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Dietary Fat (dietary + fat)
Terms modified by Dietary Fat Selected AbstractsInfluence of Dietary Fat on ,-Carotene Absorption and Bioconversion into Vitamin ANUTRITION REVIEWS, Issue 4 2002Judy D. Ribaya-Mercado Sc.D. Dietary fat facilitates the utilization of carotenoids and, based on serum ,-carotene or retinol responses following ingestion of meals containing carotene and fat sources, it has been reported that the amount of fat required in a meal may be minimal (,3-5 g). However, the dietary fat requirement for optimal carotene utilization in humans cannot be fully ascertained without longer-term dose-response studies that measure the changes in vitamin A body stores in response to varying levels of dietary fat. In humans, vitamin A body stores can be determined by use of stable isotope-dilution methods. Animal studies have shown that although the level of dietary fat has no effect on serum vitamin A concentrations of animals fed ,-carotene, higher liver vitamin A concentrations were found in those that ingested higher fat levels. Other factors that might influence the relationship of fat intake and ,-carotene utilization include the type of fat ingested, physicochemical properties of the carotenoid source, amount of carotene ingested, whether fat and ,-carotene sources are provided in the same meal, the presence of helminthic infections, age, and vitamin A status. [source] Dietary fat is a major player in obesity , but not the only oneOBESITY REVIEWS, Issue 2 2002Arne Astrup [source] Dietary fat plays a major role in obesity: noOBESITY REVIEWS, Issue 2 2002W. C. Willett Summary The percentage of dietary energy from fat has been suggested to be an important determinant of body fat, and this presumed effect has been invoked to justify the general promotion of low-fat diets. Dietary fat and the prevalence of obesity are lower in poor countries than in affluent countries. However, these contrasts are seriously confounded by differences in physical activity and food availability; within areas of similar economic development, per capita intake of fat and the prevalence of obesity have not been positively correlated. Randomized trials are the preferable method for evaluating the effect of dietary fat on adiposity because they avoid problems of confounding that are difficult to control in other studies. In short-term trials, a small reduction in body weight is typically seen in individuals randomized to diets with a lower percentage of calories from fat. In a meta-analysis of these trials, it was estimated that a decrease in 10% of energy from fat would reduce weight by 16 g d,1, which would correspond to a 9-kg weight loss by 18 months. However, compensatory mechanisms appear to operate because in trials lasting one year or longer, fat consumption within the range of 18,40% of energy has consistently had little, if any, effect on body fatness. Moreover, within the United States (US), a substantial decline in the percentage of energy from fat during the last two decades has corresponded with a massive increase in obesity, and similar trends are occurring in other affluent countries. Diets high in fat do not account for the high prevalence of excess body fat in Western countries; reductions in the percentage of energy from fat will have no important benefits and could further exacerbate this problem. The emphasis on total fat reduction has been a serious distraction in efforts to control obesity and improve health in general. [source] Orlistat 120 mg improves glycaemic control in type 2 diabetic patients with or without concurrent weight lossDIABETES OBESITY & METABOLISM, Issue 4 2009S. Jacob Background:, Both obesity and type 2 diabetes are associated with increased morbidity and mortality. Published data suggest that orlistat 120 mg, a lipase inhibitor used to treat obesity, may improve glycaemic parameters through weight loss,independent effects. Aim:, To investigate the effect of orlistat 120 mg on weight loss, and assess whether changes in glycaemic parameters [fasting plasma glucose (FPG) and haemoglobin A1c (HbA1c)] are independent of weight loss. Methods:, This retrospective analysis of pooled data from seven multicentre, double-blind, placebo-controlled studies involved overweight or obese patients with type 2 diabetes (aged 18,70 years). Patients were required to have a body mass index of 27,43 kg/m2, HbA1c of 6.5 to <13%, and stable weight for ,3 months. Subjects received orlistat 120 mg tid or placebo for 6 or 12 months. Results:, A total of 2550 overweight or obese patients with type 2 diabetes were enrolled and randomized to treatment with orlistat 120 mg tid (n = 1279) or placebo (n = 1271). For the whole population, patients treated with orlistat 120 mg had significantly greater mean decreases in FPG compared with placebo-treated patients (,1.39 mmol/l vs. ,0.47 mmol/l; p < 0.0001). In addition, orlistat 120 mg provided significantly larger mean decreases in HbA1c compared with placebo (,0.74% vs. ,0.31%; p < 0.0001). For patients with minimal weight loss (,1% of baseline body weight), orlistat 120 mg still provided a significantly greater decrease in the least squares mean value for both FPG (,0.83 mmol/l vs. ±0.02 mmol/l; p = 0.0052) and HbA1c,0.29% vs. ±0.14%; p = 0.0008). This suggested that the improvement of glycaemic control with orlistat 120 mg was independent of weight loss. Using linear regression analysis, improvement in glycaemic control (FPG and HbA1c) with orlistat 120 mg was less strongly correlated with weight loss than for placebo. Conclusion:, Orlistat 120 mg appears to improve glycaemic control more than would be predicted by weight loss alone in overweight or obese patients with type 2 diabetes. Postulated mechanisms underlying this effect include an improvement of insulin sensitivity, a slower and incomplete digestion of dietary fat, reduction of postprandial plasma non-esterified fatty acids, decreased visceral adipose tissue, and stimulation of glucagon-like peptide-1 secretion in the lower small intestine. [source] Diabetes: insulin resistance and derangements in lipid metabolism.DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 1 2005Cure through intervention in fat transport, storage Abstract We present multiple findings on derangements in lipid metabolism in type 2 diabetes. The increase in the intracellular deposition of triglycerides (TG) in muscles, liver and pancreas in subjects prone to diabetes is well documented and demonstrated to attenuate glucose metabolism by interfering with insulin signaling and insulin secretion. The obesity often associated with type 2 diabetes is mainly central, resulting in the overload of abdominal adipocytes with TG and reducing fat depot capacity to protect other tissues from utilizing a large proportion of dietary fat. In contrast to subcutaneous adipocytes, the central adipocytes exhibit a high rate of basal lipolysis and are highly sensitive to fat mobilizing hormones, but respond poorly to lipolysis restraining insulin. The enlarged visceral adipocytes are flooding the portal circulation with free fatty acids (FFA) at metabolically inappropriate time, when FFA should be oxidized, thus exposing nonadipose tissues to fat excess. This leads to ectopic TG accumulation in muscles, liver and pancreatic beta-cells, resulting in insulin resistance and beta-cell dysfunction. This situation, based on a large number of observations in humans and experimental animals, confirms that peripheral adipose tissue is closely regulated, performing a vital role of buffering fluxes of FFA in the circulation. The central adipose tissues tend to upset this balance by releasing large amounts of FFA. To reduce the excessive fat outflow from the abdominal depots and prevent the ectopic fat deposition it is important to decrease the volume of central fat stores or increase the peripheral fat stores. One possibility is to downregulate the activity of lipoprotein lipase, which is overexpressed in abdominal relatively to subcutaneous fat stores. This can be achieved by gastrointestinal bypass or gastroplasty, which decrease dietary fat absorption, or by direct means that include surgical removal of mesenteric fat. Indirect treatment consists of the compliant application of drastic lifestyle change comprising both diet and exercise and pharmacotherapy that reduces mesenteric fat mass and activity. The first step should be an attempt to effectively induce a lifestyle change. Next comes pharmacotherapy including acarbose, metformin, PPAR,, or PPAR,, agonists, statins and orlistat, estrogens in postmenopausal women or testosterone in men. Among surgical procedures, gastric bypass has been proven to produce beneficial results in advance of other surgical techniques, the evidence basis of which still needs strengthening. Copyright © 2004 John Wiley & Sons, Ltd. [source] Dorothy Hodgkin Lecture 2008 Gastric inhibitory polypeptide (GIP) revisited: a new therapeutic target for obesity,diabetes?DIABETIC MEDICINE, Issue 7 2008P. R. Flatt Abstract There is increasing realization that gastric inhibitory polypeptide (GIP) has actions outside of the pancreas and gastrointestinal tract. Most significant is the presence of functional GIP receptors on adipocytes and the appreciation that GIP, secreted strongly in response to fat ingestion, plays a role in the translation of excessive amounts of dietary fat into adipocyte tissue stores. Such effects open up the possibility of exploiting GIP receptor antagonism for the treatment of obesity and insulin resistance. This is borne out by studies in high-fat-fed mice or ob/ob mice with either genetic knockout of GIP receptor or chemical ablation of GIP action using the GIP receptor antagonist, (Pro3)GIP. By causing preferential oxidation of fat, blockade of GIP signalling clears triglyceride deposits from liver and muscle, thereby respectively restoring mechanisms for suppression of hepatic glucose output and cellular glucose uptake. Further studies are needed to determine the applicability of this research to human obesity,diabetes. However, proof of concept is provided by emerging evidence that rapid cure of diabetes in grossly obese subjects undergoing Roux-en-Y bypass surgery is mediated in part by surgical bypass of GIP-secreting K-cells in the upper small intestine. [source] The benefits of oestrogens on postprandial lipid metabolism are lost in post-menopausal women with Type 2 diabetesDIABETIC MEDICINE, Issue 7 2006M. G. Masding Abstract Aims, Women with Type 2 diabetes appear to lose the protection against cardiovascular disease (CVD) afforded by oestrogens. We examined the effects of oestrogen hormone replacement therapy (HRT) on postprandial clearance of dietary fat in non-diabetic and diabetic post-menopausal women. Methods, In a cross-sectional study, fasting subjects [HRT+ and HRT, control and diabetic women; Type 2 diabetes (DM) HRT+n = 8, DM HRT,n = 14, control HRT+n = 7, control HRT,n = 11] consumed a meal containing the stable isotope 1,1,1,[13]C-tripalmitin, with blood and breath sampled for 6 and 24 h, respectively, in the postprandial period. Results, In diabetic women, there were no differences between the HRT+ and HRT, groups for any of these parameters. In contrast, in HRT+ compared with HRT, control women, the triglyceride (TG) area under the curve was lower [AUC; HRT+ median (range) 7.7 (4.1, 12.8) mmol/l per 6 h, HRT, 9.7 (3.9, 18.5) mmol/l per 6 h, P < 0.05] and [13]C-palmitic acid in the TG fraction was also lower [HRT+ 23.2 (10.3, 41.3) ng/ml per 6 h, HRT, 47.7 (12.6, 77.2) ng/ml per 6 h, P < 0.05], suggesting the lower postprandial triglyceridaemia associated with HRT in non-diabetic women is because of better chylomicron clearance. Conclusions, The oestrogen-associated advantage in clearance of dietary lipid we observed in non-diabetic post-menopausal women is not seen in post-menopausal diabetic women. This is likely to promote an atherogenic lipoprotein profile and may contribute to the loss of CVD protection seen in diabetic women. [source] The implementation of nutritional advice for people with diabetesDIABETIC MEDICINE, Issue 10 2003Nutrition Subcommittee of the Diabetes Care Advisory Committee of Diabetes UK Abstract These consensus-based recommendations emphasize the practical implementation of nutritional advice for people with diabetes, and describe the provision of services required to provide the information. Important changes from previous recommendations include greater flexibility in the proportions of energy derived from carbohydrate and monounsaturated fat, further liberalization in the consumption of sucrose, more active promotion of foods with a low glycaemic index, and greater emphasis on the provision of nutritional advice in the context of wider lifestyle changes, particularly physical activity. Monounsaturated fats are now promoted as the main source of dietary fat because of their lower susceptibility to lipid peroxidation and consequent lower atherogenic potential. Consumption of sucrose for patients who are not overweight can be increased up to 10% of daily energy derived from carbohydrate provided that this is eaten in the context of a healthy diet and distributed throughout the day. Evidence is presented for the effectiveness of advice provided by trained dieticians. The increasing evidence for the importance of good metabolic control and the growing requirement for measures to prevent Type 2 diabetes in an increasingly obese population will require major expansion of dietetic services if the standards in National Service Frameworks are to be successfully implemented. [source] Postprandial lipemic response to alpha-linolenic acid rich oil, butter, and olive oilEUROPEAN JOURNAL OF LIPID SCIENCE AND TECHNOLOGY, Issue 9 2010Julia Svensson Abstract Postprandial lipemia varies with composition of dietary fat due to partitioning of fatty acids between ,-oxidation, incorporation into TAG, and tissue lipids. Effects of alpha-linolenic acid (ALA) are poorly characterized. Lipase-catalyzed transesterification was used to produce a novel ALA-oil (35% ALA) from rapeseed and linseed oil. We hypothesized a lower postprandial lipemic response with ALA-oil than with olive oil and butter due to higher ,-oxidation of ALA. A randomized crossover study with 26 healthy men compared the effects on plasma lipids 7,h after a breakfast containing 35,g ALA-rich oil, butter fat, or olive oil. The incremental area under curve for plasma TAG was lower with butter than with olive oil (34%, p<0.05) and ALA-oil (25%, ns). After ALA-oil percentage ALA increased, in TAG to a constant level of 7,mol% and in NEFA to 6% after 7,h. Since total NEFA increased with time the amount of exogenous ALA in NEFA also increased. Butter resulted in lower postprandial lipemia than the oils, the difference exceeding what is expected from the presence of short and medium chain fatty acids in butter. There was a considerable recirculation of ALA into the NEFA pool available for oxidation. Practical application: Enzymatic transesterification was used to produce a dietary oil rich in ALA. By randomizing the partitioning of ALA more evenly between the TAG molecules the risk of oxidation could be reduced. Analyses showed that the ALA-oil was stable during storage for at least 3 months. Enzymatic transesterification could be used as an advantageous method to design an ALA rich dietary oil with new properties regarding fatty acid composition, susceptibility to oxidation, and effects on blood lipids. [source] Skin surface lipids and skin and hair coat condition in dogs fed increased total fat diets containing polyunsaturated fatty acidsJOURNAL OF ANIMAL PHYSIOLOGY AND NUTRITION, Issue 4 2009N. A. Kirby Summary It is generally believed that diets containing increased amounts of polyunsaturated fatty acids (PUFA) result in improved canine skin and hair coat (SHC). However, the extent to which dietary fat amount and type play a role remains to be systematically investigated. The objective of this study was to investigate the role of both increased dietary fat amount and type on SHC assessments of dogs. Improvements of SHC conditions were investigated after feeding three diets containing increased total dietary fat (i.e. 13% total fat) for 12 weeks in relation to a lower fat acclimation diet (i.e. 9% total fat). The higher fat diets varied in polyunsaturated and saturated fat types and amounts but total fat was kept constant. Skin and hair coat assessments were performed at selected intervals by a trained group of veterinarians and graduate students. In addition, hair lipids were fractionated by thin layer chromatography after extraction of plucked hair samples. Significant improvements were found in hair coat glossiness and softness in all dogs fed the higher fat diets in relation to the acclimation diet. Improvements as a result of fat type were also seen but only at 12 weeks. A parallel finding was a marked increase in hair cholesteryl ester content determined at the end of the study at which time SHC scores were significantly improved. Skin and hair coat condition improvements may thus be related to increased cholesteryl ester deposited on the hair shaft surface when high fat diets are fed. Whereas this finding is preliminary, hair lipid analysis may be a useful, non-invasive technique with which to help assess dietary effects on canine SHC. [source] Changes in amino acid composition in the tissues of African catfish (Clarias gariepinus) as a consequence of dietary L-carnitine supplementsJOURNAL OF APPLIED ICHTHYOLOGY, Issue 3 2002R. O. A. Ozório A study was undertaken to examine the effect of different amounts of dietary lysine (13 and 21 g kg,1 diet), lipid (80 and 160 g kg,1 diet) and L -carnitine (0.2 and 1.0 g kg,1 diet) on growth performance, proximate composition and amino acid metabolism of the African catfish (Clarias gariepinus). Juvenile African catfish (23 ± 1.5 g/fish) were stocked into 70-L aquaria (16 aquaria, 28 fish/aquarium) connected to a recirculation system during a maximum period of 74 days. All groups were fed at a level of 24 g kg,0.8 day,1 in an experiment run at pair feeding. Animals receiving 1.0 g carnitine accumulated up to six times more carnitine in their tissues than animals receiving 0.2 g (P < 0.05). Acyl-carnitine and free L -carnitine levels increased in the whole body and in tissues. Dietary L -carnitine supplements increased protein-to-fat ratios in the body, but did not affect growth rate. Protein-to-fat ratios were only affected when the biosynthesis capacity of L -carnitine was restricted due to low lysine levels and when there was a shortage of dietary fat. When lysine was offered at 21 g kg,1 feed, dietary L -carnitine supplements did not affect the amino acid concentrations of body tissues. Dietary L -carnitine supplements raised the concentration of glutamic acid,>,aspartic acid,>,glycine > alanine > arginine > serine > threonine in skeletal muscle tissue (P < 0.05). Total amino acid concentration in muscle and liver tissues (dry-matter basis) increased from 506 to 564 and from 138 to 166 mg g,1, respectively, when diets were offered with high L -carnitine, low lysine and low fat levels. These data suggest that dietary L -carnitine supplementation may increase fatty acid oxidation and possibly decrease amino acid combustion for energy. [source] Does the capacity for energy utilization affect the survival of post-smolt Atlantic salmon, Salmo salar L., during natural outbreaks of infectious pancreatic necrosis?JOURNAL OF FISH DISEASES, Issue 7 2007K-A Rřrvik Abstract If osmotic stress and reduced seawater tolerance are predisposing factors for infectious pancreatic necrosis (IPN) outbreaks in farmed Atlantic salmon, increased survival by enhancing access to energy would be expected. The aim of the present study was, therefore, to increase energy access in 1-year old Atlantic salmon after sea transfer by increasing the level of dietary fat, by exchanging some of the dietary oil with more easily oxidized medium chain triacylglycerols, or by dietary supplementation of potentially energy enhancing additives such as clofibrate and tetradecylthioacetic acid (TTA). A natural outbreak of IPN occurred 8 weeks after sea transfer, and a significant dietary effect explaining 76% of the variation in mortality was observed. Relative percentage survival for the fish fed TTA in sea water was 70% when compared with the unsupplemented control, reducing mortality from 7.8 to 2.3%. Muscle fat content and plasma chloride were related to IPN mortality, suggesting that reduced hypoosmoregulatory capacity might be a predisposing factor to the onset of an IPN outbreak. Based on the observation of a threefold increase in white muscle mitochondrial fatty acid oxidizing activity by TTA, it is suggested that TTA has resulted in a re-allocation of dietary fatty acids from storage to energy producing oxidation. [source] Gastro-oesophageal reflux disease in AsiaJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 3 2000Khean-Lee Goh Abstract Gastro-oesophageal reflux disease (GORD) occurs more frequently in Europe and North America than in Asia but its prevalence is now increasing in many Asian countries. Many reasons have been given for the lower prevalence of GORD in Asia. Low dietary fat and genetically determined factors, such as body mass index and maximal acid output, may be important. Other dietary factors appear to be less relevant. Increased intake of carbonated drinks or aggravating medicines may influence the increasing rates of GORD in some Asian countries but no strong evidence links other factors, such as the age of the population, smoking or alcohol consumption, to GORD. The management of GORD in Asia is similar to that in Europe and North America but the lower incidence of severe oesophagitis in Asia may alter the approach slightly. Also, because Asians tend to develop stomach cancer at an earlier age, endoscopy is used routinely at an earlier stage of investigation. Gastro-oesophageal reflux disease is essentially a motility disorder, so short-term management of the disease can usually be achieved using prokinetic agents (or histamine (H2)-receptor antagonists). More severe and recurrent GORD may require proton pump inhibitors (PPI) or a combination of prokinetic agents and PPI. The choice of long-term treatment may be influenced by the relative costs of prokinetic agents and PPI. © 2000 Blackwell Science Asia Pty Ltd [source] Personalized nutrition for the prevention of cardiovascular disease: a future perspectiveJOURNAL OF HUMAN NUTRITION & DIETETICS, Issue 4 2008J. A. Lovegrove Abstract Cardiovascular disease (CVD) is responsible for significant morbidity and mortality in the Western and developing world. This multi-factorial disease is influenced by many environmental and genetic factors. At present, public health advice involves prescribed population-based recommendations, which have been largely unsuccessful in reducing CVD risk. This is, in part, due to individual variability in response to dietary manipulations, that arises from nutrient,gene interactions (defined by the term ,nutrigenetics'). The shift towards personalized nutritional advice is a very attractive proposition, where, in principle, an individual can be given dietary advice specifically tailored to their genotype. However, the evidence-base for the impact of interactions between nutrients and fixed genetic variants on biomarkers of CVD risk is still very limited. This paper reviews the evidence for interactions between dietary fat and two common polymorphisms in the apolipoprotein E and peroxisome proliferator-activated receptor-, genes. Although an increased understanding of how these and other genes influence response to nutrients should facilitate the progression of personalized nutrition, the ethical issues surrounding its routine use need careful consideration. [source] Comparison of dietary fat and fatty acid intake estimated by the duplicate diet collection technique and estimated dietary recordsJOURNAL OF HUMAN NUTRITION & DIETETICS, Issue 6 2003L. M. Brady Abstract Introduction A high saturated fatty acid intake is a well recognized risk factor for coronary heart disease development. More recently a high intake of n-6 polyunsaturated fatty acids (PUFA) in combination with a low intake of the long chain n-3 PUFA, eicosapentaenoic acid and docosahexaenoic acid has also been implicated as an important risk factor. Aim To compare total dietary fat and fatty acid intake measured by chemical analysis of duplicate diets with nutritional database analysis of estimated dietary records, collected over the same 3-day study period. Methods Total fat was analysed using soxhlet extraction and subsequently the individual fatty acid content of the diet was determined by gas chromatography. Estimated dietary records were analysed using a nutrient database which was supplemented with a selection of dishes commonly consumed by study participants. Results Bland & Altman statistical analysis demonstrated a lack of agreement between the two dietary assessment techniques for determining dietary fat and fatty acid intake. Conclusion The lack of agreement observed between dietary evaluation techniques may be attributed to inadequacies in either or both assessment techniques. This study highlights the difficulties that may be encountered when attempting to accurately evaluate dietary fat intake among the population. [source] Nutrition and diet in the clinical management of multiple sclerosisJOURNAL OF HUMAN NUTRITION & DIETETICS, Issue 5 2001A. Payne For many years, medical interest in the relationship between nutrition and multiple sclerosis (MS) has focused largely on aetiology and the influence of dietary fat on the rate and severity of disease. While the cause of MS remains unknown and the influence of dietary fat is unclear, recent studies on antioxidant intake and oxidative stress in MS are strengthening the rationale in support of a healthy eating regime following diagnosis. Dietary intake in MS and the influence of advanced disease on nutritional status are less well researched and documented. Both obesity and malnutrition may occur with detrimental consequences to functional abilities. Cognitive difficulties, dysphagia and the side-effects of drug treatment may further contribute to deterioration in nutritional status. This paper aims to provide a practical overview of dietary management in MS. It reviews the available evidence relating nutrition to MS and discusses dietary management, with particular emphasis on the identification and alleviation of factors affecting nutritional status. [source] Differential Effects of Restricted Versus Unlimited High-Fat Feeding in Rats on Fat Mass, Plasma Hormones and Brain Appetite RegulatorsJOURNAL OF NEUROENDOCRINOLOGY, Issue 7 2009T. Shiraev The rapid rise in obesity has been linked to altered food consumption patterns. There is increasing evidence that, in addition to total energy intake, the macronutrient composition of the diet may influence the development of obesity. The present study aimed to examine the impact of high dietary fat content, under both isocaloric and hypercaloric conditions, compared with a low fat diet, on adiposity, glucose and lipid metabolism, and brain appetite regulators in rats. Male Sprague,Dawley rats were exposed to one of three diets: control (14% fat), ad lib high-fat palatable (HFD, 35% fat) or high-fat palatable restricted (HFD-R, matched to the energy intake of control) and were killed in the fasting state 11 weeks later. Body weight was increased by 28% in unrestricted HFD fed rats, with an almost tripling of caloric intake and fat mass (P < 0.001) and double the plasma triglycerides of controls. Glucose intolerance and increased insulin levels were observed. HFD-R animals calorie matched to control had double their fat mass, plasma insulin and triglycerides (P < 0.05). Only ad lib consumption of the HFD increased the hypothalamic mRNA expression of the appetite-regulating peptides, neuropeptide Y and pro-opiomelanocortin. Although restricted consumption of palatable HFD had no significant impact on hypothalamic appetite regulators or body weight, it increased adiposity and circulating triglycerides, suggesting that the proportion of dietary fat, independent of caloric intake, affects fat deposition and the metabolic profile. [source] Increased Caloric Intake on a Fat-Rich Diet: Role of Ovarian Steroids and Galanin in the Medial Preoptic and Paraventricular Nuclei and Anterior Pituitary of Female RatsJOURNAL OF NEUROENDOCRINOLOGY, Issue 10 2007S. F. Leibowitz Previous studies in male rats have demonstrated that the orexigenic peptide galanin (GAL), in neurones of the anterior parvocellular region of the paraventricular nucleus (aPVN) projecting to the median eminence (ME), is stimulated by consumption of a high-fat diet and may have a role in the hyperphagia induced by fat. In addition to confirming this relationship in female rats and distinguishing the aPVN-ME from other hypothalamic areas, the present study identified two additional extra-hypothalamic sites where GAL is stimulated by dietary fat in females but not males. These sites were the medial preoptic nucleus (MPN), located immediately rostral to the aPVN, and the anterior pituitary (AP). The involvement of ovarian steroids, oestradiol (E2) and progesterone (PROG), in this phenomenon was suggested by an observed increase in circulating levels of these hormones and GAL in MPN and AP with fat consumption and an attenuation of this effect on GAL in ovariectomised (OVX) rats. Furthermore, in the same four areas affected by dietary fat, levels of GAL mRNA and peptide immunoreactivity were stimulated by E2 and further by PROG replacement in E2 -primed OVX rats and were higher in females compared to males. Because both GAL and PROG stimulate feeding, their increase on a fat-rich diet may have functional consequences in females, possibly contributing to the increased caloric intake induced by dietary fat. This is supported by the findings that PROG administration in E2 -primed OVX rats reverses the inhibitory effect of E2 on total caloric intake while increasing voluntary fat ingestion, and that female rats with higher GAL exhibit increased preference for fat compared to males. Thus, ovarian steroids may function together with GAL in a neurocircuit, involving the MPN, aPVN, ME and AP, which coordinate feeding behaviour with reproductive function to promote consumption of a fat-rich diet at times of increased energy demand. [source] Effects of microcrystalline plant sterol suspension and a powdered plant sterol supplement on hypercholesterolemia in genetically obese Zucker ratsJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 12 2003Jari Summanen ABSTRACT Because dietary fat appears to be an effective vehicle for dispensing plant sterols into the diet, a special plant-sterol-containing ingredient has recently been developed. This ingredient is a plant sterol suspension in oil in which the sterols are in microcrystalline form. The objective of the present study was to analyse the cholesterol-lowering effects and safety of two different plant sterol preparations, an orally administered microcrystalline plant sterol suspension (MPS) in rapeseed oil and a powdered plant sterol supplement, in obese Zucker rats. Dietary plant sterol supplements (0.5%, w/w) were given concurrently with a high cholesterol diet (HCD, 1% cholesterol and 18% fat, w/w). No significant changes in serum triglyceride, blood glucose, serum glutamate oxaloacetic transaminase and glutamic pyruvic transaminase values or body and liver weights were observed. The powdered plant sterol supplement lowered the serum cholesterol by 25% (P< 0.05) and the MPS diet by 35% (P< 0.001) compared with HCD by the end of the 12-week experiment. Interestingly, the plant sterol supplements also produced a marked reduction in serum ubiquinone levels, suggesting a possible effect on isoprene synthesis. Unlike the powdered plant sterol, both MPS and plain rape-seed oil decreased the serum baseline diene conjugation values, suggesting that they protect against oxidative stress-induced lipid peroxidation in rats. This lipid peroxidation diminishing effect is probably due to some antioxidative components in rapeseed oil. These findings indicate that an unesterified plant sterol, such as the microcrystalline suspension in oil, effectively prevents cholesterol absorption in obese Zucker rats. [source] Orexigenic Peptides and Alcohol Intake: Differential Effects of Orexin, Galanin, and GhrelinALCOHOLISM, Issue 11 2007Eve R. Schneider Background:, The question is which hypothalamic systems for food intake might play a role in ethanol intake and contribute to alcohol abuse. The peptide orexin was found to exhibit similar properties to galanin in its relation to dietary fat and may therefore be similar to galanin in having a stimulatory effect on alcohol intake. Methods:, Rats were trained to drink 10% ethanol, implanted with brain cannulas, and then injected in the paraventricular nucleus (PVN), lateral hypothalamus (LH), or nucleus accumbens (NAc) with galanin, orexin-A, and for comparison, ghrelin. Ethanol, food, and water intake were measured at 1, 2, and 4 hours postinjection. Results:, In the PVN, both orexin and galanin significantly increased ethanol intake, whereas ghrelin increased food intake. In the LH, orexin again induced ethanol intake, while ghrelin increased eating. In the NAc, orexin failed to influence ethanol intake but did stimulate food intake. Conclusions:, In ethanol-drinking rats, injection of orexin or galanin into the appropriate locus in the hypothalamus induced significant ethanol intake instead of food intake. Ghrelin, as a positive control, failed to influence ethanol intake at the same hypothalamic sites. In the NAc, as an anatomical control, orexin augmented eating but not ethanol intake. Thus orexin and galanin in the hypothalamus selectively stimulated ethanol intake at sites where other studies have shown that both ethanol and fat increase expression of the endogenous peptides. Thus, a neural circuit that evolved with the capability to augment food intake is apparently co-opted by ethanol and may serve as a potential positive feedback circuit for alcohol abuse. [source] Effect of Ethanol on Hypothalamic Opioid Peptides, Enkephalin, and Dynorphin: Relationship With Circulating TriglyceridesALCOHOLISM, Issue 2 2007Guo-Qing Chang Background: Recent evidence has demonstrated that ethanol intake can stimulate the expression and production of the feeding-stimulatory peptide, galanin (GAL), in the hypothalamic paraventricular nucleus (PVN), and that PVN injection of this peptide, in turn, can increase the consumption of ethanol. To test the hypothesis that other feeding-related systems are involved in ethanol intake, this study examined the effect of ethanol on the hypothalamic opioid peptides, enkephalin (ENK), and dynorphin (DYN). Method: Adult, male Sprague,Dawley rats were trained to voluntarily drink increasing concentrations of ethanol, up to 9% v/v, on a 12-hour access schedule or were given a single injection of ethanol (10% v/v) versus saline vehicle. The effect of ethanol on GAL, ENK, and DYN mRNA was measured using real-time quantitative polymerase chain reaction and radiolabeled in situ hybridization, while radioimmunoassay was used to measure peptide levels. In addition to blood alcohol, circulating levels of triglycerides (TG), leptin, and insulin were also measured. Results: The data demonstrated that: (1) rats voluntarily drinking 9% v/v ethanol (approximately 2.0 g/kg/d) show a significant increase in GAL, ENK, and DYN mRNA in the PVN compared with water-drinking rats; (2) voluntary consumption of ethanol also increases peptide levels of ENK and DYN in the PVN; (3) acute injection of 10% ethanol (1.0 g/kg of 10% v/v) similarly increases the expression of GAL, ENK, and DYN in the PVN; and (4) ethanol consumption and injection, while having little effect on leptin and insulin, consistently increase circulating levels of TG as well as alcohol, both of which are strongly, positively correlated with peptide expression in the PVN. Conclusions: These findings, together with published studies, suggest a possible role for hypothalamic opioid peptides in the drinking of ethanol. Based on evidence that dietary fat and lipid injections stimulate the PVN peptides and injection of the opiates and GAL increase ethanol intake, it is proposed that both TG and alcohol in the circulation, which are elevated by the ingestion or injection of ethanol, are involved in stimulating these peptides in the PVN, which in turn promote further consumption of ethanol. [source] Development of Alcoholic Fatty Liver and Fibrosis in Rhesus Monkeys Fed a Low n-3 Fatty Acid DietALCOHOLISM, Issue 10 2004Robert J. Pawlosky Background: The amount and type of dietary fat seem to be important factors that modulate the development of alcohol-induced liver steatosis and fibrosis. Various alcohol-feeding studies in animals have been used to model some of the symptoms that occur in liver disease in humans. Methods: Rhesus monkeys (Macaca mulatta) were maintained on a diet that had a very low concentration of ,-linolenic acid and were given free access to an artificially sweetened 7% ethanol solution. Control and ethanol-consuming animals were maintained on a diet in which the linoleate content was adequate (1.4% of energy); however, ,-linoleate represented only 0.08% of energy. Liver specimens were obtained, and the fatty acid composition of the liver phospholipids, cholesterol esters, and triglycerides of the two groups were compared at 5 years and histopathology of tissue samples were compared at 3 and 5 years. Results: The mean consumption of ethanol for this group over a 5-year period was 2.4 g · kg,1· day,1. As a consequence of the ethanol-dietary treatment, there were significantly lower concentrations of several polyunsaturated fatty acids in the liver phospholipids of the alcohol-treated group, including arachidonic acid and most of the n-3 fatty acids and particularly docosahexaenoic acid, when compared with dietary controls. Liver specimens from animals in the ethanol group at 5 years showed a marked degree of steatosis, both focal and diffuse cellular necrosis, and an increase in the development of fibrosis compared with specimens obtained at 3 years and with those from dietary controls, in which there was no evidence of fibrotic lesions. Conclusion: These findings suggest that the advancement of ethanol-induced liver disease in rhesus monkeys may be modulated by the amount and type of dietary essential fatty acids and that a marginal intake of n-3 fatty acids may be a permissive factor in the development of liver disease in primates. [source] Dietary Cholate Is Required for Antiatherogenic Effects of Ethanol in Mouse ModelsALCOHOLISM, Issue 9 2003Mark A. Deeg Background: Human consumption of moderate amounts of ethanol is associated with reduced cardiovascular events. Studies examining the effect of ethanol on atherosclerosis in mouse models have yielded conflicting results that may be due to differences in dietary fat and cholate content. To determine if dietary cholate influences ethanol's effect on atherosclerosis, we fed apolipoprotein E,/, and low-density lipoprotein receptor (LDLR),/, mice different liquid diets with or without ethanol. Methods: Apolipoprotein E,/, mice were fed a low-fat or high saturated fat, cholate-containing diet with or without ethanol for 3 to 10 weeks, and LDLR,/, mice were fed a low-fat, high saturated fat, or high saturated fat diet with cholate with or without ethanol for 7 weeks. At the end of the feeding study, aortic root lesion size was determined and compared with serum cholesterol, triglycerides, and high-density lipoprotein cholesterol. Because dietary cholate increases hepatic nuclear factor (NF)-,B and ethanol inhibits NF-,B, we also examined the effect of ethanol on aortic NF-,B binding activity. Results: Adding ethanol to a low-fat diet had no effect on lesion size. Similarly, ethanol had no effect on lesion size in LDLR,/, mice consuming a high saturated fat diet. Adding ethanol to a high-fat, cholate-containing diet for either strain resulted in a 25% to 50% reduction in lesion size. Dietary cholate increased and ethanol reduced NF-,B binding activity in the aorta. Conclusions: These results suggest that ethanol inhibits atherosclerosis in the presence of dietary cholate, which may occur via an anti-inflammatory mechanism. [source] Correlations of dietary patterns with prostate healthMOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 1 2008Maria Stacewicz-Sapuntzakis Abstract Both genetic and environmental influences may be involved in etiology of prostate health and prostate cancer. These include ethnic origin, family history, smoking, and diet. Adiposity and excess energy intake are potentially distinct risk factors and positive associations with prostate cancer risk for both were observed among case-control and cohort studies. Some epidemiological studies support an association between dietary fat, particularly saturated or animal fats, and prostate cancer risk. Of these, several suggest reduced risk with low-fat diets high in n-3 fatty acids and increased risk with high-fat diets rich in n-6 fatty acids. Others suggested association with higher meat intake, possibly due to heterocyclic amines and polycyclic aromatic hydrocarbons, produced during grilling or frying. Positive association of prostate cancer risk with dairy intake could involve ,-methylacyl-CoA racemase activity (required for ,-oxidation of phytanic acid present in dairy products and red meat) or the suppression of vitamin D activity by calcium. Inverse associations were observed with dietary intake of plant foods. These include cereals, soy products, and fruit and vegetable sources of carotenoids. Numerous plant constituents may act synergistically in the prevention and inhibition of prostate disorders. These diet-risk associations may lead to future individualized diet recommendations based upon genetic polymorphisms. [source] Nutrition in the genomics era: Cardiovascular disease risk and the Mediterranean dietMOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 10 2007Jose M. Ordovas Abstract The effect of dietary changes on phenotypes (i.e., plasma lipid measures, body weight and blood pressure) differs significantly between individuals. This phenomenon has been more extensively researched in relation to changes in dietary fat and plasma lipid concentrations for the prevention of cardiovascular disease (CVD) compared to other pathological conditions. Although common knowledge associates low fat diets with reductions in total and plasma LDL cholesterol, the clinical evidence shows dramatic inter-individual differences in response that are partially due to genetic factors. The discovery of the cardioprotective and other healthy properties of the Mediterranean diet has popularized the consumption of Mediterranean products such as olive oil. Molecular, clinical, and epidemiological studies have begun to shed some light about how various components of this diet may protect the cardiovascular system and to decrease the risk of other diseases such as cancer. However, it is also possible that the right combination of genetic, cultural, socioeconomic factors is needed to achieve full benefit. It has been proposed that the Mediterranean diet may be closer to the ancestral foods that were part of human development and our metabolism may have evolved to work optimally on such a diet rather than with the current diets richer in saturated fat and highly refined and processed foods. Therefore, it is possible that alleles that are associated with increase disease risk may be silenced in the presence of that more ancestral and traditional diet and lifestyle. This knowledge may provide the basis for successful public health as well individual approaches for disease prevention. [source] The RISCK study: testing the impact of the amount and type of dietary fat and carbohydrate on metabolic riskNUTRITION BULLETIN, Issue 2 2007S. A. Jebb [source] Influence of Dietary Fat on ,-Carotene Absorption and Bioconversion into Vitamin ANUTRITION REVIEWS, Issue 4 2002Judy D. Ribaya-Mercado Sc.D. Dietary fat facilitates the utilization of carotenoids and, based on serum ,-carotene or retinol responses following ingestion of meals containing carotene and fat sources, it has been reported that the amount of fat required in a meal may be minimal (,3-5 g). However, the dietary fat requirement for optimal carotene utilization in humans cannot be fully ascertained without longer-term dose-response studies that measure the changes in vitamin A body stores in response to varying levels of dietary fat. In humans, vitamin A body stores can be determined by use of stable isotope-dilution methods. Animal studies have shown that although the level of dietary fat has no effect on serum vitamin A concentrations of animals fed ,-carotene, higher liver vitamin A concentrations were found in those that ingested higher fat levels. Other factors that might influence the relationship of fat intake and ,-carotene utilization include the type of fat ingested, physicochemical properties of the carotenoid source, amount of carotene ingested, whether fat and ,-carotene sources are provided in the same meal, the presence of helminthic infections, age, and vitamin A status. [source] Nutrition and Physical Activity Interventions to Reduce Cardiovascular Disease Risk in Health Care Settings: A Quantitative Review with a Focus on WomenNUTRITION REVIEWS, Issue 7 2001Sara Wilcox Ph.D. The authors conducted a quantitative literature review of the impact of 32 diet and physical activity (PA) interventions delivered in health care settings on cardiovascular disease risk factors. Intervention effects were relatively modest but statistically significant for PA, body mass index or weight, dietary fat, blood pressure, and total and low-density lipoprotein serum cholesterol. Intervention effects were generally larger for samples with a mean age >50 years and for studies with <6 months follow-up. Type of comparison group, type of intervention, and use of a behavior theory did not have a consistent impact on intervention effects. Few studies focused on persons of color, although the results from these studies are promising. [source] Dietary fat plays a major role in obesity: noOBESITY REVIEWS, Issue 2 2002W. C. Willett Summary The percentage of dietary energy from fat has been suggested to be an important determinant of body fat, and this presumed effect has been invoked to justify the general promotion of low-fat diets. Dietary fat and the prevalence of obesity are lower in poor countries than in affluent countries. However, these contrasts are seriously confounded by differences in physical activity and food availability; within areas of similar economic development, per capita intake of fat and the prevalence of obesity have not been positively correlated. Randomized trials are the preferable method for evaluating the effect of dietary fat on adiposity because they avoid problems of confounding that are difficult to control in other studies. In short-term trials, a small reduction in body weight is typically seen in individuals randomized to diets with a lower percentage of calories from fat. In a meta-analysis of these trials, it was estimated that a decrease in 10% of energy from fat would reduce weight by 16 g d,1, which would correspond to a 9-kg weight loss by 18 months. However, compensatory mechanisms appear to operate because in trials lasting one year or longer, fat consumption within the range of 18,40% of energy has consistently had little, if any, effect on body fatness. Moreover, within the United States (US), a substantial decline in the percentage of energy from fat during the last two decades has corresponded with a massive increase in obesity, and similar trends are occurring in other affluent countries. Diets high in fat do not account for the high prevalence of excess body fat in Western countries; reductions in the percentage of energy from fat will have no important benefits and could further exacerbate this problem. The emphasis on total fat reduction has been a serious distraction in efforts to control obesity and improve health in general. [source] Effects of various corn distillers by-products on growth, feed efficiency, and body composition of channel catfish, Ictalurus punctatusAQUACULTURE NUTRITION, Issue 2 2010M.H. LI Abstract A study was conducted to examine the use of corn distillers' by-products in diets and the effects of additional dietary fat on channel catfish, Ictalurus punctatus, performance. Juvenile channel catfish (initial weight: 12.6 g per fish) were stocked in flow-through aquaria and fed one of six practical diets for 9 weeks. Fish fed the control + fat diet consumed more diet and had higher feed efficiency ratio (FER) than fish fed the control diet, but weight gain was not significantly different between fish fed these two diets. Fish fed the diet containing 300 g kg,1 distillers dried grains with solubles (DDGS) consumed more diet and gained more weight, but had similar FER compared with fish fed the control + fat diet. The diet containing 200 g kg,1 high-protein distillers grains (HPDDG) resulted in similar diet consumption, weight gain and FER as the control + fat diet. Fish fed the diet containing 100 g kg,1 distillers solubles (DS) consumed more diet, but had similar weight gain and FER compared with fish fed the 300 g kg,1 DDGS diet. The presence of distillers solubles in the diet (300 g kg,1 DDGS, 100 g kg,1 DS, 100 g kg,1 EDS diets) appears to increase diet consumption, weight gain, and FER over the control diets with or without additional fat. [source] | ||||||||||||||||||||||||||||