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Fátima Pérez de Heredia, Elvira Larqué, Salvador Zamora, and Marta Garaulet

, Sánchez et al . 2008 ). In addition, DHEA-S can modulate fatty acid (FA) metabolism, through up-regulation of hepatic enzymes involved in β-oxidation ( Waxman 1996 , Depreter et al . 2002 ). The relevance of FAs is far beyond their role as energy

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Z Cheng, M Elmes, S E Kirkup, E C Chin, D R E Abayasekara, and D C Wathes

Introduction Dietary polyunsaturated fatty acids (PUFAs) provide the body with energy, contribute structural components to cell membranes and also act as the precursors for prostaglandin (PG) synthesis. Linoleic acid (LA; 18:2 n -6

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Sabina Paglialunga, Patrick Schrauwen, Christian Roy, Esther Moonen-Kornips, Huiling Lu, Matthijs K C Hesselink, Yves Deshaies, Denis Richard, and Katherine Cianflone

as the quotient of VCO 2 /VO 2 . Plasma assays Fasting plasma samples were taken at the time of killing by cardiac puncture. Plasma TGs and non-esterified fatty acids (NEFA) were measured using colorimetric

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Rengasamy Palanivel, Vivian Vu, Min Park, Xiangping Fang, and Gary Sweeney

contractile performance is derived from fatty acids while the remainder (∼30%) is principally obtained via metabolism of glucose ( Stanley et al . 2005 , An & Rodrigues 2006 ). Well-controlled fatty acid metabolism is also important to prevent triglyceride

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William WN Jr, RB Ceddia, and R Curi

Leptin directly increases the rate of exogenous glucose and fatty acids oxidation in isolated adipocytes. However, the effects of leptin on fatty acid metabolism in white adipose tIssue have not been examined in detail. Here, we report that in adipocytes incubated for 6 h in the presence of leptin (10 ng/ml), the insulin-stimulated de novo fatty acid synthesis was inhibited by 36% (P<0.05), while the exogenous oxidation of acetic and oleic acids was increased by 50% and 76% respectively. Interestingly, leptin did not alter the oxidation of intracellular fatty acids. Leptin-incubated cells presented a 16-fold increase in the incorporation of oleic acid into triglyceride (TG) and a 123% increase in the intracellular TG hydrolysis (as measured by free fatty acids release). Fatty acid-TG cycling was not affected by leptin. By employing fatty acids radiolabeled with (3)H and (14)C, we could determine the concomitant influx of fatty acids (incorporation of fatty acids into TG) and efflux of fatty acids (intracellular fatty acids oxidation and free fatty acids release) in the incubated cells. Leptin increased by 30% the net efflux of fatty acids from adipocytes. We conclude that leptin directly inhibits de novo synthesis of fatty acids and increases the release and oxidation of fatty acids in isolated rat adipocytes. These direct energy-dissipating effects of leptin may play an important role in reducing accumulation of fatty acids into TG of rat adipose cells.

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Brendan J Waddell, Maike Bollen, Caitlin S Wyrwoll, Trevor A Mori, and Peter J Mark

activity. In addition, we measured urinary levels of corticosterone and aldosterone and adrenal expression of key genes that promote adrenal steroidogenesis. The interactive effects of a postnatal, high-omega-3 fatty acid diet were also assessed because our

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Luana Lopes Souza, Aline Cordeiro, Lorraine Soares Oliveira, Gabriela Silva Monteiro de Paula, Larissa Costa Faustino, Tania Maria Ortiga-Carvalho, Karen Jesus Oliveira, and Carmen Cabanelas Pazos-Moura

have important implications, both at physiological and pharmacological levels. Fatty acids are described as PPAR endogenous agonists, being polyunsaturated fatty acids of the omega 3 family (n-3 PUFA) high-affinity agonists ( Bordoni et al . 2006

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The fatty acid patterns of the cholesterol ester, triglyceride and phospholipid fractions of serum from thirteen hypothyroid subjects have been determined using gas-liquid chromatography.

A comparison was made with the results of similar analyses performed on sixteen apparently normal subjects and on eighteen patients with ischaemic heart disease. A trend towards increasing saturation was found in each of the fractions from the hypothyroid subjects. This was most marked in the cholesterol esters.

The mechanism of the production of this trend is discussed and it is suggested that it is secondary to the hyperlipidaemia of hypothyroidism.

Attention is drawn to the implication of these findings in interpreting the reported changes in the fatty acid composition of the serum lipids in atherosclerosis.

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C Gravena, PC Mathias, and SJ Ashcroft

Fatty acids have both stimulatory and inhibitory effects on insulin secretion. Long-term exposure to fatty acids results in impaired insulin secretion whilst acute exposure has generally been found to enhance insulin release. However, there are conflicting data in the literature as to the relative efficacy of various fatty acids and on the glucose dependency of the stimulatory effect. Moreover, there is little information on the responses of human islets in vitro to fatty acids. We have therefore studied the acute effects of a range of fatty acids on insulin secretion from rat and human islets of Langerhans at different glucose concentrations. Fatty acids (0.5 mM) acutely stimulated insulin release from rat islets of Langerhans in static incubations in a glucose-dependent manner. The greatest effect was seen at high glucose concentration (16.7 mM) and little or no response was elicited at 3.3 or 8.7 mM glucose. Long-chain fatty acids (palmitate and stearate) were more effective than medium-chain (octanoate). Saturated fatty acids (palmitate, stearate) were more effective than unsaturated (palmitoleate, linoleate, elaidate). Stimulation of insulin secretion by fatty acids was also studied in perifused rat islets. No effects were observed at 3.3 mM glucose but fatty acids markedly potentiated the effect of 16.7 mM glucose. The combination of fatty acid plus glucose was less effective when islets had been first challenged with glucose alone. The insulin secretory responses to fatty acids of human islets in static incubations were similar to those of rat islets. In order to examine whether the responses to glucose and to fatty acids could be varied independently we used an animal model in which lactating rats are fed a low-protein diet during early lactation. Islets from rats whose mothers had been malnourished during lactation were still able to respond effectively to fatty acids despite a lowered secretory response to glucose. These data emphasise the complex interrelationships between nutrients in the control of insulin release and support the view that fatty acids play an important role in glucose homeostasis during undernutrition.

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Georgia Frangioudakis and Gregory J Cooney

protein kinase B (PKB) under conditions of physiological insulin elevation ( Frangioudakis et al . 2005 ). Insulin resistance can also be induced by an acute infusion of lipid to elevate circulating fatty acid (FA; Chalkley et al . 1998 , Ye et al