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Introduction It is well-known that n-3 polyunsaturated fatty acids (PUFAs), especially eicosapentanoic acid (EPA, 20:5, n-3) and docosahexanoic acid (DHA, 22:6, n-3), have positive effects in a wide range of health and disease conditions. For

amphetamine-related transcript (CART), ultimately leading to changes in food intake ( Blouet & Schwartz 2010 ). These neurons integrate information of peripheral signals, such as i) changes in the levels of nutrients/metabolites like glucose, fatty acids and

-inositol states could impact placental lipid metabolism with consequences for fetal development. In this study we sought to address the specific hypothesis that myo-inositol treatment alters the processing of fatty acids in normal human term placenta. We

Introduction Highly unsaturated fatty acids with 20 or more carbon atoms and three or more double bonds (HUFA) are essential components of cellular membranes and can modulate physiological processes, including membrane transport

Overview Fatty acids (FAs) are organic acids largely defined by the length and saturation of the aliphatic side chain attached to a carboxylic acid. In animals, these side chains normally contain an even number of carbon atoms and FAs are grouped

neuroendocrine system occurs mainly during the postnatal period, in contrast to primates, in which it occurs during the third trimester ( Matthews 2002 ). Dietary fatty acids are important regulators of gene expression, acting as intracellular messengers or

fatty acids (FFA) in vitro leads to enhanced rates of insulin secretion ( Sako & Grill 1990 , Newsholme et al. 2007 ), whereas more prolonged treatment can be associated with toxicity ( Lupi et al. 2002 , El-Assaad et al. 2003

availability of substrates for mitochondrial oxidation (from glucose, amino acids and fatty acids). The consequences of failure of these adaptive responses are clearly demonstrated in the syndrome of adrenal insufficiency (in Addison's disease or

different energy requirements. Energy metabolism in normal hearts depends on ATP production from mitochondrial oxidation of glucose and fatty acids (FA; Taegtmeyer 1994 , Stanley & Chandler 2002 ). FA oxidation is the main cardiac energy source accounting

obesity and T2D is characterized as ‘diabesity’ ( Koulouridis 2004 ). A multitude of factors contribute to the pathogenesis of T2D including inflammatory cytokines, increased concentrations of free fatty acids (FFA), adipokines, impaired mitochondrial