Understanding the Role of Vitamin D in Heart Failure.

Vitamin D is now believed to have a significant role in cardiac signal transduction and regulation of gene expression, and thus influences normal cardiomyocyte function. It has been reported to provide cardioprotection through its anti-inflammatory, anti-apoptotic and anti-fibrotic actions; and to prevent cardiac remodeling, -handling defects, and abnormal electrophysiological patterns. A vitamin D deficient state has been associated in the pathogenesis of heart failure; however, while many clinical studies report a benefit of vitamin D to heart function, other clinical studies are inconsistent with these findings.

Maternal supplementation with dietary arachidonic and docosahexaenoic acids during lactation elevates bone mass in weanling rat and guinea pig offspring even if born small sized.

Whether post-natal long chain polyunsaturated fatty acids (LCPUFA) elevates bone mineral content (BMC) of small and normal neonates was studied using pregnant rats and guinea pigs fed a control (C) diet or low protein (LP) diet to induce small neonates followed by C or LCPUFA diets during lactation. Measurements (days 3 and 21 post-partum) included BMC and density (BMD) plus bone metabolism. In rats LP reduced birth weight but at day 21 elevated weight and whole body BMC; LCPUFA enhanced spine BMC, tibia BMC and BMD and whole body BMD.

Bone mass in First Nations, Asian and white newborn infants.

To compare bone mass in newborn infants of First Nations, white and Asian mothers while accounting for vitamin D status. Fifty infants born healthy at term age were measured for bone mass using dual energy x-ray absorptiometry (DXA) within 15 days of life. Vitamin D status was measured as 25(OH)D in cord plasma.

Dietary conjugated linoleic acid in the cis-9, trans-11 isoform reduces parathyroid hormone in male, but not female, rats.

Previously, a mixture of conjugated linoleic acid (CLA) isoforms reduced parathyroid hormone (PTH) in male rats over 8 weeks. The objective herein was to determine which isoform caused the reduction in PTH; whether the effect was sex specific; and whether CLA-induced reductions in PTH were sustained. Male and female weanling rats (n=48) were randomized to a control diet or one made with 0.

Minimal enteral feeding within 3 d of birth in prematurely born infants with birth weight < or = 1200 g improves bone mass by term age.

Background: Evidence-based practice guidelines for aggressive nutritional intervention by using parenteral amino acids (AAs) and minimal enteral feeding (MEF) as early as the first day of life have not been tested for benefits to bone mass.

Objective: We investigated whether early introduction of parenteral AAs and MEF improves growth and bone mass achieved by term age in infants born prematurely.

Design: Twenty-seven infants who were < or = 1200 g and < or = 32 wk gestation at birth were randomly assigned by using a 2 x 2 design to treatment of either 1 g AAs/kg within the first 24 h or 12 mL MEF x kg(-1) x d(-1) within the first 72 h of life.

Maternal and cord blood long-chain polyunsaturated fatty acids are predictive of bone mass at birth in healthy term-born infants.

Long-chain polyunsaturated fatty acids (LC PUFA) are associated with bone mass in animals and human adults, yet no data exist for human infants. Thus, the objective of this study was to establish that LC PUFA status is associated with bone mass in healthy infants. Thirty mother-infant pairs were studied for LC PUFA status by measuring maternal and cord blood red blood cells (RBC) for arachidonic acid (AA), eicosapentaenoic acid (EPA), and DHA.

Vitamin D deficiency and whole-body and femur bone mass relative to weight in healthy newborns.

Background: Vitamin D is required for normal bone growth and mineralization. We sought to determine whether vitamin D deficiency at birth is associated with bone mineral content (BMC) of Canadian infants.

Methods: We measured plasma 25-hydroxyvitamin D [25(OH)D] as an indicator of vitamin D status in 50 healthy mothers and their newborn term infants.

Low levels of dietary arachidonic and docosahexaenoic acids improve bone mass in neonatal piglets, but higher levels provide no benefit.

In piglets, feeding arachidonic acid (AA) and docosahexaenoic acid (DHA) in a 5:1 ratio leads to elevated bone mass, but the optimal total quantity requires clarification. We studied bone mass and modeling of piglets that were randomized to receive 1 of 4 formulas for 15 d: control formula or the same formula with various levels of AA:DHA (0.5:0.

Dietary soy protein attenuates renal disease progression after 1 and 3 weeks in Han:SPRD-cy weanling rats.

Compared with casein, dietary soy protein slows disease progression in animal models of chronic renal injury. To determine whether dietary soy protein feeding can alter early disease progression, male Han:SPRD-cy rats (n = 87) in a very early stage of chronic kidney disease were fed soy protein compared with casein-based diets for 1 or 3 wk. Kidneys were assessed for fibrosis, cyst growth, fatty acid composition and prostaglandin E(2) (PGE(2)) production.

Conjugated linoleic acid reduces parathyroid hormone in health and in polycystic kidney disease in rats.

Background: Feeding conjugated linoleic acid (CLA) is reported to reduce prostaglandin E(2) synthesis, which is required for parathyroid hormone (PTH) release.

Objective: This study was undertaken to determine whether CLA would suppress hyperparathyroidism and the resulting high-turnover bone disease in a rat model of polycystic kidney disease (PKD).

Design: Outcome measurements were conducted after 8 wk of feeding diets supplemented with and without CLA (1% of dietary fat) to Han:SPRD-cy male rats (n = 52).

Dose response of bone mass to dietary arachidonic acid in piglets fed cow milk-based formula.

Background: The addition of arachidonic acid (AA) and docosahexaenoic acid (DHA) to infant formula was recently approved in North America. In piglets, dietary AA is linked to elevations in bone mass.

Objective: The objective was to investigate the effects of varied amounts of dietary AA on bone modeling and bone mass with the use of the piglet model for infant nutrition.

Dietary conjugated linoleic acid reduces PGE2 release and interstitial injury in rat polycystic kidney disease.

Background: Conjugated linoleic acid (CLA) describes positional isomers of linoleic acid (LA). Experimental health benefits of CLA include amelioration of malignancy and inflammatory disease and reduction of adiposity. The Han:SPRD-cy rat model of polycystic kidney disease (PKD) features prominent renal interstitial inflammation and fibrosis that is amenable to dietary modification.

Dietary arachidonic acid suppresses bone turnover in contrast to low dosage exogenous prostaglandin E(2) that elevates bone formation in the piglet.

This study was designed to compare the effects of dietary arachidonic acid (AA) versus prostaglandin E(2) (PGE(2)) on bone cell metabolism and bone mass. Twenty-eight piglets from 7 litters were randomized to 1 of 4 treatments for 15 days: fatty acid supplemented formula (FA: 0.8% of total fatty acids as AA and 0.

Activation of phospholipases A2 and D of a human neuroblastoma cell line (LA-N-2) by N-dodecyl-L-lysine amide (compound 24), a putative G protein activator: characteristics of inhibition by (-)-nicotine.

Compound 24, an alkyl-substituted amino acid amide, previously found to activate pertussis toxin-sensitive G proteins in cell membranes and membrane protein fractions, was used as a tool to determine the mechanism/location of nicotine inhibition of amyloid beta peptide-stimulated phospholipase A2 and D activities in a human neuroblastoma cell line, LA-N-2, in vitro. In contrast to our previous findings with amyloid beta peptide, these phospholipase activations by compound 24 were not inhibited by (-)-nicotine, cholera toxin or tetanus toxin pretreatment. The contrasting activation of these phospholipases by amyloid beta peptide and compound 24 are discussed.

Elevated bone turnover in rat polycystic kidney disease is not due to prostaglandin E2.

Hyperparathyroidism, secondary to renal disease, is thought to cause high bone turnover via prostaglandin E2 (PGE2). Diets high in n-3 fatty acids reduced PGE2. Thus the objective was to compare the effect of diets high in n-6 and n-3 fatty acids on hyperparathyroidism, bone turnover, and PGE2 in Han:SPRD- cy rats that develop polycystic kidney disease (PKD).

Modulation of essential (n-6):(n-3) fatty acid ratios alters fatty acid status but not bone mass in piglets.

Dietary (n-6) and (n-3) fatty acids have been implicated as important regulators of bone metabolism. The main objective of this research was to define the response of whole-body growth, fatty acid status and bone mass to a reduced dietary (n-6):(n-3) fatty acid ratio. A secondary objective was to determine whether there is an amount of fat x fatty acid ratio interaction for these outcomes.

Leptin predicts bone and fat mass after accounting for the effects of diet and glucocorticoid treatment in piglets.

The role of leptin in neonatal growth and bone metabolism has been investigated, but not simultaneously. The objectives of this study were to determine if leptin relates to bone mass during rapid growth; if consumption of maternal milk is related to elevated circulating concentrations of leptin resulting in higher fat mass; and if glucocorticoids result in higher fat mass and reduced bone mass due to elevated leptin. Thirty-two piglets were randomized to either a suckling or milk substitute plus either dexamethasone (DEX) or placebo injection for 15 days beginning at 5 days of age.

Dietary long-chain polyunsaturated fatty acids minimize dexamethasone-induced reductions in arachidonic acid status but not bone mineral content in piglets.

The primary objective of this study was to determine whether exogenous arachidonic acid (AA) in a supplemented formula substitute for piglets or sow milk would attenuate reductions in AA status, growth, and bone mineral content (BMC) as a result of exogenous glucocorticoid excess using dexamethasone (DEX). A secondary objective was to confirm a positive effect of exogenous AA on growth and BMC of piglets fed formula and not treated with DEX as well as to determine whether the elevation in BMC was related to greater production of prostaglandin E(2) in bone. Forty-eight 5-d-old male piglets were randomized to be suckled or receive either a standard formula or the same formula, but containing AA (0.