scholarly journals Effects of dietary fat and conjugated linoleic acid on plasma metabolite concentrations and metabolic responses to homeostatic signals in pigs

2002 ◽  
Vol 88 (6) ◽  
pp. 625-634 ◽  
Author(s):  
E. Ostrowska ◽  
R. F. Cross ◽  
M. Muralitharan ◽  
D. E. Bauman ◽  
F. R. Dunshea

Sixteen female cross-bred (Large White × Landrace) pigs (initial weight 65 kg) with venous catheters were randomly allocated to four treatment groups in a 2×2 factorial design. The respective factors were dietary fat (25 or 100 g/kg) and dietary conjugated linoleic acid (CLA; 0 or 10 g CLA-55/kg). Pigs were fed every 3 h (close to ad libitum digestible energy intake) for 8 d and were bled frequently. Plasma glucose and non-esterified fatty acid (NEFA) responses to insulin and adrenaline challenges were determined on day 8. Plasma concentrations of NEFA were significantly increased (10·5 and 5·4 % for low- and high-fat diets respectively, P=0·015) throughout the experiment, suggesting that there was a possible increase in fat mobilisation. The increase in lipolysis, an indicator of ß-adrenergic stimulated lipolysis, was also evident in the NEFA response to adrenaline. However, the increase in plasma triacylglycerol (11·0 and 7·1 % for low- and high-fat diets respectively, P=0·008) indicated that CLA could have reduced fat accretion via decreased adipose tissue triacylglycerol synthesis from preformed fatty acids, possibly through reduced lipoprotein lipase activity. Plasma glucose, the primary substrate for de novo lipid synthesis, and plasma insulin levels were unaffected by dietary CLA suggesting that de novo lipid synthesis was largely unaffected (P=0·24 and P=0·30 respectively). In addition, the dietary CLA had no effect upon the ability of insulin to stimulate glucose removal.

2000 ◽  
Vol 25 (6) ◽  
pp. 495-523 ◽  
Author(s):  
David J. Dyck

Although there remains controversy regarding the role of macronutrient balance in the etiology of obesity, the consumption of high-fat diets appears to be strongly implicated in its development. Evidence that fat oxidation does not adjust rapidly to acute increases in dietary fat, as well as a decreased capacity to oxidize fat in the postprandial state in the obese, suggest that diets high in fat may lead to the accumulation of fat stores. Novel data is also presented suggesting that in rodents, high-fat diets may lead to the development of leptin resistance in skeletal muscle and subsequent accumulations of muscle triacylglycerol. Nevertheless, several current fad diets recommend drastically reduced carbohydrate intake, with a concurrent increase in fat content. Such recommendations are based on the underlying assumption that by reducing circulating insulin levels, lipolysis and lipid oxidation will be enhanced and fat storage reduced. Numerous supplements are purported to increase fat oxidation (carnitine, conjugated linoleic acid), increase metabolic rate (ephedrine, pyruvate), or inhibit hepatic lipogenesis (hydroxycitrate). All of these compounds are currently marketed in supplemental form to increase weight loss, but few have actually been shown to be effective in scientific studies. To date, there is little or no evidence supporting that carnitine or hydroxycitrate supplementation are of any value for weight loss in humans. Supplements such as pyruvate have been shown to be effective at high dosages, but there is little mechanistic information to explain its purported effect or data to indicate its effectiveness at lower dosages. Conjugated linoleic acid has been shown to stimulate fat utilization and decrease body fat content in mice but has not been tested in humans. The effects of ephedrine, in conjunction with methylxanthines and aspirin, in humans appears unequivocal but includes various cardiovascular side effects. None of these compounds have been tested for their effectiveness or safety over prolonged periods of time. Key words: carnitine, conjugated linoleic acid, ephedrine, pyruvate, hydroxycitrate


1997 ◽  
Vol 77 (2) ◽  
pp. 327-336 ◽  
Author(s):  
Lilian B. M. Tuburg ◽  
Edward Haddeman ◽  
Gerard A. A. Kivits ◽  
Jan A. Weststrate ◽  
Elizabeth J. Brink

Vitamin E is the major lipid-soluble antioxidant in human subjects and is crucial in protecting polyunsaturated fatty acids (PUFA) against lipid peroxidation. Dietary PUFA have been suggested to inhibit the absorption of vitamin E. The present study in young male rats was designed to investigate the effect of increasing concentrations of dietary linoleic acid on the faecal excretion of vitamin E. The rats were fed on semi-synthetic diets containing two concentrations of fat (59 g/kg diet, 15 energy % (en%) or 131 g/kg, 30 en%) for 3 weeks. Triacylglycerol rich in linoleic acid was added at the expense of triacylglycerol rich in saturated fatty acids to obtain dietary concentrations of 13,39 or 66 g linoleic acid/kg diet for the high-fat diet (131 g fat/kg) and 12, 24 or 36 g linoleic acid/kg diet for the reduced-fat diet (59 g fat/kg). The results from the present study demonstrate that the faecal excretion of vitamin E was significantly lower in rats fed on diets with high levels of linoleic acid compared with rats fed on lower levels of linoleic acid irrespective of the dietary fat content. The concentration of vitamin E in liver and plasma was significantly lower in animals fed on the highest concentration of linoleic acid compared with those fed on the lowest level. Results from the present study also demonstrate that at the same concentration of linoleic acid, the faecal excretion of vitamin E in rats fed on reduced-fat diets was significantly lower than in rats fed on high-fat diets. Our findings indicate that the apparent absorption of vitamin E is not inhibited by dietary PUFA. Results from the present study also demonstrate that a reduction of dietary fat content from 30 en% to 15 en% does not lower the apparent absorption of vitamin E


2020 ◽  
Vol 98 (3) ◽  
Author(s):  
Logan R Kilburn ◽  
Karin Allenspach ◽  
Albert E Jergens ◽  
Agnes Bourgois-Mochel ◽  
Jonathan P Mochel ◽  
...  

Abstract Pet foods may be formulated with decreased starch to meet consumer demands for less processed diets. Fats and oils may be added to low-starch diets to meet energy requirements, but little is known about its effects on canine health. The study objective was to evaluate the effects of feeding healthy adult dogs low carbohydrate, high-fat diets on apparent total tract digestibility, fecal characteristics, and overall health status. Eight adult Beagles were enrolled in a replicated 4 × 4 Latin Square design feeding trial. Dogs were randomly assigned to one of four dietary fat level treatments (T) within each period: 32% (T1), 37% (T2), 42% (T3), and 47% (T4) fat on a dry matter basis. Fat levels were adjusted with the inclusion of canola oil added to a commercial diet. Each dog was fed to exceed its energy requirement based on NRC (2006). Blood samples were analyzed for complete blood counts, chemistry profiles, and canine pancreatic lipase immunoreactivity levels. Apparent total tract digestibility improved (P < 0.05) as the fat level increased for dry matter, organic matter, fat, and gross energy. Fecal output decreased as levels of fat increased in the diet (P = 0.002). There was no effect of fat level on stool quality or short-chain fatty acid and ammonia concentrations in fecal samples (P ≥ 0.20). Blood urea nitrogen levels decreased with increased fat level (P = 0.035). No significant differences were seen in canine pancreatic lipase immunoreactivity (P = 0.110). All blood parameters remained within normal reference intervals. In summary, increased dietary fat improved apparent total tract digestibility, did not alter fecal characteristics, and maintained the health status of all dogs.


2000 ◽  
Vol 84 (4) ◽  
pp. 417-427 ◽  
Author(s):  
Patrick Schrauwen ◽  
Klaas R. Westerterp

The prevalence of obesity is increasing in westernized societies. In the USA the age-adjusted prevalence of BMI ≫30 kg/m2 increased between 1960 and 1994 from 13 % to 23 % for people over 20 years of age. This increase in the prevalence of obesity has been attributed to an increased fat intake and a decreased physical activity. However, the role of the impact of the level of dietary fat intake on human obesity has been challenged. High-fat diets, due to their high energy density, stimulate voluntary energy intake. An increased fat intake does not stimulate its own oxidation but the fat is stored in the human body. When diet composition is isoenergetically switched from low to high fat, fat oxidation only slowly increases, resulting in positive fat balances on the short term. Together with a diminished fat oxidation capacity in pre-obese subjects, high-fat diets can therefore be considered to be fattening. Another environmental factor which could explain the increasing prevalence of obesity is a decrease in physical activity. The percentage of body fat is negatively associated with physical activity and exercise has pronounced effects on energy expenditure and substrate oxidation. High-intensity exercise, due to a lowering of glycogen stores, can lead to a rapid increase in fat oxidation, which could compensate for the consumption of high-fat diets in westernized societies. Although the consumption of high-fat diets and low physical activity will easily lead to the development of obesity, there is still considerable inter-individual variability in body composition in individuals on similar diets. This can be attributed to the genetic background, and some candidate genes have been discovered recently. Both leptin and uncoupling protein have been suggested to play a role in the prevention of diet-induced obesity. Indeed, leptin levels are increased on a high-fat diet but this effect can be attributed to the increased fat mass observed on the high-fat diet. No effect of a high-fat diet per se on leptin levels is observed. Uncoupling proteins are increased by high-fat diets in rats but no data are available in human subjects yet. In conclusion, the increased intake of dietary fat and a decreasing physical activity level are the most important environmental factors explaining the increased prevalence of obesity in westernized societies.


2007 ◽  
Vol 74 (2) ◽  
pp. 160-166 ◽  
Author(s):  
Amanda Aparecida Hayashi ◽  
Sérgio Raposo de Medeiros ◽  
Marina Hojaij Carvalho ◽  
Dante Pazzanese Duarte Lanna

Conjugated linoleic acid (CLA) has a range of biological properties, including effects on lipid metabolism, milk and body composition in animals. This study investigated the effects of dietary CLA on lactating rats and development of the suckling pups. Dams were fed either a control diet or the same diet supplemented with 25 g/kg of a fat supplement containing 540 g CLA/kg (final concentration of 13·5 g CLA/kg diet) from parturition to the 15th day post-partum. The CLA mixture used in this study contained the following isomers (per 100 g): cis-9, trans-11 (24 g); cis-10, trans-12 (35 g); cis-8, trans-10 (15 g); cis-11, trans-13 (17 g) and others (9 g). On d 15 post partum, CLA supplementation reduced milk fat content by 33% and pup growth by 21%. The milk fatty acid profile, with decreased content of short and medium chain acids, suggests CLA inhibition was more pronounced for de novo lipid synthesis. Consistent with these results, activities of fatty acid synthase, glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase were reduced by CLA treatment in the mammary gland and liver. In contrast, the activity of NADP-malate dehydrogenase was unchanged.


2021 ◽  
Vol 22 (2) ◽  
pp. 834
Author(s):  
Xiaofei Wang ◽  
Zhaopeng Zhong ◽  
Xiangyin Chen ◽  
Ziyun Hong ◽  
Weimin Lin ◽  
...  

HFD (high-fat diet) induces obesity and metabolic disorders, which is associated with the alteration in gut microbiota profiles. However, the underlying molecular mechanisms of the processes are poorly understood. In this study, we used the simple model organism honey bee to explore how different amounts and types of dietary fats affect the host metabolism and the gut microbiota. Excess dietary fat, especially palm oil, elicited higher weight gain, lower survival rates, hyperglycemic, and fat accumulation in honey bees. However, microbiota-free honey bees reared on high-fat diets did not significantly change their phenotypes. Different fatty acid compositions in palm and soybean oil altered the lipid profiles of the honey bee body. Remarkably, dietary fats regulated lipid metabolism and immune-related gene expression at the transcriptional level. Gene set enrichment analysis showed that biological processes, including transcription factors, insulin secretion, and Toll and Imd signaling pathways, were significantly different in the gut of bees on different dietary fats. Moreover, a high-fat diet increased the relative abundance of Gilliamella, while the level of Bartonella was significantly decreased in palm oil groups. This study establishes a novel honey bee model of studying the crosstalk between dietary fat, gut microbiota, and host metabolism.


Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1678
Author(s):  
Kamila P. Liput ◽  
Adam Lepczyński ◽  
Agata Nawrocka ◽  
Ewa Poławska ◽  
Magdalena Ogłuszka ◽  
...  

The aim of the study was to evaluate the effect of different types of high-fat diets (HFDs) on the proteomic profile of mouse liver. The analysis included four dietary groups of mice fed a standard diet (STD group), a high-fat diet rich in SFAs (SFA group), and high-fat diets dominated by PUFAs with linoleic acid (LA, C18:2n–6) to α-linolenic acid (ALA, C18:3n–3) ratios of 14:1 (14:1 group) and 5:1 (5:1 group). After three months of diets, liver proteins were resolved by two-dimensional gel electrophoresis (2DE) using 17 cm non-linear 3–10 pH gradient strips. Protein spots with different expression were identified by MALDI-TOF/TOF. The expression of 13 liver proteins was changed in the SFA group compared to the STD group (↓: ALB, APOA1, IVD, MAT1A, OAT and PHB; ↑: ALDH1L1, UniProtKB—Q91V76, GALK1, GPD1, HMGCS2, KHK and TKFC). Eleven proteins with altered expression were recorded in the 14:1 group compared to the SFA group (↓: ARG1, FTL1, GPD1, HGD, HMGCS2 and MAT1A; ↑: APOA1, CA3, GLO1, HDHD3 and IVD). The expression of 11 proteins was altered in the 5:1 group compared to the SFA group (↓: ATP5F1B, FTL1, GALK1, HGD, HSPA9, HSPD1, PC and TKFC; ↑: ACAT2, CA3 and GSTP1). High-PUFA diets significantly affected the expression of proteins involved in, e.g., carbohydrate metabolism, and had varying effects on plasma total cholesterol and glucose levels. The outcomes of this study revealed crucial liver proteins affected by different high-fat diets.


2001 ◽  
Vol 71 (6) ◽  
pp. 339-346 ◽  
Author(s):  
Yi-Fa Lu ◽  
Chia-Feng Chiang

The aim of this study was to investigate the effect of dietary fat levels, with or without cholesterol, on lipid peroxidation and the activities of antioxidant enzymes in rats. Thirty-two Wistar rats aged 4 weeks were divided into 4 groups and fed high (20%; HF) or low (5%; LF) fat, with or without l% cholesterol, for 6 weeks. Cholesterol feeding resulted in significantly higher concentrations of serum cholesterol, but lowered serum triacylglycerol levels. Cholesterol feeding also led to markedly decreased levels of hepatic thiobarbituric acid reactive substances (TBARS) and lower activities of hepatic superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase, and glucose-6-phosphate dehydrogenase (G6PDH) when compared with cholesterol-free counterparts in both HF and LF diets. On the other hand, rats fed high-fat diets showed increased serum and liver TBARS, but decreased hepatic GSH-Px, SOD, and G6PDH activities. Hepatic catalase activity was lower in rats fed cholesterol-containing diets, but higher in rats fed high-fat diets, and interaction existed between cholesterol and fat feeding. These results suggested that dietary cholesterol might delay lipid peroxidation and decrease the activities of the hepatic antioxidant enzymes. The degree of lipid peroxidation was also influenced by dietary fat levels.


Lipids ◽  
1997 ◽  
Vol 32 (4) ◽  
pp. 369-375 ◽  
Author(s):  
Jennifer A. Johnson ◽  
Mary L. Blackburn ◽  
Arthur W. Bull ◽  
Clifford W. Welsch ◽  
J. Throck Watson

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