The lipase inhibitor, orlistat, is used in the treatment of obesity and reduces fat absorption by about 30%. However, the mean weight loss induced by orlistat is less than expected for the degree of fat malabsorption. It was hypothesised that lipase inhibition with orlistat attenuates the suppressive effects of oral fat on subsequent energy intake in normal-weight subjects. Fourteen healthy, lean subjects (nine males, five females; aged 25±1·3 years) were studied twice, in a double-blind fashion. The subjects received a high-fat yoghurt ‘preload’ (males 400g (2562kJ); females 300g (1923kJ)), containing orlistat (120mg) on one study day (and no orlistat on the other ‘control’ day), 30min before ad libitum access to food and drinks; energy intake was assessed during the following 8h. Blood samples were taken at regular intervals for the measurement of plasma cholecystokinin (CCK). Each subject performed a 3d faecal fat collection following each study. Energy intake during the day was greater following orlistat (10220 (sem 928) kJ) v. control (9405 (sem 824) kJ) (P=0·02). On both days plasma CCK increased (P<0·05) after the preload. Plasma CCK 20min following ingestion of the preload was less after orlistat (4·1 (sem 0·9) pmol/l) v. control (5·3) (sem 0·9) pmol/l (P=0·028); however there was no difference in the area under the curve 0–510min between the two study days. Fat excretion was greater following orlistat (1017 (sem 168) kJ) v. control (484 (sem 90) kJ) (P=0·004). In conclusion, in healthy, lean subjects the acute inhibitory effect of fat on subsequent energy intake is attenuated by orlistat and the increase in energy intake approximates the energy lost due to fat malabsorption.

The objective of the present study was to investigate the effects of starches with differing rates of hydrolysis on exposure to pancreatin in vitro on postprandial carbohydrate metabolism in healthy subjects and in subjects with type 2 diabetes. Two test starches, prepared from uncooked native granular starch products, and naturally enriched with 13C, were consumed in a randomized crossover design by eight healthy and thirteen type 2 diabetic subjects. One starch was characterized in vitro as being rapidly hydrolysed (R, 94% after 180min), and the other was more slowly hydrolysed (S, 51% after 180min). Each subject consumed 50g of each test starch. In addition, the type 2 diabetic subjects consumed 89·7g of the S starch on a separate occasion. Blood samples were taken at 10min intervals for 3h, and at 20min intervals for a further 3h during a 6h postprandial period. Breath 13CO2 enrichment was measured at the same time points, and indirect calorimetry was performed for seven 20min sessions immediately before and during the 6h postprandial period. With the R starch, plasma glucose concentrations and serum insulin concentrations rose faster and the maximum glucose change was approximately 1·8 times that for the S starch, averaged across both subject groups. The areas under the curves for glucose and insulin were, respectively, 1·7 and 1·8 times higher for the R starch compared with the S starch, averaged across both subject groups. The rate of 13CO2 output and the proportion of 13C recovered in breath after consumption of the R starch was similar for both subject groups. The results provide evidence that starches which have different rates of hydrolysis in vitro result in different patterns of glycaemia and insulinaemia in both healthy adults and in diet-controlled type 2 diabetic subjects. Data from the hydrolysis of novel starch products in vitro, therefore, are useful in predicting glycaemic responses in vivo.

To determine the optimum indispensable (I) amino acid (AA) balance in Atlantic salmon (Salmo salar L.) fry, a single protocol established for the pig was adapted. The balance was calculated from the reduction in N gain after replacing about 45% of a single IAA by a mixture of dispensable AA in isonitrogenous diets. We confirmed that the mixture of AA simulating the AA pattern of cod-meal protein and gelatine (46:3, w/w) was used with the same efficiency as cod-meal protein and gelatine. From the deletion experiment an optimum balance between the IAA was derived. Expressed relative to lysine=100, the optimal balance was: arginine 76 (se 0·2), histidine 28 (se 2·2), methionine+cystine 64 (se 1·7), phenylalanine + tyrosine 105 (se 1·6), threonine 51 (se 2·4), tryptophan 14 (se 0·7), valine 59 (se 1·7). No estimates were made for isoleucine and leucine. Expressed as g/16g N, the optimal balance was: arginine 4·0 (se 0·0), histidine 1·5 (se 0·1), lysine 5·3 (se 0·2), methionine+cystine 3·4 (se 0·1), phenylaline+tyrosine 5·6 (se 0·1), threonine 2·7 (se 0·1), tryptophan 0·7 (se 0·0), valine 3·1 (se 0·1). This AA composition is close to that of the Atlantic salmon whole-body, but using it as an estimation of the IAA requirements may lead to an overestimation of the branched-chain AA requirements and an underestimation of aromatic and S-containing AA requirements. The results are discussed in accordance with the key assumptions associated with the model used (broken-line model, IAA efficiencies and maintenance requirements).

Milk enriched in conjugated linoleic acid (CLA) was obtained from cows on pasture supplemented with full-fat rapeseeds (FFR; 2·26g cis 9, trans 11 (c9, t11)-CLA/100g fatty acid methyl esters) and full-fat soyabeans (1·83g c9, t11-CLA/100g fatty acid methyl esters). A control milk fat (1·69g c9, t11-CLA/100g fatty acid methyl esters) was obtained from cows fed on pasture only. The present study assessed the potency of the CLA-enriched milk fats to modulate biomarkers that had previously been observed to respond to c9, t11-CLA in the MCF-7 and SW480 cell lines. Cell numbers decreased (P<0·05) by up to 61 and 58% following the incubation of MCF-7 and SW480 cells, respectively, for 4d with milk fats (yielding CLA concentrations between 60·2 and 80·6μM). The FFR milk fat, containing the highest CLA content, increased (P<0·05) [14C]arachidonic acid (AA) uptake into the monoacylglycerol fraction of MCF-7 and SW480 cells while it decreased (P<0·05) uptake into the phospholipid fraction of the latter. This milk fat also decreased (P<0·05) [14C]AA conversion to prostaglandin (PG) E2 while increasing conversion to PGF2α in both cell lines. All milk-fat samples increased (P<0·05) lipid peroxidation as measured by 8-epi-PGF2α in both cell lines. In SW480 cells the milk-fat samples decreased (P<0·05) bcl-2 and cytosolic glutathione levels while increasing (P<0·05) membrane-associated annexin V levels. All milk-fat samples decreased (P<0·05) the expression of ras in SW480 cells. These data suggest that milk-fat CLA was effective at modulating synthetic CLA-responsive biomarkers.

In the present study the effects of some C18 fatty acids on hepatic fatty acid metabolism have been compared. Male rats were fed cholesterol-free diets containing either C18:0, C18:1cis or C18:1trans isomers as the variables. In accordance with previous work, oleic acid in the diet caused an increase in cholesterol concentration in the liver and in the lipoprotein fraction of density (d; kg/l)<1·006. Oleic acid also reduced the triacylglycerol:cholesterol value in this fraction. Surprisingly, the C18:1trans isomers diet induced a decrease in the amount of cholesterol in total plasma as well as in the 1·019<d<1·063 lipoprotein fraction. Both oleic acid and C18:1trans isomers increased the concentration of triacylglycerols in the liver. The two C18:1 fatty acids differently influenced the hepatic activities of carnitine palmitoyltransferase-I and 3-hydroxy-acyl-CoA dehydrogenase; both enzymes were inhibited by C18:1trans isomers, while no change was induced by oleic acid. The activity of the citrate carrier was lower in the oleic acid- and C18:1trans isomers-fed rats, when compared with the rats fed stearic acid. No diet effects were seen for the activities of acetyl-CoA carboxylase, fatty acid synthase, diacylglycerol acyltransferase, citrate synthase and phosphofructokinase. The results are interpreted in that oleic acid raised liver triacylglycerol by reducing the secretion of it with the d<1·006 lipoprotein fraction whereas the C18:1trans isomers enhanced liver triacylglycerol by lowering the hepatic oxidation of fatty acids.

The aim of the present study was to investigate the influence of dietary-fibre (DF)-rich barley-based diets on bile acids (BA) and neutral sterols (NS) in the intestinal tract of rats. For this purpose, young male Wistar rats (n 50; ten per group) weighing about 67g were fed either a barley-free diet (control group) or diets containing 500g barley meal extrudates/kg or a barley meal–Novelose mixture (groups A–D) for 6 weeks. These barley products contained 7–24g resistant starch/100g and 7–12g (1→3),(1→4)-β-glucan/100g. More steroids were transported towards the lower parts of the intestinal tract when higher concentrations of macromolecular DF were present in the diets (P<0·001). Tauroconjugated and primary BA dominated in the contents of the small intestine. Intense enzymic conversion of BA occurred in the caecum and colon. The fermentation of DF affected indirectly the amount of formed secondary BA. The main BA present in the caecal contents were muricholic acids, hyodeoxycholic acid and cholic acid. The BA spectrum in the colonic contents was different from that in the caecum. A higher concentration of NS appeared in the intestinal contents of the groups fed the barley-based diets than in the controls (P<0·005). The microbial conversion of cholesterol to coprostanol, cholestanone and coprostanone was influenced by the amount and composition of the DF in the gut. DF in the diet may affect the concentration and spectrum of steroids in the intestinal tract. The results are relevant for the discussion of mechanisms behind the cholesterol-lowering effects of DF.

The present study was designed to evaluate the differential effects of dietary glucose, lactose and starch on small-intestinal morphology, organ weights, pH of chyme and haptoglobin levels in blood plasma of weaned piglets. It was hypothesised that lactose consumption would ameliorate the weaning-induced decrease in gut integrity. A total of forty-two barrows were used. Piglets were weaned at 27 (sd 0·8) d of age and weighed 8·0 (sd 0·51) kg. On the day before weaning (day −1) all pigs were blocked according to body weight and randomly assigned to seven groups (n 6 per group). The groups differed in diet and day of dissection. On the day of weaning, dissection was performed on one group of six piglets. The remaining groups were fed one of three experimental diets in which glucose, lactose or starch had been iso-energetically exchanged, supplying 24% dietary energy. The piglets received a liquid diet (air-dry meal:water of 1:2, w/w). The piglets were given access to a maximum of dietary energy in order to prevent confounding between feed intake and villus architecture. The piglets were dissected and sampled on days 0, 3, or 10 post-weaning. The results show that the carbohydrate source did not affect growth performance, organ weights, villus architecture, pH of chyme and plasma haptoglobin level. The weaning transition resulted in decreased villus height and increased haptoglobin levels. In the contents of the caecum and large intestine, the pH decreased after weaning. It is concluded that at least under conditions of similar feed intake and low infectious pressure, dietary lactose does not ameliorate the weaning-induced compromise of small-intestinal integrity when compared with either glucose or starch.

Conjugated linoleic acids (CLA) have been shown to decrease body fat content in pigs. It is possible that feeding pigs diets rich in CLA may increase carcass lipid CLA to levels that could provide health benefits when included as a part of a healthy diet. Therefore, the aim of the present study was to determine whether dietary CLA supplementation has any effect on the fatty acid composition of subcutaneous and intramuscular adipose tissue in pigs. Thirty-five female cross bred (Large White×Landrace) pigs (initial weight 57·2kg and initial P2 back fat 11·5mm) were used in the present study. Pigs were housed individually and randomly allocated to one of six dietary treatments (0·00, 1·25, 2·50, 5·00, 7·50 and 10·00g CLA55 (55g CLA isomers/100g total fatty acids; Natural Lipids Ltd, Hovdebygda, Norway)/kg) and fed their respective diets for 8 weeks. Twelve CLA isomers in the diet and in pig tissue lipids were separated by Ag+-HPLC. CLA was incorporated at fivefold higher levels in subcutaneous fat as compared with intramuscular fat and in a dose-dependant manner. Overall, the transfer efficiency of CLA was maximized at 5·00g CLA55/kg. However, there was clear selectivity in the uptake or incorporation of cis,trans-9,11 isomer over the trans,cis-10,12 isomer. In general, CLA supplementation produced significant changes in skeletal muscle and adipose tissue fatty acid composition, indicating that dietary CLA had a potent affect on lipid transport and metabolism in vivo. Significant increases in myristic, palmitic and palmitoleic acids and a reduction in arachidonic acid were observed, suggesting an alteration in activity of Δ5-, Δ6- and Δ9-desaturases in pig adipose tissue. In conclusion, feeding pigs diets supplemented with CLA increases carcass lipid CLA, but also results in changes in the fatty acid profile in pig fat that could potentially outweigh the benefits of CLA.

The malnutrition caused by liver cirrhosis (LC) often worsens the course of the disease. Patients affected by LC often have a low bioavailability of the anabolic liver peptide insulin-like growth factor (IGF)-I. The present study was undertaken to investigate the effect of low doses of IGF-I on the nutritional status and in vivo jejunal transport of d-galactose in anatomically, pathologically and biochemically confirmed moderate, non-ascitic, cirrhotic rats. LC was experimentally induced in growing rats by inhalation of CCl4 and addition of phenobarbital to drinking water. Both the nutritional status, as evaluated by N balance, and in vivo intestinal transport of d-galactose, were significantly impaired in cirrhotic rats. As compared with healthy rats, administration of 20μg human recombinant IGF-I/kg body weight for 14d to cirrhotic rats significantly improved N balance variables and restored in vivo intestinal transport of the sugar. However, IGF-I had no effect on the steatorrhoea associated with LC. These results suggest that low doses of IGF-I may have beneficial effects on the malnutrition associated with moderate LC.

The influence of propionate supplementation on the splanchnic metabolism of amino acids (AA) and other N compounds (urea-N and NH3-N) and the supply of AA and NH3-N to the hindlimb was investigated in growing lambs. Six rumen-cannulated and multicatheterised lambs (32·2kg) were fed frozen rye grass at 690kJ metabolisable energy intake/d per kg average metabolic body weight. They were infused intraruminally with a salt solution (control) or with propionate solutions at 0·23mol/l (P1) or 0·41mol/l (P2) infused at a maximal rate of 1·68 (sd 0·057) ml/min according to a repeated Latin square design. The propionate infusion did not increase the net portal appearance of total AA (TAA)-N but increased that of some branched-chain AA (valine and to a lesser extent isoleucine). Simultaneously, the propionate treatment (especially P2) induced an increased TAA utilisation by the liver. This was due mainly to an increased (+79%; P<0·07) utilisation of the essential AA and particularly the branched-chain AA. A stimulation of protein synthesis in the liver is hypothesised since (1) propionate stimulated insulin secretion and (2) utilisation of non-essential AA were less influenced by the propionate treatment in the liver (except for alanine), suggesting that the AA utilised by the liver were directed towards protein synthesis rather than towards oxidation or urea synthesis. At the splanchnic level, the propionate treatment did not have any effect on the TAA, non-essential AA and essential AA, except for a net splanchnic release that was decreased for leucine (P<0·02) and methionine (P<0·01) and increased for threonine (P<0·05). The propionate treatment did not have any effect on the hindlimb uptake of AA (essential and non-essential). As a consequence, even though the propionate treatment induced some major alterations in the splanchnic metabolism of AA, there were no changes in the net AA balance in the hindlimb (and hence probably on muscle growth). The role of the splanchnic tissues in the regulation of the AA supply to the peripheral tissues (such as muscle) therefore appears to be prominent in the regulation of muscle growth. Whether the peripheral tissues regulate their own supply by interacting with the splanchnic tissues (and especially the liver) or the liver is the only regulator of the AA supply to the muscle remains in doubt.

The changes in metabolic efficiency, body composition, and nutrient partitioning induced by high-fat feeding were evaluated in adult rats (90d of age). The alterations in serum free triiodothyronine, insulin, and leptin levels, as well as in hepatic and skeletal muscle metabolism, were also assessed. Rats were fed either a low- or a high-fat diet for 2 weeks. Relative to the low-fat feeding, energy intake and expenditure, as well as body-energy gain, lipid gain, and energetic efficiency, were increased by the high-fat feeding. Increased serum leptin levels accompanied these variations. A positive correlation between serum leptin levels and percentage of body fat was found in the rats fed the low- or high-fat diet, with a significant divergence between the slope of the regression lines. Furthermore, a negative correlation between serum leptin level and energy intake was found in the rats fed the low-fat diet, while a positive correlation was found in the rats fed the high-fat diet. Finally, the high-fat feeding decreased the hepatic and skeletal muscle mitochondrial oxidative capacity. It is concluded that, in adult rats, a nutritional factor such as a high level of fat in the diet induces obesity, leptin resistance, and impairment of mitochondrial capacity, all phenomena typical of unrestrained aged rats.

According to the report of the World Health Organization (1985), total energy expenditure (TEE) in human subjects can be calculated as BMR×physical activity level (PAL). However, other reports have pointed out limitations in the suggested procedure related to the % body fat of the subjects. The purpose of the present study was to evaluate the World Health Organization (1985) procedure in thirty-four healthy women with BMI 18–39kg/m2. BMR and TEE were measured using indirect calorimetry (BMRmeas) and the doubly-labelled water method (TEEref) respectively. When assessed using the doubly-labelled water and skinfold-thickness methods, the women had 34 (sd 8) and 33 (sd 6) % body fat respectively. On the basis of guidelines provided by the World Health Organization (1985), 1·64 was selected to represent the average PAL of the women. Furthermore, PAL was also assessed by means of an accelerometer (PALacc), heart-rate recordings (PALHR) and a questionnaire (PALq). These estimates were: PALacc 1·71 (sd 0·17), PALHR 1·76 (sd 0·24), PALq 1·86 (sd 0·27). These values were lower than TEEref/BMRref, which was 1·98 (sd 0·21). BMR assessed using equations recommended by the World Health Organization (1985) (BMRpredicted) overestimated BMR by 594 (sd 431) kJ/24h. However, when TEE was calculated as BMRpredicted×PALacc, BMRpredicted×PALHR and BMRpredicted×PALq respectively, average results were in agreement with TEEref. Furthermore, TEE values based on BMRpredicted and PALacc, PALHR, PALq as well as on PAL=1·64, minus TEEref, were significantly correlated with body fatness. When the same PAL value (1·64) was used for all subjects, this correlation was particularly strong. Thus, the World Health Organization (1985) procedure may give TEE results that are biased with respect to the body fatness of subjects.

The present investigation was undertaken to evaluate whether mitochondrial energy metabolism is altered in a model of malnutrition induced by dexamethasone (DEX) treatment (1·5mg/kg per d for 5d). The gastrocnemius and liver mitochondria were isolated from DEX-treated, pair-fed (PF) and control (CON) rats. Body weight was reduced significantly more in the DEX-treated group (−16%) than in the PF group (−9%). DEX treatment increased liver mass (+59% v. PF, +23% v. CON) and decreased gastrocnemius mass. Moreover, in DEX-treated rats, liver mitochondria had an increased rate of non-phosphorylative O2 consumption with all substrates (approximately +42%). There was no difference in enzymatic complex activities in liver mitochondria between rat groups. Collectively, these results suggest an increased proton leak and/or redox slipping in the liver mitochondria of DEX-treated rats. In addition, DEX decreased the thermodynamic coupling and efficiency of oxidative phosphorylation. We therefore suggest that this increase in the proton leak and/or redox slip in the liver is responsible for the decrease in the thermodynamic efficiency of energy conversion. In contrast, none of the variables of energy metabolism determined in gastrocnemius mitochondria was altered by DEX treatment. Therefore, it appears that DEX specifically affects mitochondrial energy metabolism in the liver.

Despite the importance of human milk fatty acids for infant growth and development, there are few reports describing infant intakes of individual fatty acids. We have measured volume, fat content and fatty acid composition of milk from each breast at each feed over a 24h period to determine the mean daily amounts of each fatty acid delivered to the infant from breast milk at 1, 2, 4, 6, 9 and 12 months of lactation in five women. Daily (24h) milk production was 336·60 (sem 26·21) and 414·49 (sem 28·39) ml and milk fat content was 36·06 (sem 1·37) and 34·97 (sem 1·50) g/l for left and right breasts respectively over the course of the first year of lactation. Fatty acid composition varied over the course of the day (mean CV 14·3 (sd 7·7) %), but did not follow a circadian rhythm. The proportions (g/100g total fatty acids) of fatty acids differed significantly between mothers (P<0·05) and over the first year of lactation (P<0·05). However, amounts (g) of most fatty acids delivered to the infant over 24h did not differ during the first year of lactation and only the amounts of 18:3n-3, 22:5n-3 and 22:6n-3 delivered differed between mothers (P<0·05). Mean amounts of 18:2n-6, 18:3n-3, 20:4n-6 and 22:6n-3 delivered to the infant per 24h over the first year of lactation were 2·380 (sd 0·980), 0·194 (sd 0·074), 0·093 (sd 0·031) and 0·049 (sd 0·021) g respectively. These results suggest that variation in proportions of fatty acids may not translate to variation in the amount delivered and that milk production and fat content need to be considered.

The objective of the present study was to determine the accuracy of two foot-to-foot (FF) bioelectrical impedance analysers (BIA) to assess body composition in overweight and obese adolescents, compared with dual-energy X-ray absorptiometry (DXA) and hand-to-foot (HF) BIA. Body composition was assessed in fifty-three overweight or obese adolescents (BMI 27·9 (sd 4·1) kg/m2; aged 13–16 years) by DXA (Hologic QDR-4500; Hologic Inc., Bedford, MA, USA) and BIA (HF (BIA 101, RJL System, Detroit, IL, USA) and FF (Body Fat Monitor Scale BF-625, Tanita Corporation of America Inc., Arlington Heights, IL, USA; Téfal Bodymaster Vision, Téfal, Rumilly, France)). Bland–Altman tests showed that, compared with DXA, FF-Tanita and FF-Téfal underestimated (P<0·05) fat mass (FM) less than HF-BIA (−1·7 (sd 3·1), −0·7 (sd 5·8) and −2·3 (sd 2·2) kg respectively, P<0·001). However, the limits of agreement between DXA and FF-Tanita or FF-Téfal were much greater than those obtained with HF-BIA (−7·7 and +4·3, −12·0 and +10·6 v. −2·1 and +6·7kg respectively). The differences between FM assessed using the FF-Tanita or the FF-Téfal analyser and DXA increased with the waist:hip ratio, and were higher in boys than in girls. The major limiting factor of FF-BIA was the inter-individual variability in FM estimates. In conclusion, FF-BIA and DXA are not interchangeable methods. FF-BIA could be acceptable to assess body composition in large groups of overweight or obese adolescents, but cannot be recommended for body composition assessment in obese subjects because of the large errors in individual estimates.