Leucine supplementation favors liver protein status but does not reduce body fat in rats during 1 week of food restriction

An important role in protein-energy metabolism has been attributed to leucine because of its long-term effects on body fat reduction and on the improvement of some indicators of protein status in rodents. The present study investigated the influence of leucine supplementation on the body composition and protein status of rats during the early phase of weight loss, which is characterized by a rapid loss of body weight. Thirty adult male Wistar rats were divided into 2 groups, a control and a leucine group (diet supplemented with 0.59% L-leucine), and were submitted to 1 week of 50% food restriction. The following parameters were evaluated: chemical carcass composition, protein and RNA content in liver and gastrocnemius muscle, and serum concentrations of insulin-like growth factor-1 and corticosterone. A higher liver weight and liver protein content were observed in the supplemented group (p < 0.05). However, no difference in body fat was found between groups (p > 0.05). The results indicate that low-dose leucine supplementation favors liver protein status but does not reduce body fat in rats during the early phase of rapid weight loss.

Effect of Short-term High-Dose Creatine Supplementation on Measured GFR in a Young Man With a Single Kidney

It currently is unknown whether creatine supplementation is safe for people with or at risk of kidney disease. We report on the short-term effects of creatine supplementation on kidney function in a young man with a single kidney and mildly decreased glomerular filtration rate (GFR). A 20-year-old man who had undergone unilateral nephrectomy and presented with mildly decreased GFR without kidney damage underwent a trial with 35 days of creatine supplementation (20 g/d for 5 days followed by 5 g/d for the next 30 days) and had his kidney function monitored. After the intervention, (51)Cr-EDTA clearance (pre, 81.6 mL/min/1.73 m(2); post, 82.0 mL/min/1.73 m(2)), proteinuria (protein excretion: pre, 130 mg/d; post, 120 mg/d), and electrolyte levels were unchanged. Albuminuria, serum urea level, and estimated creatinine clearance were decreased (pre, 4.6 mg/d; post, 2.9 mg/d; pre, 37 mg/d; post, 28 mg/dL; and pre, 88 mL/min/1.73 m(2); post, 71 mL/min/1.73 m(2), respectively), whereas serum creatinine level was slightly increased (pre, 1.03 mg/dL; post, 1.27 mg/dL), falsely suggesting kidney function impairment. This prospective report suggests that short-term creatine supplementation may not affect kidney function in an individual with a single kidney, mild decreased GFR, and ingesting a high-protein diet (ie, 2.8 g/kg/d). This finding has great relevance considering that creatine-induced kidney disease has been a growing concern, even for healthy people. Am J Kidney Dis 55: e7-e9. (C) 2010 by the National Kidney Foundation, Inc.

Decreasing dietary sodium while following a self-selected potassium-rich diet reduces blood pressure

Reducing dietary sodium reduces blood pressure (BP), a major risk factor for cardiovascular disease, but few studies have specifically examined the effect on BP of altering dietary sodium in the context of a high potassium diet. This randomized, crossover study compared BP values in volunteer subjects self-selecting food intake and consuming low levels of sodium (Na+; 50 mmol/d) with those consuming high levels of sodium (> or =20 mmol/d), in the context of a diet rich in potassium (K+). Sodium supplementation (NaSp) produced the difference in Na+ intake. Subjects (n = 108; 64 women, 44 men; 16 on antihypertensive therapy) had a mean age of 47.0 ± 10.1 y. Subjects were given dietary advice to achieve a low sodium (LS) diet with high potassium intake (50 mmol Na+/d, >80 mmol K+/d) and were allocated to NaSp (120 mmol Na+/d) or placebo treatment for 4 wk before crossover. The LS diet decreased urinary Na+ from baseline, 138.7 ± 5.3 mmol/d to 57.8 ± 3.8 mmol/d (P < 0.001). The NaSp treatment returned urinary Na+ to baseline levels 142.4 ± 3.7 mmol/d. Urinary K+ increased from baseline, 78.6 ± 2.3 to 86.6 ± 2.1 mmol/d with the LS diet and to 87.1 ± 2.1 mmol/d with NaSp treatment (P < 0.001). The LS diet reduced home systolic blood pressure (SBP) by 2.5 ± 0.8 mm Hg (P = 0.004), compared with the NaSp treatment. Hence, reducing Na+ intake from 140 to 60 mmol/d significantly decreased home SBP in subjects dwelling in a community setting who consumed a self-selected K+-rich diet, and this dietary modification could assist in lowering blood pressure in the general population.

Failure of conjugated linoleic acid supplementation to enhance biosynthesis of docosahexaenoic acid from α-linolenic acid in healthy human volunteers

A rate-limiting step in docosahexaenoic acid (DHA) formation from α-linolenic acid (ALA) involves peroxisomal oxidation of 24:6n-3 to DHA. The aim of the study was to determine whether conjugated linoleic acid (CLA) would enhance conversion of ALA to DHA in humans on an ALA-supplemented diet. The subjects (n=8 per group) received daily supplementation of ALA (11g) and either CLA (3.2g) or placebo for 8 weeks. At baseline, 4 and 8 weeks, blood was collected for plasma fatty acid analysis and a number of physiological measures were examined. The ALA-supplemented diet increased plasma levels of ALA and eicosapentaenoic acid (EPA). The addition of CLA to the ALA diet resulted in increased plasma levels of CLA, as well as ALA and EPA. Plasma level of DHA was not increased with either the ALA alone or ALA plus CLA supplementation. The results demonstrated that CLA was not effective in enhancing DHA levels in plasma in healthy volunteers.

Calcium supplementation: the bare bones

An adequate calcium intake is an essential part of the prevention and treatment of osteoporosis. Two to threeserves of calcium-rich foods each day provides sufficient calcium for most non-pregnant adults. If this target is not achievable, calcium supplementation is generally effective, cheap and safe for most people. Calciumcarbonate(without vitamin and mineral additives) is the preferred supplement in most cases. Problems with calcium absorption arise due to factors including high·fibre vegetarian diets, achlorhydria, long·term glucocorticoid therapy and vitamin D deficiency. Vitamin D deficiency is extremely common in some ethnic groups and the elderly who are housebound or in residential care. These at risk groups generally require vitamin D supplementation to achieve adequate intestinal absorption of calcium.

Low dose supplementation with two different marine oils does not reduce pro-inflammatory eicosanoids and cytokines in vivo

In view of the reported potential anti-inflammatory activity of the New Zealand green lipped mussel (NZGLM), we aimed to compare the effect of low dose marine oil supplementation, from mussels and fish, in reducing blood markers of inflammation. Thirty apparently healthy males and females were recruited from the general public in Melbourne, Australia to participate in a double blind, randomised, parallel intervention study. Subjects were consuming approximately 73 mg of omega-3 long chain polyunsaturated fatty acids (n-3 LCPUFA) daily in their background diet prior to the commencement of the intervention. Subjects were randomly assigned to consume either 2 mL/day of the NZGLM oil preparation (mixed with olive oil and dl-alpha-tocopherol) or fish oil preparation (also mixed with olive oil and dl-alpha-tocopherol) for six weeks. Two mL of the oils contained 241 mg and 181 mg of n-3 LCPUFA, respectively. Neutrophil phospholipid fatty acids, serum thromboxane B2 (TXB2), stimulated monocyte production of prostaglandin E2 (PGE2), interleukin-1 beta (IL-1 beta) and tumor necrosis factor alpha (TNFalpha) were measured. During the intervention, the total intakes of n-3 LCPUFA from the background diet and the supplements were 199 mg/d and 173 mg/day for the NZGLM and FO groups, respectively. Following six weeks of supplementation, both groups showed a small, but significant increase in neutrophil phospholipid proportion of eicosapentaenoic acid. The NZGLM group also showed a significant increase in docosahexaenoic acid levels. There were no significant changes with time or treatment for TXB2, PGE2, IL-1 beta or TNFalpha. This study showed that low dose supplementation with n-3 LCPUFA from two different marine oil preparations showed no difference in inflammatory markers in this group of healthy individuals. Further studies are warranted including dose response trials and studies in populations with inflammatory conditions.

Squalene supplementation alters genes associated with liver cholesterol metabolism

Background – Squalene is a component of shark liver oil and has been speculated to have cholesterol reducing properties. High levels of total and LDL cholesterol have been shown to contribute to the development of chronic heart disease. The liver is central to the regulation of cholesterol metabolism and dietary intervention has long been recognized as a primary means to reduce the risks of chronic heart disease and related ailments.
Objectives – To determine the effect of dietary squalene supplementation on gene transcripts associated with liver cholesterol metabolism. Specifically the effect of squalene supplementation on mRNA levels for proteins that
regulate cholesterol biosynthesis (HMDH & ERG1), cholesterol elimination (SRB1), bile synthesis (CP7A1 & CP27A) and cholesterol excretion by the liver into bile (ABCG5 & ABCG8) was investigated.
Design – Rats (n=32) were divided into four groups and supplemented for 12 weeks. Groups one and two were fed a cholesterol rich diet for six weeks followed by six weeks of a cholesterol rich diet plus 1.75mg/day of squalene or 3.5 mg/day. Group three was fed a cholesterol rich diet for 12 weeks and group four was fed standard rat chow for 12 weeks. Blood lipid levels were monitored during the study and liver gene expression was determined at the
conclusion of the feeding trial via RT-PCR.
Outcomes – 3.5 mg/day of squalene lowered total and LDL cholesterol in rats consuming a cholesterol rich diet. This dose of squalene also resulted in constant levels of HMDH and ERG1 whereas the cholesterol rich diet halved mRNA levels of these enzymes. Furthermore 3.5 mg/day of squalene caused a greater than 3.0 fold increase in mRNA levels of the proteins SRB1, CP7A1, CP27A and ABCG5.
Conclusion – Dietary squalene supplementation at a dose of 3.5 mg/day lowers total and LDL cholesterol in rats consuming a cholesterol rich diet. These reductions in cholesterol levels may be due to increased cholesterol
elimination, bile synthesis and cholesterol excretion by the liver into bile mediated by changes in gene expression of key enzymes involved in these metabolic pathways

α-Linolenic acid supplementation and conversion to n-3 long-chain polyunsaturated fatty acids in humans

Blood levels of polyunsaturated fatty acids (PUFA) are considered biomarkers of status. Alpha-linolenic acid, ALA, the plant omega-3, is the dietary precursor for the long-chain omega-3 PUFA eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and docosahexaenoic acid (DHA). Studies in normal healthy adults consuming western diets, which are rich in linoleic acid (LA), show that supplemental ALA raises EPA and DPA status in the blood and in breast milk. However, ALA or EPA dietary supplements have little effect on blood or breast milk DHA levels, whereas consumption of preformed DHA is effective in raising blood DHA levels. Addition of ALA to the diets of formula-fed infants does raise DHA, but no level of ALA tested raises DHA to levels achievable with preformed DHA at intakes similar to typical human milk DHA supply. The DHA status of infants and adults consuming preformed DHA in their diets is, on average, greater than that of people who do not consume DHA. With no other changes in diet, improvement of blood DHA status can be achieved with dietary supplements of preformed DHA, but not with supplementation of ALA, EPA, or other precursors.

The effect of cocoa supplementation on hepatic steatosis, reactive oxygen species and LFABP in a rat model of NASH

Background: Non alcoholic steatohepatitis is hypothesised to develop via a mechanism involving fat accumulation and oxidative stress. The current study aimed to investigate if an increase in oxidative stress was associated with changes in the expression of liver fatty acid binding protein in a rat model of non alcoholic steatohepatitis and whether cocoa supplementation attenuated those changes.

Methods: Female Sprague Dawley rats were fed a high fat control diet, a high fat methionine choline deficient diet, or one of four 12.5% cocoa supplementation regimes in combination with the high fat methionine choline deficient diet.

Results: Liver fatty acid binding protein mRNA and protein levels were reduced in the liver of animals with fatty liver disease when compared to controls. Increased hepatic fat content was accompanied by higher levels of oxidative stress in animals with fatty liver disease when compared to controls. An inverse association was found between the levels of hepatic liver fatty acid binding protein and the level of hepatic oxidative stress in fatty liver disease. Elevated NADPH oxidase protein levels were detected in the liver of animals with increased severity in inflammation and fibrosis. Cocoa supplementation was associated with partial attenuation of these pathological changes, although the severity of liver disease induced by the methionine choline deficient diet prevented complete reversal of any disease associated changes. Red blood cell glutathione was increased by cocoa supplementation, whereas liver glutathione was reduced by cocoa compared to methionine choline deficient diet fed animals.

Conclusion: These findings suggest a potential role for liver fatty acid binding protein and NADPH oxidase in the development of non alcoholic steatohepatitis. Furthermore, cocoa supplementation may have be of therapeutic benefit in less sever forms of NASH.

Effects of Dietary Vitamin B6 Supplementation on Fillet Fatty Acid Composition and Fatty Acid Metabolism of Rainbow Trout Fed Vegetable Oil Based Diets

Fish oil replacement in aquaculture feeds results in major modifications to the fatty acid makeup of cultured fish. Therefore, in vivo fatty acid biosynthesis has been a topic of considerable research interest. Evidence suggests that pyridoxine (vitamin B₆) plays a role in fatty acid metabolism, and in particular, the biosynthesis of LC-PUFA has been demonstrated in mammals. However, there is little information on the effects of dietary pyridoxine availability in fish fed diets lacking LC-PUFA. This study demonstrates a relationship between dietary pyridoxine supplementation and fatty acid metabolism in rainbow trout. In particular, the dietary pyridoxine level was shown to modulate and positively stimulate the activity of the fatty acid elongase and Δ-6 and Δ-5 desaturase enzymes, deduced by the whole-body fatty acid balance method. This activity was insufficient to compensate for a diet lacking in LC-PUFA but does highlight potential strategies to maximize this activity in cultured fish, especially when fish oil is replaced with vegetable oils.

Maternal dietary creatine supplementation does not alter the capacity for creatine synthesis in the newborn spiny mouse

We have previously reported that maternal creatine supplementation protects the neonate from hypoxic injury. Here, we investigated whether maternal creatine supplementation altered expression of the creatine synthesis enzymes (arginine:glycine amidinotransferase [AGAT], guanidinoaceteate methyltransferase [GAMT]) and the creatine transporter (solute carrier family 6 [neurotransmitter transporter, creatine] member 8: SLC6A8) in the term offspring. Pregnant spiny mice were fed a 5% creatine monohydrate diet from midgestation (day 20) to term (39 days). Placentas and neonatal kidney, liver, heart, and brain collected at 24 hours of age underwent quantitative polymerase chain reaction and Western blot analysis. Maternal creatine had no effect on the expression of AGAT and GAMT in neonatal kidney and liver, but mRNA expression of AGAT in brain tissues was significantly decreased in both male and female neonates born to mothers who were fed the creatine diet. SLC6A8 expression was not affected by maternal dietary creatine loading in any tissues. Maternal dietary creatine supplementation from midgestation in the spiny mouse did not alter the capacity for creatine synthesis or transport.

Maternal dietary supplementation with saturated, but not monounsaturated or polyunsaturated fatty acids, leads to tissue-specific inhibition of offspring Na+,K+-ATPase

In rats, a maternal diet rich in lard is associated with reduced Na+,K+-ATPase activity in adult offspring kidney. We have addressed the role of different fatty acids by evaluating Na+,K+-ATPase activity in offspring of dams fed diets rich in saturated (SFA), monounsaturated (MUFA) or polyunsaturated (PUFA) fatty acids. Female Sprague–Dawley rats were fed, during pregnancy and suckling, a control diet (4% w/w corn oil) or a fatty acid supplemented diet (24% w/w). Offspring were reared on chow (4% PUFA) and studied at 6 months. mRNA expression (real-time PCR) of Na+,K+-ATPase α subunit and protein expression of Na+,K+-ATPase subunits (Western blot) were assessed in kidney and brain. Na+,K+-ATPase activity was reduced in kidney (P < 0.05 versus all groups) and brain (P < 0.05 versus control and MUFA offspring) of the SFA group. Neither Na+,K+-ATPase α1 subunit mRNA expression, nor protein expression of total α, α1, α2, α3 or β1 subunits were significantly altered in kidney in any dietary group. In brains of SFA offspring α1 mRNA expression (P < 0.05) was reduced compared with MUFA and PUFA offspring, but not controls. Also in brain, SFA offspring demonstrated reduced (P < 0.05) α1 subunit protein and increased phosphorylation (P < 0.05) of the Na+,K+-ATPase modulating protein phospholemman at serine residue 63 (S63 PLM). Na+,K+-ATPase activity was similar to controls in heart and liver. In utero and neonatal exposure to a maternal diet rich in saturated fatty acids is associated with altered activity and expression of Na+,K+-ATPase in adulthood, but mechanisms appear tissue specific.

Protein-enriched diet, with the use of lean red meat, combined with progressive resistance training enhances lean tissue mass and muscle strength and reduces circulating IL-6 concentrations in elderly women: a cluster randomized controlled trial.

Physical inactivity, inadequate dietary protein, and low-grade systemic inflammation contribute to age-related muscle loss, impaired function, and disability.

Randomized controlled trial examining the effects of fish oil and multivitamin supplementation on the incorporation of n-3 and n-6 fatty acids into red blood cells

The present randomized, placebo-controlled, double-blind, parallel-groups clinical trial examined the effects of fish oil and multivitamin supplementation on the incorporation of n-3 and n-6 fatty acids into red blood cells. Healthy adult humans (n = 160) were randomized to receive 6 g of fish oil, 6 g of fish oil plus a multivitamin, 3 g of fish oil plus a multivitamin or a placebo daily for 16 weeks. Treatment with 6 g of fish oil, with or without a daily multivitamin, led to higher eicosapentaenoic acid (EPA) composition at endpoint. Docosahexaenoic acid (DHA) composition was unchanged following treatment. The long chain LC n-3 PUFA index was only higher, compared to placebo, in the group receiving the combination of 6 g of fish oil and the multivitamin. Analysis by gender revealed that all treatments increased EPA incorporation in females while, in males, EPA was only significantly increased by the 6 g fish oil multivitamin combination. There was considerable individual variability in the red blood cell incorporation of EPA and DHA at endpoint. Gender contributed to a large proportion of this variability with females generally showing higher LC n-3 PUFA composition at endpoint. In conclusion, the incorporation of LC n-3 PUFA into red blood cells was influenced by dosage, the concurrent intake of vitamin/minerals and gender.

Recovery of omega-3 profiles of cultivated abalone by dietary macroalgae supplementation

Formulated feeds for cultivated abalone have received considerable attention to improve the feeding costs, efficiency and productivity of the growing cultivated abalone industry in Australia. Less attention has been given to the resulting quality of the seafood product from formulated feeds and the effect of the reduction of marine ingredients in these feeds. Marine n-3 fatty acids are particularly important nutritional factors of seafood that are lacking from feed ingredients at the base of the aquaculture production chain. Considering that this important category of nutrients is already deficient in the western diet, further erosion through cultivated seafood products is of concern. This study tested the effect of three diet categories on the fatty acid profiles of commercially farmed abalone. Two commercial formulated feeds, Ulva spp. macroalgae, and combinations of the formulated feeds and macroalgae were fed to six replicate baskets of 20 abalone (~62 mm) for 12 months in Victoria, Australia. The macroalgae diets represented overall lower fatty acid content, including eicosapentaenoic (EPA) and docosahexaenoic (DHA), but higher relative amounts of alpha linolenic acid (ALA) and docosapentaenoic acid (DPA), than the formulated feeds. The total lipid content of abalone tissue did not vary substantially across diet categories; however, the ratio of n-6:n-3 fatty acids decreased incrementally with the increasing macroalgae content in the diet and by a factor of two with a 100 % macroalgae diet. Also, equal or higher content of all important long chain n-3 fatty acids was achieved with a macroalgae diet despite the lower dietary content of some of these fatty acids. Marine fatty acid-deplete aquaculture feeds can result in decreased n-3 fatty acid content in the abalone tissue. The inclusion of macroalgae in the diet of abalone can offset this reduction.