2-Mercaptoacetate administration depresses the β-oxidation pathway through an inhibition of long-chain acyl-CoA dehydrogenase activity

Bauché, Françoise; Sabourault, D; Giudicelli, Yves; Nordmann, J; Nordmann, Roger

doi:10.1042/bj1960803

Cited by 76 publications

(36 citation statements)

References 31 publications

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“…MA suppresses fatty acid oxidation by inhibiting the long-chain acyl-CoA dehydrogenases that catalyze mitochondrial ␤-oxidation (9). Bauché et al reported that octanoate oxidation was also markedly decreased after MA administration (14). Therefore the suppression of food intake by MCT preloading may be related to the hepatic ATP content.…”

Section: Discussionmentioning

confidence: 99%

Decrease of Food Intake in Rats after Ingestion of Medium-Chain Triacylglycerol

Ooyama

Kojima

Aoyama

et al. 2009

J Nutr Sci Vitaminol

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Summary Previous studies have demonstrated that fatty acid oxidation in the liver may affect food intake. This study examined the influence of preloading of medium-chain triacylglycerol (MCT) on food intake in comparison with long-chain triacylglycerol (LCT). Male rats were fasted for 18 h and then administered LCT or MCT emulsion orally. Each group of rats was allowed to rest for 30 min, and then food intake during 1 h was measured. Food intake in the MCT group was significantly lower than that in the LCT group. To examine the influence of hepatic oxidation, the MCT ϩ MA group was injected intraperitoneally with mercaptoacetate (MA), an inhibitor of fatty acid oxidation, 2 h before ingestion of MCT emulsion. Then, 30 min after ingestion of LCT or MCT emulsion, food intake was measured for 1 h. Food intake in the MCT group was significantly lower than that in the LCT group, but there was no significant difference between the MCT ϩ MA group and the LCT group. Food intake in the MCT ϩ MA group was significantly higher than that in the MCT group. The hepatic ATP content after MCT ingestion was significantly higher than that after LCT ingestion, but there was no significant difference between the MCT ϩ MA group and the LCT group. The hepatic ATP content after MCT ϩ MA ingestion was significantly lower than that after MCT ingestion. These results suggest that ingestion of medium-chain fatty acid (MCFA) increases the liver ATP content in fasted rats, consequently decreasing food intake.

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Section: Discussionmentioning

confidence: 99%

Decrease of Food Intake in Rats after Ingestion of Medium-Chain Triacylglycerol

Ooyama

Kojima

Aoyama

et al. 2009

J Nutr Sci Vitaminol

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“…MA is a blocker of FA oxidation that acts through inhibition of long-chain acyl-CoA dehydrogenase activity in the mitochondrial matrix (2). Whether it also inhibits microsomal ␤-oxidation is unknown.…”

Section: Response Of Lipid and Glucose Metabolism To Mamentioning

confidence: 99%

Blockade of fatty acid oxidation mimics phase II-phase III transition in a fasting bird, the king penguin

Bernard¹,

Mioskowski²,

Groscolas³

2002

American Journal of Physiology-Regulatory, Integrative and Comp

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This study tests the hypothesis that the metabolic and endocrine shift characterizing the phase II-phase III transition during prolonged fasting is related to a decrease in fatty acid (FA) oxidation. Changes in plasma concentrations of various metabolites and hormones and in lipolytic fluxes, as determined by continuous infusion of [2-3 H]glycerol and [1-14 C]palmitate, were examined in vivo in spontaneously fasting king penguins in the phase II status (large fat stores, protein sparing) before, during, and after treatment with mercaptoacetate (MA), an inhibitor of FA oxidation. MA induced a 7-fold decrease in plasma ␤-hydroxybutyrate and a 2-to 2.5-fold increase in plasma nonesterified fatty acids (NEFA), glycerol, and triacylglycerols. MA also stimulated lipolytic fluxes, increasing the rate of appearance of NEFA and glycerol by 60-90%. This stimulation might be partly mediated by a doubling of circulating glucagon, with plasma insulin remaining unchanged. Plasma glucose level was unaffected by MA treatment. Plasma uric acid increased 4-fold, indicating a marked acceleration of body protein breakdown, possibly mediated by a 2.5-fold increase in circulating corticosterone. Strong similarities between these changes and those observed at the phase II-phase III transition in fasting penguins support the view that entrance into phase III, and especially the end of protein sparing, is related to decreased FA oxidation, rather than reduced NEFA availability. MA could be therefore a useful tool for understanding mechanisms underlying the phase II-phase III transition in spontaneously fasting birds and the associated stimulation of feeding behavior.protein sparing; lipolytic fluxes; isotopic tracers; mercaptoacetate; seabirds PROLONGED FASTING IS CHARACTERIZED by the preferential utilization of lipid, with relative sparing of body protein (4, 6, 25). Previous studies indicated that protein sparing depends on the availability of lipid fuels (17). The conservation of body protein that characterizes the so-called phase II of fasting (9, 17) is no longer maintained when a lower threshold in fat stores is reached (6,17,22,25). Then a metabolic shift occurs, with a simultaneous acceleration in the catabolism of body protein and a decrease in the contribution of lipid to energy production, the signature of the so-called phase III of fasting (6,22,25). Entrance into phase III is also accompanied by hormonal changes, such as an increase in the level of circulating glucocorticoids thought to contribute to the stimulation of protein breakdown (10). How fat store availability determines body protein sparing during phase II or accelerated catabolism during phase III is not well understood. Is protein sparing during phase II linked to the availability of nonesterified fatty acids (NEFA) mobilized from adipose tissue, or does it depend on their oxidation? Arguments suggest that NEFA may specifically modulate the breakdown of myofibrillar proteins independently of their oxidation as a fuel for muscle (26). This suggestion agrees with ...

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“…injection of sodium 2-mercaptoacetate (MA; Sigma) after collection of the first blood sample. The drug, which blocks β-oxidation of fatty acids by inhibiting mitochondrial acyl-CoA dehydrogenase [19,20], was freshly prepared in ultra-pure water and injected at doses of 400 or 800 µmol/kg BW. These doses were chosen because MA at doses of 400 to 800 µmol/kg induces food intake in a dose-dependent manner during the light phase in rats maintained on a fat-supplemented diet [14].…”

Section: Experimental Protocolsmentioning

confidence: 99%

Acute Lipoprivation Suppresses Pulsatile Luteinizing Hormone Secretion without Affecting Food Intake in Female Rats

Shahab

Sajapitak

Tsukamura

et al. 2006

Journal of Reproduction and Development

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Abstract. The present study examined the effect of acute lipoprivation on pulsatile luteinizing hormone (LH) secretion in both normal-fat diet, ad libitum-fed and fasted female rats. To produce an acute lipoprivic condition, mercaptoacetate (MA), an inhibitor of fatty acid oxidation, was administered intraperitoneally to ad libitum-fed or 24-h fasted ovariectomized (OVX) rats with or without an estradiol (E2) implant, that produces a negative feedback effect on LH pulses. The steroid treatment was performed to determine the effect of estrogen on lipoprivic changes in LH release, because estrogen enhances fasting-or glucoprivation-induced suppression of LH pulses. Pulsatile LH secretion was suppressed by MA administration in a dose-dependent manner in the ad libitum-fed OVX and OVX+E2 rats. LH pulses were more severely suppressed in the 24-h-fasted OVX and OVX+E2 rats compared to the ad libitum-fed rats. Estrogen slightly enhanced lipoprivic suppression but the effect was not significant. In the present study, increased plasma glucose and free-fatty acid concentrations may indicate a blockade of fatty acid metabolism by the MA treatment, but food intake was not affected by any of the MA doses. Acute vagotomy did not block lipoprivic suppression of LH pulses. Thus, the present study indicates that lipid metabolism is important for maintenance of normal reproductive function even in rats fed a normal-fat diet and lipoprivation may be more critical in fasted animals that probably rely more heavily on fatty acid oxidation to maintain appropriate metabolic fuel levels. In addition, failure of blockade of lipoprivic LH inhibition by vagotomy suggests that lipoprivic information resulting in LH suppression is not transmitted to the brain via the vagus nerve. Key words: Fatty acids, Mercaptoacetate, Gonadotropin, Vagotomy (J. Reprod. Dev. 52: [763][764][765][766][767][768][769][770][771][772] 2006) nergy availability has been considered to be a critical factor maintaining gonadal functions [1] at various reproductive stages in mammalian species, not only in the adult animal [2], but also at the onset of puberty [3,4] and during lactation [5]. Experimentally, food restriction [3,6] or acute food deprivation [7] inhibits pulsatile luteinizing hormone (LH) secretion in rats through central mechanisms [8] and causes suppression of gonadal function. Pulsatile LH release is sensitive to the

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2-Mercaptoacetate administration depresses the β-oxidation pathway through an inhibition of long-chain acyl-CoA dehydrogenase activity

Cited by 76 publications

References 31 publications

Decrease of Food Intake in Rats after Ingestion of Medium-Chain Triacylglycerol

Decrease of Food Intake in Rats after Ingestion of Medium-Chain Triacylglycerol

Blockade of fatty acid oxidation mimics phase II-phase III transition in a fasting bird, the king penguin

Acute Lipoprivation Suppresses Pulsatile Luteinizing Hormone Secretion without Affecting Food Intake in Female Rats

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