Conjugated linoleic acid reduces parathyroid hormone in health and in polycystic kidney disease in rats.
ABSTRACT Feeding conjugated linoleic acid (CLA) is reported to reduce prostaglandin E(2) synthesis, which is required for parathyroid hormone (PTH) release.
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).
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). PTH, bone formation, and resorption were assessed in addition to femur bone mass with use of dual-energy X-ray absorptiometry.
CLA feeding resulted in attenuation of PTH concentrations in both PKD-affected and nonaffected rats (by 60%) but did not significantly alter bone formation and resorption.
Reduction in PTH may open possibilities for CLA as an adjunctive therapy in secondary hyperparathyroidism.
Article: The effect of trans-10, cis-12 conjugated linoleic acid on gene expression profiles related to lipid metabolism in human intestinal-like Caco-2 cells.[show abstract] [hide abstract]
ABSTRACT: We conducted an in-depth investigation of the effects of conjugated linoleic acid (CLA) on the expression of key metabolic genes and genes of known importance in intestinal lipid metabolism using the Caco-2 cell model. Cells were treated with 80 mumol/L of linoleic acid (control), trans-10, cis-12 CLA or cis-9, trans-11 CLA. RNA was isolated from the cells, labelled and hybridized to the Affymetrix U133 2.0 Plus arrays (n = 3). Data and functional analysis were preformed using Bioconductor. Gene ontology analysis (GO) revealed a significant enrichment (P < 0.0001) for the GO term lipid metabolism with genes up-regulated by trans-10, cis-12 CLA. Trans-10, cis-12 CLA, but not cis-9, trans-11 CLA, altered the expression of a number of genes involved in lipid transport, fatty acid metabolism, lipolysis, beta-oxidation, steroid metabolism, cholesterol biosynthesis, membrane lipid metabolism, gluconeogenesis and the citrate cycle. These observations warrant further investigation to understand their potential role in the metabolic syndrome.Genes & Nutrition 03/2009; 4(2):103-12. · 2.51 Impact Factor