From fat to FAT (CD36/SR-B2):Understanding the regulation of cellular fatty acid uptake

The molecular mechanisms underlying the cellular uptake of long-chain fatty acids and the regulation of this process have been elucidated in appreciable detail in the last decades. Two main players in this field, each discovered in the early 1990s, are (i) a membrane-associated protein first identified in adipose ('fat') tissue and referred to as putative fatty acid translocase (FAT)/CD36 (now officially designated as SR-B2) which facilitates the transport of fatty acids across the plasma membrane, and (ii) the family of transcription factors designated peroxisome proliferator-activated receptors (PPAR alpha, PPAR gamma, and PPAR(beta/delta) for which fatty acids and fatty acid metabolites are the preferred ligand. CD36/SR-B2 is the predominant membrane protein involved in fatty acid uptake into intestinal enterocytes, adipocytes and cardiac and skeletal myocytes. The rate of cellular fatty acid uptake is regulated by the subcellular vesicular recycling of CD36/SR-B2 from endosomes to the plasma membrane. Fatty acid-induced activation of PPARs results in the upregulation of the expression of genes encoding various proteins and enzymes involved in cellular fatty acid utilization. Both CD36/SR-B2 and the PPARs have been implicated in the derangements in fatty acid and lipid metabolism occurring with the development of pathophysiological conditions, such as high fat diet-induced insulin resistance and diabetic cardiomyopathy, and have been suggested as targets for metabolic intervention. In this brief review we discuss the discovery and current understanding of both CD36/SR-B2 and the PPARs in metabolic homeostasis. (C) 2016 Elsevier B.V. and Societe Francaise de Biochimie et Biologie Moleculaire (SFBBM). All rights reserved

One-dimensional Disordered Density Waves and Superfluids: The Role of Quantum Phase Slips and Thermal Fluctuations

The low temperature phase diagram of 1D disordered quantum systems like charge or spin density waves, superfluids and related systems is considered by a full finite T renormalization group approach, presented here for the first time. At zero temperature the consideration of quantum phase slips leads to a new scenario for the unpinning (delocalization) transition. At finite T a rich cross-over diagram is found which reflects the zero temperature quantum critical behavior.Comment: 4 pages, 2 figure

Effects of different Papua New Guinea sweetpotato varieties on performance and level of enteric pathogens in chickens

Published: 23 April 2019In the last decade, research has targeted the evaluation of local feed ingredients for use in monogastric diets to alleviate the high cost of production of livestock at smallholder levels in Papua New Guinea (PNG). The PNG smallholder poultry production system involves many families who rear multiple batches of meat birds every year. This study was conducted to evaluate the levels of enteric pathogens in the caeca of broilers fed with sweetpotato diets with varying levels of non-starch polysaccharides (NSP). Selection of a sweetpotato variety for use in broiler diets should be based on the total NSP content. In particular, varieties with low soluble NSPs are economical to use as Apparent Metabolizable Energy (AME) values are within the desired range for poultry and there is minimal need to include enzymes to improve NSP digestibility. The use of varieties with a low total NSP is also advantageous as the numbers of Clostridium perfringens was lower in broilers fed with these sweetpotato varieties. The level of Campylobacter and Salmonella levels were high in the ceca of birds fed with the sweetpotato varieties with high total NSP. These levels can be reduced with the inclusion of enzymes. This information will assist in the efficient use of local varieties of sweetpotato in PNG by small holder poultry farmers for sustainable poultry production and the commercial industry.Janet Pandi, Phil Glatz, Rebecca Forder and Kapil Chousalka

Thermoelectric performance of granular semiconductors

We study thermoelectric properties of granular semiconductors with weak tunneling conductance between the grains, g_t < 1. We calculate the thermopower and figure of merit taking into account the shift of the chemical potential and the asymmetry of the density of states in the vicinity of the Fermi surface due to n- or p-type doping in the Efros-Shklovskii regime for temperatures less than the charging energy. We show that for weakly coupled semiconducting grains the figure of merit is optimized for grain sizes of order 5nm for typical materials and its values can be larger than one. We also study the case of compensated granular semiconductors and show that in this case the thermopower can be still finite, although two to three orders of magnitude smaller than in the uncompensated regime.Comment: 4 pages, 4 figure

Caffeine-stimulated fatty acid oxidation is blunted in CD36 null mice

Aim: The increase in skeletal muscle fatty acid metabolism during exercise has been associated with the release of calcium. We examined whether this increase in fatty acid oxidation was attributable to a calcium-induced translocation of the fatty acid transporter CD36 to the sarcolemma, thereby providing an enhanced influx of fatty acids to increase their oxidation.Methods: Calcium release was triggered by caffeine (3 mM) to examine fatty acid oxidation in intact soleus muscles of WT and CD36-KO mice, while fatty acid transport and mitochondrial fatty acid oxidation were examined in giant vesicles and isolated mitochondria, respectively, from caffeine-perfused hindlimb muscles of WT and CD36-KO mice. Western blotting was used to examine calcium-induced signalling.Results: In WT, caffeine stimulated muscle palmitate oxidation (+136%), but this was blunted in CD36-KO mice (-70%). Dantrolene inhibited (WT) or abolished (CD36-KO) caffeine-induced palmitate oxidation. In muscle, caffeine-stimulated palmitate oxidation was not attributable to altered mitochondrial palmitate oxidation. Instead, in WT, caffeine increased palmitate transport (+55%) and the translocation of fatty acid transporters CD36, FABPpm, FATP1 and FATP4 (26-70%) to the sarcolemma. In CD36-KO mice, caffeine-stimulated FABPpm, and FATP1 and 4 translocations were normal, but palmitate transport was blunted (-70%), comparable to the reductions in muscle palmitate oxidation. Caffeine did not alter the calcium-/calmodulin-dependent protein kinase II phosphorylation but did increase the phosphorylation of AMPK and acetyl-CoA carboxylase comparably in WT and CD36-KO.Conclusion: These studies indicate that sarcolemmal CD36-mediated fatty acid transport is a primary mediator of the calcium-induced increase in muscle fatty acid oxidation