in healthy adults was shown.

Bioavailability of calcium of fresh cheeses, enteral food and mineral water. A study with stable calcium isotopes in young adult women.

True fractional Ca absorption from six foods was measured in twelve normal healthy women, aged 20-29 years. The tested foods were commercially available fresh cheese, fresh cheese prepared by new technology and rich in Ca, similar cheese with added Fe, enteral food, mineral water alone and combined with a spaghetti meal. The aim of the study was to investigate: (1) Ca absorption from a new Ca-rich fresh cheese and to compare it with that from the traditional commercial type of fresh cheese; (2) the effect of Fe enrichment of the new cheese on Ca absorption; (3) Ca absorption from the mineral water and the enteral product and to compare it with that from the dairy products; (4) the effect of a meal combined with the mineral water on Ca absorption. All test foods were consumed by all subjects according to a design with two Latin squares. Each treatment of 2 d was followed by a wash-out period of 2 weeks. Ca absorption was measured using a double stable-isotope (44Ca and 48Ca) extrinsic labelling technique. Mean fractional Ca absorption from the new fresh cheese was not significantly different from that from the traditional type (37.7 (SD 10.2)% v. 42.2 (SD 11.6)%). The addition of Fe to the new cheese did not significantly influence Ca absorption. Ca-absorption values from the mineral water (37.0 (SD 9.8)%) and from the enteral product (42.6 (SD 11.4)%) were not significantly different from those from the dairy products (37.7-42.2%, SD 10.2-11.6%). The co-ingestion of a spaghetti meal with the mineral water significantly enhanced Ca absorption from 37 (SD 9.8)% to 46.1 (SD 11.7)%. It is concluded that a new process leading to a fresh cheese with a higher Ca concentration does not alter Ca bioavailability compared with the standard technology and for a constant Ca supply. Thus this new fresh cheese would probably provide more Ca than the standard one. The fractional Ca-absorption values for mineral water and the enteral product indicate that these products can make an interesting contribution to Ca supply for populations with a low Ca intake and patients with specific diseases respectively.

Effects of moderate amounts of emulsified dietary fat on postprandial lipemia and lipoproteins in normolipidemic adults.

Eight normolipidemic males ingested a meal containing either 42 g fat or 31 g fat in the form of emulsions (9.0 and 9.2 m2) and a fixed amount of retinyl palmitate. Fasting and postmeal blood samples were obtained for 7 h. Serum and chylomicron triglyceride responses were related to the amount of fat ingested and peaked after 2-3 h. The chylomicron retinyl palmitate response was lower (P < or = 0.05) with the 31-g fat supply. After the 42-g fat intake, but not after the 31-g fat intake, serum free cholesterol and phospholipids increased and esterified cholesterol decreased postprandially. Significantly different responses were observed after both meals for low-density-lipoprotein (LDL) free cholesterol, very-low-density-lipoprotein (VLDL) and LDL esterified cholesterol, and high-density-lipoprotein (HDL) phospholipids. These data show that ingesting 31 g instead of 42 g fat in a meal reduces postmeal lipoprotein variations and suggest that a threshold level of dietary fat should be overcome to promote significant postprandial changes in lipoprotein particles.

Effect of chronic acetaldehyde intoxication on ethanol tolerance and membrane fatty acids.

Recent studies have suggested that acetaldehyde participates directly in the pathogenesis of alcoholism. Its action has been attributed mainly to its physico-chemical properties. Results of direct intoxication of laboratory animals with acetaldehyde have been reported, but only for short periods of exposure and at high doses. These are probably not representative of the conditions found during alcohol intoxication. The pulmonary route of administration described here enables long term intoxication with acetaldehyde, at levels corresponding to values measured during chronic ethanol intoxication. Chronic administration of acetaldehyde during 3 weeks induced a metabolic tolerance to ethanol as tested by the sleeping time after a challenge dose of ethanol; behavioural tolerance (measured by blood alcohol levels on waking) was not observed. At the end of the intoxication, phospholipid fatty acids of erythrocyte and synaptosome membranes were also analysed. Small changes in levels of the shorter fatty acids were observed in the phosphatidyl-choline fraction. By comparison with the effects of ethanol on the same membrane preparations, only a small part of this effect can be attributed to acetaldehyde. The first metabolite of ethanol has, however, a sure effect on the pattern of fatty acid phospholipids.

Ethanol tolerance in the rat after inhalation of acetaldehyde for a period of 21 days.

Ethanol tolerance is related to alterations in fatty acid content and physical properties of membranes. Studies have suggested a specific role for acetaldehyde in the pathogenesis of alcoholism. We measured tolerance to EtOH and erythrocyte membrane fatty acid composition after intoxication by continuous inhalation of AcH vapor for a period of 21 days. Pathophysiological and nutritional parameters were compared between treated and pair weight controls. We showed that: intoxication with AcH is technically possible via the pulmonary route, producing plasma AcH levels comparable to those seen after ethanol intoxication. The dose of AcH needs to be increased progressively to maintain constant plasma levels this indicates metabolic tolerance. the AcH-intoxicated animals had a metabolic tolerance to EtOH. AcH intoxication led to alterations in fatty acid composition similar to those seen after EtOH intoxication, especially in the saturated/unsaturated ratio of the phosphatidyl-choline and phosphatidyl-inositol fractions. AcH probably plays a part in the phenomenon of tolerance to EtOH.