Phosphorus Supplementation Mitigates Perivascular Adipose Inflammation-Induced Cardiovascular Consequences in Early Metabolic Impairment.

Background The complexity of the interaction between metabolic dysfunction and cardiovascular complications has long been recognized to extend beyond simple perturbations of blood glucose levels. Yet, structured interventions targeting the root pathologies are not forthcoming. Growing evidence implicates the inflammatory changes occurring in perivascular adipose tissue (PVAT) as early instigators of cardiovascular deterioration. Methods and Results We used a nonobese prediabetic rat model with localized PVAT inflammation induced by hypercaloric diet feeding, which dilutes inorganic phosphorus (Pi) to energy ratio by 50%, to investigate whether Pi supplementation ameliorates the early metabolic impairment. A 12-week Pi supplementation at concentrations equivalent to and twice as much as that in the control diet was performed. The localized PVAT inflammation was reversed in a dose-dependent manner. The increased expression of UCP1 (uncoupling protein1), HIF-1α (hypoxia inducible factor-1α), and IL-1ß (interleukin-1ß), representing the hallmark of PVAT inflammation in this rat model, were reversed, with normalization of PVAT macrophage polarization. Pi supplementation restored the metabolic efficiency consistent with its putative role as an UCP1 inhibitor. Alongside, parasympathetic autonomic and cerebrovascular dysfunction function observed in the prediabetic model was reversed, together with the mitigation of multiple molecular and histological cardiovascular damage markers. Significantly, a Pi-deficient control diet neither induced PVAT inflammation nor cardiovascular dysfunction, whereas Pi reinstatement in the diet after a 10-week exposure to a hypercaloric low-Pi diet ameliorated the dysfunction. Conclusions Our present results propose Pi supplementation as a simple intervention to reverse PVAT inflammation and its early cardiovascular consequences, possibly through the interference with hypercaloric-induced increase in UCP1 expression/activity.

Urinary minerals excretion among primary schoolchildren in Dubai-United Arab Emirates.

INTRODUCTION: Urinary excretion of calcium (Ca), magnesium (Mg), phosphorus (P), iodine and fluoride is used to assess their statuses and/or the existence of metabolic abnormalities. In the United Arab Emirates (UAE), the urinary concentration of these minerals among children have not been documented. MATERIALS AND METHODS: A cross-sectional study, including 593 subjects (232 boys and 361 girls), was conducted among healthy 6 to 11-year-old Emirati children living in Dubai. Non-fasting morning urine samples and anthropometrical measurements were collected and analyzed. Results were expressed as per mg of creatinine (Cr). RESULTS: On average, estimated Cr excretion was 17.88±3.12 mg/kg/d. Mean urinary Ca/Cr, Mg/Cr and P/Cr excretions were 0.08±0.07 mg/mg, 0.09±0.04 mg/mg, and 0.57±0.26 mg/mg respectively. Urinary excretion of Ca, Mg and P were found to decrease as age increased. Urinary excretion and predicted intake of fluoride were lower than 0.05 mg/kg body weight per day. Surprisingly, more than 50% of the children were found to have urinary iodine excretion level above adequate. CONCLUSION: The Emirati schoolchildren had comparable levels of urinary Ca, Mg and P excretion to other countries. The 95% percentile allows the use of the current data as a reference value for the detection of mineral abnormalities. Fluoride excretion implies that Emirati children are at low risk of fluorosis. The level of urinary iodine excretion is slightly higher than recommended and requires close monitoring of the process of salt iodization to avoid the harmful impact of iodine overconsumption.

Iron Fortification and Supplementation: Fighting Anemia of Chronic Diseases or Fueling Obesity?

The significant worldwide increase in obesity has become a major health problem. Excess adiposity has been extensively linked to inflammation. Recently, studies have shown that dietary intake and microbiota dysbiosis can affect the health of the gut and lead to low-grade systemic inflammation, worsening the state of obesity and further exacerbating inflammation. The latter is shown to decrease iron status and potentially increase the risk of anemia by inhibiting iron absorption. Hence, anemia of obesity is independent of iron intake and does not properly respond to increased iron ingestion. Therefore, countries with a high rate of obesity should assess the health impact of fortification and supplementation with iron due to their potential drawbacks. This review tries to elucidate the relation between inflammation and iron status to better understand the etiology of anemia of obesity and chronic diseases and wisely design any dietary or medical interventions for the management of anemia and/or obesity.

The effect of central obesity on inflammation, hepcidin, and iron metabolism in young women.

BACKGROUND/OBJECTIVES: In overweight and obesity (OW/OB), greater total body fat predicts higher serum hepcidin (SHep) which can impair iron homeostasis and increase risk for iron deficiency (ID). However, the effect of body fat distribution on SHep and iron homeostasis is unclear. In central obesity, interleukin (IL)-6 released from visceral adipose tissue into portal blood could strongly stimulate hepatic hepcidin synthesis. Thus, our hypothesis was that higher amounts of android fat, rather than gynoid fat, would predict impaired iron metabolism in OW/OB. SUBJECTS/METHODS: In this cross-sectional study, we enrolled 117 otherwise-healthy women into two groups: normal weight; BMI < 25 (n = 36) and OW/OB; BMI ≥ 25 (n = 81); we then subdivided the OW/OB using DEXA into tertiles based on the ratio of android fat/total body fat (AF/TBF). We measured inflammation and iron status, and assessed iron absorption in two ways: by measuring erythrocyte isotope incorporation from a labeled test meal containing 6 mg 57Fe (representing dietary iron); and by measuring change in serum iron (ΔSeFe) after a 100 mg oral iron challenge (representing supplemental iron). RESULTS: Greater AF/TBF correlated with higher CRP, AGP, SHep, and TIBC, and lower transferrin saturation and SeFe/SHep ratio (for all, p < 0.05). Greater AF/TBF correlated with lower supplemental iron absorption (ΔSeFe) (p = 0.08) but not lower dietary iron absorption. In multiple regressions, AF/TBF positively predicted CRP (p < 0.001) and SHep (p < 0.05); a model including AF/TBF and serum ferritin as covariates explained 65% of the variance in SHep. AF/TBF negatively predicted TSAT (p < 0.05) and iron absorption (ΔSeFe) (p = 0.07). In contrast, the ratio of gynoid fat/total body fat was not significantly associated with these variables. CONCLUSION: Body fat distribution affects iron metabolism: women with greater central adiposity have higher SHep, greater impairments in iron homeostasis, and reduced iron absorption from a supplemental iron dose.

Concomitant lysine and phosphorus addition to a wheat gluten protein diet highly amplified growth measures of rats.

OBJECTIVE: In humans, the effects of lysine-fortified wheat on growth measures was much lower than that of animal experimentations that used phosphorus-containing mineral mix. It is known that wheat contains a limited amount of available phosphorus, which is believed to support growth. The aim of this study was to determine the involvement of phosphorus in growth measures of rats maintained on a lysine-supplemented wheat gluten diet. METHODS: Forty male Sprague-Dawley (6 wk old) rats were randomly divided into four equal groups and fed wheat gluten protein (10%)-based diets with added lysine (0.6%), phosphorus (0.3%), or both (0.6% lysine and 0.3% phosphorus), ad libitum for 9 wk. Rats were monitored for changes in food intake, body weight, body and liver compositions, plasma urea nitrogen, and albumin. RESULTS: The addition of lysine or phosphorus to wheat gluten-based diets increased energy intake modestly (∼15%), whereas their combination caused a higher increase (∼45%). Similarly, the magnitude of improvement in weight gain and energy efficiency by the addition of lysine or phosphorus (∼1g/d and 2.7g/MJ, respectively) was much lower than that of the combination (∼4g/d and 8.7g/MJ). In the phosphorus-containing groups, plasma urea nitrogen was significantly reduced and this was associated with higher body protein (%) and hepatic fat (%); whereas plasma albumin was significantly increased in the lysine-containing groups. CONCLUSION: When using gluten protein, concomitant lysine and phosphorus availability is required to support growth measures, although phosphorus seems to have an independent effect on protein metabolism. Thus, human interventions should consider the improvement of the amino acid profile and phosphorus availability.

Phosphorus ingestion with a high-carbohydrate meal increased the postprandial energy expenditure of obese and lean individuals.

OBJECTIVES: Phosphorus ingestion with glucose was reported to stimulate the postprandial peripheral uptake of both phosphorus and glucose, a process that favors energy production. The aim of this study was to determine whether phosphorus ingestion with a meal can affect energy metabolism. METHODS: Overnight fasted men (eight lean and seven obese) consumed a high-carbohydrate meal (648 kcal) with either placebo or phosphorus (500 mg) tablets in a random order. Energy expenditure and substrate oxidation were monitored for 240 min using ventilated hood indirect calorimetry. RESULTS: Phosphorus ingestion with a meal increased the postprandial energy expenditure of both lean and obese individuals (P < 0.001), although in different patterns. Alterations in postprandial substrate oxidation was highly noticeable from time 120 min onward, where phosphorus-treated lean participants exhibited a significant decrease in respiratory quotient. CONCLUSION: Phosphorus ingestion with a high-carbohydrate meal alters postprandial energy metabolism mainly by enhancing postprandial energy expenditure that may ultimatly favor weight loss.

Postprandial energy expenditure of protein is affected by its phosphorus content.

Postprandial energy expenditure (PEE) is largely dependent on ATP production, which is may be affected by phosphorus (P) availability. Proteins are known to have high levels of P and induce high levels of PEE. This study aimed at assessing the effect of P in PEE of normal and high protein meals. A single-blind randomized crossover study was conducted with two groups of 12 healthy lean male subjects who received iso-caloric (554 Kcal) meals. Group1: normal protein (NPr) meal with or without P (500 mg) and group 2: high protein (HPr) meal with or without P (500 mg), on two visits separated by a minimum of 1-week washout period. Energy expenditure and substrate oxidation were measured at baseline and every 30 min for 4 h after meal ingestion using a ventilated hood for indirect calorimetry. NPr and HPr meals had similar postprandial energy expenditure and this was significantly increased (P = 0.005) by P ingestion. Our work shows that PEE of protein meal is highly affected by P content of the meal.

Lebanese children are iodine deficient and urinary sodium and fluoride excretion are weak positive predictors of urinary iodine.

PURPOSE: To assess iodine and fluoride status among Lebanese children. METHODS: A nationally representative cross-sectional study of 6- to 10-year-old schoolchildren was conducted using multistage cluster sampling. Spot urine samples were collected from 1403 children, and urinary iodine, fluoride, creatinine and sodium levels were measured. Salt samples from markets (n = 30) were tested for iodine concentration by titration. RESULTS: Median urinary iodine concentration was 66.0 µg/l, indicating mild deficiency, and almost 75 % of Lebanese children had a urinary iodine concentration (UIC) <100 µg/l. UIC was higher among children from private schools and in areas of higher socioeconomic status. Most salt samples were fortified at levels far below the legislated requirement, and 56 % of samples contained less than 15 ppm iodine. Fluoride-to-creatinine ratio (F/Cr) was 0.250 (0.159-0.448) mg/g. There were weak positive correlations between UIC and urinary sodium (r 2 = 0.039, P value <0.001) and UIC and urinary fluoride (r 2 = 0.009, P value <0.001). CONCLUSIONS: Lebanese elementary school children are iodine deficient due to inadequately iodized salt. The weak correlation between UIC and urinary sodium suggests most dietary iodine does not come from iodized salt. The poor correlation between UIC and urinary fluoride suggests that fluoride intake is not affecting iodine metabolism. Efforts are needed in Lebanon to improve industry compliance with salt fortification through improved monitoring and enforcement of legislation.

Phosphorus Supplementation Mitigated Food Intake and Growth of Rats Fed a Low-Protein Diet.

Background: Low protein intake is associated with various negative health outcomes at any life stage. When diets do not contain sufficient protein, phosphorus availability is compromised because proteins are the major sources of phosphorus. However, whether mineral phosphorus supplementation mitigates this problem is unknown, to our knowledge. Objective: Our goal was to determine the impact of dietary phosphorus supplementation on food intake, weight gain, energy efficiency, body composition, blood metabolites, and liver histology in rats fed a low-protein diet for 9 wk. Methods: Forty-nine 6-wk-old male Sprague-Dawley rats were randomly allocated to 5 groups and consumed 5 isocaloric diets ad libitum that varied only in protein (egg white) and phosphorus concentrations for 9 wk. The control group received a 20% protein diet with 0.3% P (NP-0.3P). The 4 other groups were fed a low-protein (10%) diet with a phosphorus concentration of 0.015%, 0.056%, 0.1%, or 0.3% (LP-0.3P). The rats' weight, body and liver composition, and plasma biomarkers were then assessed. Results: The addition of phosphorus to the low-protein diet significantly increased food intake, weight gain, and energy efficiency, which were similar among the groups that received 0.3% P (LP-0.3P and NP-0.3P) regardless of dietary protein content. In addition, phosphorus supplementation of low-protein diets reduced plasma urea nitrogen and increased total body protein content (defatted). Changes in food intake and efficiency, body weight and composition, and plasma urea concentration were highly pronounced at a dietary phosphorus content <0.1%, which may represent a critical threshold. Conclusions: The addition of phosphorus to low-protein diets improved growth measures in rats, mainly as a result of enhanced energy efficiency. A dietary phosphorus concentration of 0.3% mitigated detrimental effects of low-protein diets on growth parameters.

Phosphorus Supplementation Recovers the Blunted Diet-Induced Thermogenesis of Overweight and Obese Adults: A Pilot Study.

Diet-induced thermogenesis (DIT) is believed to be largely related to ATP production, which is dependent on phosphorus (P) availability. We aimed to test the effect of P addition on DIT of lean and overweight/obese healthy subjects. DIT was measured with or without P in 10 lean and 13 overweight/obese adults in a double-blind randomized cross-over pilot study with one week washout period. After 10 h overnight fast, resting metabolic rate, respiratory quotient, and substrate utilization were measured at fasting and every 30 min for 3 h after subjects drank a standardized glucose solution, with P (500 mg) or placebo pills. Subjective ratings of hunger and satiety were assessed before and after the end of each experiment using validated visual analogue scale (VAS) questionnaires. Overweight/obese subjects had a blunted DIT with placebo, while P supplementation induced a 23% increase in their DIT area under the curve (p < 0.05), which was associated with a significant increase in carbohydrate oxidation. Subjects had lower appetite following P supplementation, which was expressed as a significantly (p = 0.02) lower desire to eat a meal (4.0 ± 0.7 cm) compared with placebo (5.8 ± 0.9 cm). P supplementation recovers the blunted diet-induced thermogenesis in overweight and obese subjects and enhances their postprandial satiety.

Urinary Magnesium, Calcium, and Phosphorus to Creatinine Ratios of Healthy Elementary School Lebanese Children.

Urinary magnesium (Mg), calcium (Ca), and phosphorus (P) excretions are known to vary greatly between populations due to dietary habits, physical activity, mineral content of water, climate, genetics, and race. Thus, it is essential to determine the normal values in each population in order to assess the status as well as to diagnose any possible abnormality of metabolisms especially hypercalciuria. A study was conducted to determine urinary Mg/creatinine (Cr), Ca/Cr, and P/Cr ratios of healthy Lebanese elementary schoolchildren. Using a multi-stage cluster sampling at district, school, and class levels, a sample of 1403 children (781 boys and 622 girls), from 26 different schools, was selected. Non-fasting morning urine samples and anthropometric data were collected and analyzed. The mean Mg/Cr, Ca/Cr, and P/Cr ratios were 0.122 ± 0.075 mg/mg (0.568 ± 0.348 mM/mM), 0.084 ± 0.101 mg/mg (0.237 ± 0.286 mM/mM), and 0.692 ± 0.417 mg/mg (2.527 ± 1.524 mM/mM), respectively, with no significant difference between boys and girls (P = 0.706, 0.161, and 0.604; respectively). The 95th percentile of Mg/Cr, Ca/Cr, and P/Cr ratios fluctuated with age, showing a sharp decrease in Ca/Cr and P/Cr at the age of 10. The mean Mg/Cr, Ca/Cr, and P/Cr ratios were comparable to those of similar age groups in other populations. The 95th percentiles of Mg/Cr, Ca/Cr, and P/Cr ratios were 0.26 mg/mg (1.23 mM/mM), 0.27 mg/mg (0.76 mM/mM), and 1.48 mg/mg (5.40 mM/mM), respectively. These values can be used as cutoffs to detect abnormalities in these three minerals' metabolisms among healthy Lebanese children.

Phosphorus ingestion improves oral glucose tolerance of healthy male subjects: a crossover experiment.

BACKGROUND: Fasting serum phosphorus (P) was reported to be inversely related to serum glucose and insulin, while the impact of P ingestion is not well documented. The effect of P intake with or before glucose ingestion on postprandial glucose and insulin statuses was investigated. METHOD: Two cross over experiments using healthy male subjects were conducted. Experiment 1: Overnight fasted subjects (n = 7) randomly received: 500 mg of P tablets, glucose (75 g) solution with placebo or 500 mg of P tablets. Experiment 2: Overnight fasted subjects (n = 8) underwent similar procedures to those of experiment 1, except that placebo or 500 mg P tablets were given 60 min prior to glucose ingestion. RESULTS: In both experiments, serum P decreased following glucose ingestion. Co-ingestion of P with glucose improved, at time 60 min, postprandial glucose (P < 0.05), insulin (P < 0.05), and insulin sensitivity index (p < 0.006), while P pre-ingestion failed to exert similar effect. CONCLUSION: This study suggests that postprandial glucose and insulin are affected by exogenous P supply, especially when co-ingested with glucose.

Meal pattern of male rats maintained on amino acid supplemented diets: the effect of tryptophan, lysine, arginine, proline and threonine.

The macronutrient composition of the diet has been shown to affect food intake, with proteins having distinct effects. The present study investigated the effect of diet supplementation with individual amino acids (tryptophan, lysine, arginine, proline and threonine) on meal pattern among male rats. Meal pattern and body weight were monitored for two weeks. Proline and threonine had minimal effects on meal pattern, while the most pronounced changes were observed in the tryptophan group. Both tryptophan and lysine decreased overall food intake, which was translated into a reduction in body weight. The reduced food intake of the tryptophan group was associated with an increase in meal size, intermeal intervals (IMI) and meal time and a decrease in meal number. The decrease in the food intake of the lysine group was associated with a reduction in both IMI and meal number, and this was accompanied by an increase in meal time. Arginine increased meal number, while decreasing IMI. Proline and threonine had a minimal effect on meal pattern. Lysine seems to increase satiety, and arginine seems to decrease it, while tryptophan seems to increase satiety and decrease satiation. Accordingly, changes in meal patterns are associated with the type of amino acid added to the diet.

Phosphorus supplement alters postprandial lipemia of healthy male subjects: a pilot cross-over trial.

BACKGROUND: Epidemiological studies have found a U-shaped relationship between serum phosphorus and cardiovascular disease (CVD). The mechanism(s) behind such a relationship are poorly understood. Phosphorus (P) is reported to improve insulin sensitivity, which is involved in lipid metabolism, and thus we were interested in determining the impact of phosphorus ingestion on postprandial lipemia, a recognized CVD risk factor. FINDINGS: A within-subject study design was conducted, whereby 8 healthy male subjects received a high fat meal (330 Kcal; 69% energy from fat; 35 mg of phosphorus) with placebo or phosphorus (500 mg) in a random order. Postprandial blood samples (~10 ml) were collected every hour for 6 hours after meal ingestion. Changes in different parameters were analyzed using a 2-factor repeated-measure ANOVA. In the phosphorus (P) supplemented group, postprandial serum P increased (p=0.00), while changes in insulin, non-esterified fatty acids (NEFA) and triglyceride (TG) were not significantly different than that of placebo. Concurrently, phosphorus supplementation increased postprandial concentrations of apolipoprotein B48 (ApoB48) (p<0.05) and decreased that of apolipoprotein B100 (ApoB100) (p<0.05). CONCLUSIONS: Phosphorus supplementation (500 mg) of the meal seems to alter the different components of postprandial lipemia. These findings highlight the potential role of phosphorus in CVD.

Combined fish oil and high oleic sunflower oil supplements neutralize their individual effects on the lipid profile of healthy men.

Both n-3 and n-9 fatty acids share a common metabolic pathway and can potentially and individually improve cardiovascular disease risk factors. Dietary n-6 is known to weaken the efficacy of n-3 fatty acids due to competition for the same enzymes. Still unclear is whether a similar competition exists between n-3 and n-9 fatty acids. Thus, a 12-week intervention study was conducted to investigate the effect of different combinations of fish oil and high-oleic sunflower oil (OSO) on healthy subjects. Included were five groups (98 subjects): three groups received a fixed amount of n-9 (8 g/day) with varying amounts of n-3 (1, 2 or 4 g/day), one group was given n-3 fatty acids only (2 g/day) and another was given n-9 only (8 g/day). We found that fish oil supplement (2 g/day) was able to decrease TAG by about 13 %, this effect was diminished with the co-ingestion of n-9 (OSO). Intake of OSO (8 g/day) reduced both total and LDL cholesterol by about 10 %, this effect was reduced by the addition of fish oil. Both fish oil and OSO failed to have any significant effect on both glycemic and blood pressure parameters. In conclusion; the impact of oleic acid (n-9) on total and LDL cholesterol was altered by the addition fish oil (n-3). These effects may have been the result of enzymatic competition between the two types of fatty acids.

Effect of lysine, vitamin B(6), and carnitine supplementation on the lipid profile of male patients with hypertriglyceridemia: a 12-week, open-label, randomized, placebo-controlled trial.

BACKGROUND: Fat metabolism is known to be altered in hypertriglyceridemia. Fat oxidation requires carnitine, which can be obtained either from the diet (animal or dairy products) or through synthesis in the body using both lysine and vitamin B(6). OBJECTIVE: The goal of this study was to investigate the effect of lysine, vitamin B(6), and carnitine supplementation on both glycemia and the lipid profiles, specifically triglyceride (TG) levels, in men with hypertriglyceridemia. METHODS: This 12-week, randomized, placebo-controlled clinical trial was conducted at a Lebanese medical center. A total of 85 hypertriglyceridemic (TG> 150 mg/dL) male patients were randomized to 1 of 5 groups and given supplements of lysine (1 g/d), vitamin B(6) (50 mg/d), lysine (1 g/d) + vitamin B(6) (50 mg/d), carnitine (1 g/d), or placebo for 12 weeks. The lipid profile (TG, total cholesterol, LDL-C, and HDL-C) and fasting plasma glucose levels were assessed at baseline and at 6 and 12 weeks. RESULTS: Adults (∼50 years) Lebanese males from a low socioeconomic status in Beirut were given the appropriate supplements. Vitamin B(6) supplementation was associated with a significant reduction in total cholesterol and HDL-C of ∼10%. In addition, plasma TG was reduced by 36.6 mg/dL at 6 weeks, whereas levels in the placebo group increased by 18 mg/dL; this difference failed to reach statistical significance. No major changes in the lipid profile were observed in the lysine and carnitine groups or when lysine was added to vitamin B(6). CONCLUSION: Vitamin B(6) supplementation in these male patients with hypertriglyceridemia reduced plasma total cholesterol and HDL-C concentrations.

Stimulation of postprandial in vivo glycogenesis and lipogenesis of rats fed high fructose diet with varied phosphate content.

It has been reported that increased fructose intake is associated with the development of the metabolic syndrome. The phosphate (P) sequestering capacity of fructose is likely to affect the phosphorylation capacity of different metabolites, and this, in turn, may be the basis for several metabolic derangements, especially in the P requiring reactions, for example, glycogenesis and lipogenesis. We hypothesized that P enrichment of the diet can balance P status and, consequently, affect glycogenesis and lipogenesis. An animal experiment was executed in which adult male Sprague-Dawley rats were maintained for 4 days on high-fructose diets with different P content (0.15%, 0.165%, 0.30%, and 1.65%). At the end of the feeding period, overnight fasted rats were tube fed a test meal, injected with (3)H(2)O and euthanized 1 hour later. Final plasma glucose, insulin, uric acid, and triacylglycerol concentrations, as well as in vivo rates of glycogen and lipid synthesis and hepatic glycogen content, were measured. Results showed that increased P content of the diet was associated with an increase in postprandial epididymal fat pad (P = .007) and hepatic lipogenesis (P = .029), as well as glycogenesis (P = .024). In conclusion, P content of the diet was found to stimulate both glycogenesis and lipogenesis. These alterations in carbohydrate and fat metabolism point to the potential of P in influencing nutritional status.

Fish oil and the management of hypertriglyceridemia.

Hypertriglyceridemia, regarded as one of the independent clinical markers of metabolic syndrome, is a frequently observed disorder that has been shown to be common in the Arab region. Epidemiologic and clinical trials demonstrated that omega-3 fatty acids have the potential to reduce the incidence of cardiovascular disease (CVD); one of the mechanisms by which this effect is achieved is through reducing plasma triglyceride levels. There is strong scientific evidence from human trials that omega-3 fatty acids from either fish or fish oil supplements significantly reduce blood triglyceride levels and these benefits appear to be dose-dependent. The active ingredients of fish oils include the long chain fatty acids EPA and DHA. The ideal amount of omega-3 fatty acid that should be incorporated into the diet without provoking detrimental effects on other lipid components such as decreasing HDL-C and/or increasing LDL-C has not yet been elucidated. Presently, a prescription form of omega-3 fatty acid has been approved by the United States Food and Drug Administration (USFDA) as an adjunct to the diet for the treatment of very high triglyceride levels (> or = 500 mg/dl) in adults. Patients with hypertriglyceridemia have been shown to respond well to the use of omega-3 fatty acids even when used in conjunction with statins where greater improvements in the lipid profile were found as compared to treatment with statins alone. A determinant of the responsiveness to fish oil could be attributed to the ApoE genotype of individuals.

Plasma copper, zinc, and selenium levels and correlates with metabolic syndrome components of lebanese adults.

Zinc, copper, and selenium statuses were reported to be linked to the development of chronic diseases, especially coronary heart disease (CHD). Metabolic syndrome, a known CHD risk factor, was found to be highly prevalent in Lebanon. Nevertheless, no data are available on the statuses of plasma zinc, copper, and selenium, especially in terms of their relation to the components of the metabolic syndrome. A sample of 398 men and women aged 18-65 years was drawn from 23 health centers across Lebanon; anthropometric measurements and biochemical analyses of fasting plasma samples were performed. Subjects were found to have normal plasma statuses of copper and selenium but were at elevated risk of zinc deficiency. Plasma selenium levels correlated positively with all the components of the metabolic syndromes, while that of copper correlated only with total, high-density lipoprotein and low-density lipoprotein cholesterol. Plasma zinc did not correlate with any of the metabolic syndrome components.

Meal pattern of male rats maintained on histidine-, leucine-, or tyrosine-supplemented diet.

OBJECTIVE: Food intake is known to be affected by macronutrient composition of the diet, and protein manipulation has been reported to alter food intake, but the effect of individual amino acids on eating behavior has not been fully studied. This study investigated the effect of diet supplementation with three individual amino acids on meal pattern in male rats. RESEARCH METHODS AND PROCEDURES: Thirty-two Sprague-Dawley rats were randomly divided into four equal groups and fed control diet or histidine (5%)-, leucine (5%)-, or tyrosine (5%)-supplemented diet for 2 weeks and were monitored for their meal pattern. RESULTS: Total food intake and feeding rate of the different groups were not affected, although other components of meal pattern were altered. Histidine supplementation reduced diurnal meal size by 42% (p < 0.05), whereas that of leucine increased nocturnal meal size by approximately 35% (p < 0.05). Tyrosine supplementation increased food intake of the nocturnal period and decreased that of the diurnal period. Both histidine and tyrosine supplementation elevated fasting plasma insulin levels and suppressed fasting glucose significantly. DISCUSSION: Individual amino acids were found to alter meal pattern differently. Further investigations are required to dissect the involvement of central and peripheral factors in these alterations.