Lipoprotein lipid and protein responses to dietary fat and diabetes in rats

Dietary and insulin-deficiency types of hyperlipidemia were compared in adult normal and streptozotocin-induced diabetes in male breeder rats. Experimental diets--high-beef tallow (BT; 38% of calories as beef fat and 2% as corn oil), high-corn oil (CO; 40% corn oil) or low-fat (LF; 2% corn oil)--were fed ad libitum for two months. To accentuate effect of type of fat, a group of normal rats was fed first BT diet for two months and then switched to CO diet (NCO) for another two months; the reverse switch was done with an additional group of normal rats (CO to BT; NBT). In all animals, glucose and insulin were measured in plasma, and phospholipids (PL), total cholesterol (TC), free cholesterol (FC), cholesteryl ester (CE), triglycerides (TG) and apoproteins in very low density (VLDL), low density (LDL) and high density (HDL) lipoproteins;Normal rats consumed the same amount of energy per day but average weight gain was higher in BT and CO than LF rats. Dietary treatment did not affect plasma glucose or insulin; VLDL-, LDL-, or HDL-PL; TC or CE in VLDL, LDL or HDL; VLDL- or LDL-FC; VLDL- or HDL-TG; LDL- or HDL-total protein or VLDL-apo-E. HDL-FC was higher in CO and LF than BT rats. LDL-TG was lower in CO and LF than BT rats. A dietary change from CO to BT (=NBT) resulted in a marked elevation of TG, with NBT similar to diabetic rats. VLDL-apo-B was lower in LF than BT rats. Feeding high-fat diets for four compared to two months resulted in an increase in apo-E and decrease in apo-C. In LDL, apo-B was lower and apo-E higher in LF-than high-fat-fed rats. HDL-apo-E was higher and HDL-apo-Al lower in LF- than high-fat-fed rats. HDL-apo-C was higher in LF than NCO rats;Compared to normal rats, total LDL- or HDL-protein or VLDL-CE were not affected in diabetic rats. Diabetic rats had higher plasma glucose, VLDL-TC and FC, VLDL-TG, LDL-apo-B, HDL-apo-B and HDL-apo-C levels and lower plasma insulin, LDL- and HDL-TC and CE, HDL-FC, LDL- and HDL-apo-E levels than normal rats. LDL-TG were higher in diabetic than all normal except NBT rats. VLDL-apo-B was lower in LF than diabetic rats. HDL-apo-Al was higher in diabetic than CO and LF but not BT rats. The results related to lipoprotein composition support the hypothesis that excess intake of a diet high in saturated fat may contribute to a metabolic pattern which resembles that of a diabetic state

Biotic Element Analysis in Biogeography

Biotic element analysis is an alternative to the areas-of-endemism approach for recognizing the presence or absence of vicariance events in a given region. If an ancestral biota was fragmented by vicariance events, biotic elements or clusters of distribution areas should emerge. We propose a statistical test for clustering of distribution areas based on a Monte Carlo simulation with a null model that considers the spatial autocorrelation in the data. The hypothesis tested is that the observed degree of clustering of ranges can be explained by the range size distribution, the varying number of taxa per cell, and the spatial autocorrelation of the occurrences of a taxon alone. A method for the delimitation of biotic elements which uses model-based Gaussian clustering is introduced. We demonstrate our methods and show the importance of grid size by means of a case study, an analysis of the distribution patterns of southern African species of the weevil genus Scobius. The example highlights the difficulties in delimiting areas of endemism if dispersal has occurred and illustrates the advantages of the biotic element approac

The Randomized Dependence Coefficient

We introduce the Randomized Dependence Coefficient (RDC), a measure of non-linear dependence between random variables of arbitrary dimension based on the Hirschfeld-Gebelein-R\'enyi Maximum Correlation Coefficient. RDC is defined in terms of correlation of random non-linear copula projections; it is invariant with respect to marginal distribution transformations, has low computational cost and is easy to implement: just five lines of R code, included at the end of the paper

Impact of Nutrition on Pollutant Toxicity: An Update with New Insights Into Epigenetic Regulation

Exposure to environmental pollutants is a global health problem and is associated with the development of many chronic diseases, including cardiovascular disease, diabetes and metabolic syndrome. There is a growing body of evidence that nutrition can both positively and negatively modulate the toxic effects of pollutant exposure. Diets high in proinflammatory fats, such as linoleic acid, can exacerbate pollutant toxicity, whereas diets rich in bioactive and anti-inflammatory food components, including omega-3 fatty acids and polyphenols, can attenuate toxicant-associated inflammation. Previously, researchers have elucidated direct mechanisms of nutritional modulation, including alteration of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling, but recently, increased focus has been given to the ways in which nutrition and pollutants affect epigenetics. Nutrition has been demonstrated to modulate epigenetic markers that have been linked either to increased disease risks or to protection against diseases. Overnutrition (i.e. obesity) and undernutrition (i.e. famine) have been observed to alter prenatal epigenetic tags that may increase the risk of offspring developing disease later in life. Conversely, bioactive food components, including curcumin, have been shown to alter epigenetic markers that suppress the activation of NF-κB, thus reducing inflammatory responses. Exposure to pollutants also alters epigenetic markers and may contribute to inflammation and disease. It has been demonstrated that pollutants, via epigenetic modulations, can increase the activation of NF-κB and upregulate microRNAs associated with inflammation, cardiac injury and oxidative damage. Importantly, recent evidence suggests that nutritional components, including epigallocatechin gallate (EGCG), can protect against pollutant-induced inflammation through epigenetic regulation of proinflammatory target genes of NF-κB. Further research is needed to better understand how nutrition can modulate pollutant toxicity through epigenetic regulation. Therefore, the objective of this review is to elucidate the current evidence linking epigenetic changes to pollutant-induced diseases and how this regulation may be modulated by nutrients allowing for the development of future personalized lifestyle interventions

Manufactured Aluminum Oxide Nanoparticles Decrease Expression of Tight Junction Proteins in Brain Vasculature

Manufactured nanoparticles of aluminum oxide (nano-alumina) have been widely used in the environment; however, their potential toxicity provides a growing concern for human health. The present study focuses on the hypothesis that nano-alumina can affect the blood-brain barrier and induce endothelial toxicity. In the first series of experiments, human brain microvascular endothelial cells (HBMEC) were exposed to alumina and control nanoparticles in dose- and time-responsive manners. Treatment with nano-alumina markedly reduced HBMEC viability, altered mitochondrial potential, increased cellular oxidation, and decreased tight junction protein expression as compared to control nanoparticles. Alterations of tight junction protein levels were prevented by cellular enrichment with glutathione. In the second series of experiments, rats were infused with nano-alumina at the dose of 29 mg/kg and the brains were stained for expression of tight junction proteins. Treatment with nano-alumina resulted in a marked fragmentation and disruption of integrity of claudin-5 and occludin. These results indicate that cerebral vasculature can be affected by nano-alumina. In addition, our data indicate that alterations of mitochondrial functions may be the underlying mechanism of nano-alumina toxicity