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Shalinee Dhayal, Francesco P Zummo, Matthew W Anderson, Patricia Thomas, Hannah J Welters, Catherine Arden and Noel G Morgan

Introduction Chronic exposure of pancreatic β-cells to long-chain saturated fatty acids in vitro is associated with a phenomenon often referred to as ‘lipotoxicity’ in which the cells display secretory dysfunction and, ultimately, an

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Cristina Velasco, Cristina Otero-Rodiño, Sara Comesaña, Jesús M Míguez and José L Soengas

) and fish ( Delgado et al. 2017 ). Accordingly, several mechanisms are present in brain areas, especially hypothalamus, detecting changes in the levels of glucose, fatty acids and amino acids as demonstrated in mammals ( Efeyan et al. 2015 , Bruce

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Cristina Velasco, Sara Comesaña, Marta Conde-Sieira, Jesús M Míguez and José L Soengas

hypothalamus and hindbrain are able to detect changes in the levels of specific long-chain fatty acids (LCFA) through fatty acid-sensing mechanisms. These are based on carnitine palmitoyl transferase-1 (CPT-1), fatty acid translocase (FAT/CD36), increased

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Horng-Yih Ou, Hung-Tsung Wu, Feng-Hwa Lu, Yu-Chu Su, Hao-Chang Hung, Jin-Shang Wu, Yi-Ching Yang, Chao-Liang Wu and Chih-Jen Chang

carcinoma. However, there is still no effective treatment for hepatic steatosis, and life style modification remains the best therapeutic option ( Ferre & Foufelle 2010 ). Free fatty acid receptor 1 (FFAR1), also named G-protein-coupled receptor 40, is a

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Guojun Shi, Chen Sun, Weiqiong Gu, Minglan Yang, Xiaofang Zhang, Nan Zhai, Yan Lu, Zhijian Zhang, Peishun Shou, Zhiguo Zhang and Guang Ning

. 2012 ), and more details of T1D pathogenesis need to be explored in both human patients and animal models. Short-chain fatty acids (SCFAs) are fatty acids with aliphatic tails of fewer than six carbons, mainly derived from the fermentation of dietary

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Carmela Santangelo, Paola Matarrese, Roberta Masella, Maria Chiara Di Carlo, Angela Di Lillo, Beatrice Scazzocchio, Elio Vecci, Walter Malorni, Riccardo Perfetti and Emanuela Anastasi

hyperlipidemia contribute to β-cells dysfunction and a decrease of β-cell mass ( Dickson & Rhodes 2004 ). Free fatty acids (FFAs), at physiological concentrations, modulate the process of basal and glucose-induced insulin secretion in pancreatic β

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Yanxia Tang and GuoDong Li

increased plasma levels of free fatty acids (FFAs) resulting from lack of appropriate suppression of adipocyte lipolysis due to insulin resistance and deficiency ( Reaven 1988 , Imrie et al . 2010 ). Furthermore, circulating levels of FFAs are usually

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M J Watt, R J Southgate, A G Holmes and M A Febbraio

Introduction Skeletal muscle is a major site of fatty acid uptake and oxidation at rest and during contraction (for review see van der Vusse & Reneman 1996 ) and aberrant control of fatty acid metabolism is related to obesity and

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CP Briscoe, S Hanif, Arch JR and M Tadayyon

The effect of treatment with a 0.03% fatty acid (FA) cocktail on leptin-receptor-mediated STAT (signal transducers and activators of transcription) activation in the rat insulinoma cell line BRIN-BD11 was investigated. Leptin (10 nM) stimulated the tyrosine phosphorylation of STAT3 and STAT5b. Acute treatment with FAs prevented leptin-stimulated STAT3 tyrosine phosphorylation and significantly raised basal STAT5 phosphorylation. A chronic treatment (5 days) of BRIN-BD11 cells with FAs similarly attenuated leptin-stimulated STAT tyrosine phosphorylation. Chronic FA treatment also attenuated prolactin-stimulated STAT5b tyrosine phosphorylation but not interleukin-6-stimulated STAT3 tyrosine phosphorylation, suggesting that the effect is receptor/ligand specific. TaqMan analysis of gene expression following chronic FA treatment showed neither a decrease in the amount of leptin receptor (Ob-R) mRNA, nor an increase in the negative regulators of STAT signalling, SOCS3 (suppressors of cytokine signalling) or cytokine inducible sequence (CIS). These data demonstrate that FAs modulate leptin and prolactin signalling in beta-cells, implying that high levels of circulating FAs present in obese individuals affect the action of selective cytokines in beta-cell function.

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I Issemann, R A Prince, J D Tugwood and S Green

ABSTRACT

The peroxisome proliferator-activated receptor (PPAR) is a member of the steroid hormone receptor superfamily and is activated by a variety of fibrate hypolipidaemic drugs and non-genotoxic rodent hepatocarcinogens that are collectively termed peroxisome proliferators. A key marker of peroxisome proliferator action is the peroxisomal enzyme acyl CoA oxidase, which is elevated about tenfold in the livers of treated rodents. We have previously shown that a peroxisome proliferator response element (PPRE) is located 570 bp upstream of the rat peroxisomal acyl CoA oxidase gene and that PPAR binds to it. We show here that the retinoid X receptor (RXR) is required for PPAR to bind to the PPRE, and that the RXR ligand, 9-cis retinoic acid, enhances PPAR action. Retinoids may therefore modulate the action of peroxisome proliferators and PPAR may interfere with retinoid action, perhaps providing one mechanism to explain the toxicity of peroxisome proliferators. We have also shown that a variety of hypolipidaemic drugs and fatty acids can activate PPAR. This supports the suggestion that the physiological role of PPAR is to regulate fatty acid homeostasis, and provides further evidence that PPAR is the target of the fibrate class of hypolipidaemic drugs. Finally, we have demonstrated that a metabolically stabilized fatty acid is a potent PPAR activator, suggesting that fatty acids, or their acyl CoA derivatives, may be the natural ligands of PPAR.