Inhibition by 5‐(tetradecyloxy)‐2‐furoic acid of fatty acid and cholesterol synthesis in isolated rat hepatocytes

E, Panek; Cook, George A.; Cornell, Neal W.

doi:10.1007/bf02533270

Cited by 38 publications

(18 citation statements)

References 18 publications

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“…As expected, oleate (1 mM) decreased both the rate of endogenous lipogenesis (Table 1; Mayes & Topping, 1974) and that in the presence of dihydroxyacetone. In confirmation of the results of Panek et al (1977), 5-(tetradecyloxy)-2-furoic acid inhibited the endogenous rate of lipogenesis by at least 80% in hepatocytes from both virgin and lactating rats. The inhibition may be due to decreased transport of citrate from the mitochondria (Ribereau-Gayon, 1976) or alternatively to inhibition of acetyl-CoA carboxylase (Kariya & Wille, 1978).…”

Section: Resultssupporting

confidence: 66%

“…To test this point we have examined the effects of 5-(tetradecyloxy)-2-furoic acid, an inhibitor of the transmitochondrial membrane transport of citrate (Ribereau-Gayon, 1976), on the metabolism of hepatocytes from fed virgin and lactating rats. This compound has been shown to decrease lipogenesis in hepatocytes from fed rats (Panek et al, 1977) and in mammary-gland acini from lactating rats (Robinson & Williamson, 1977). Hepatocytes from lactating rats were chosen because they have a lower rate of ketogenesis compared with hepatocytes from virgin rats (Whitelaw & Williamson, 1977), and studies with liver slices suggest they may Vol, 176 have a higher rate of lipogenesis (Smith, 1973).…”

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confidence: 99%

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Evidence for a reciprocal relationship between lipogenesis and ketogenesis in hepatocytes from fed virgin and lactating rats

Benito¹,

Williamson²

1978

Biochemical Journal

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Lipogenesis is increased in hepatocytes from fed lactating rats compared with virgin rats. Inhibition of lipogenesis with 5-(tetradecyloxy)-2-furoic acid resulted in increased ketogenesis from endogenous substrate, but not from oleate. Dihydroxyacetone increased lipogenesis and esterification of [1-14C]oleate and decreased ketogenesis; these changes were reversed by the inhibitor. The reciprocal relationship between lipogenesis and ketogenesis in hepatocytes from fed rats may be due to alterations in [malonyl-CoA]

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Section: Resultssupporting

confidence: 66%

mentioning

confidence: 99%

Evidence for a reciprocal relationship between lipogenesis and ketogenesis in hepatocytes from fed virgin and lactating rats

Benito¹,

Williamson²

1978

Biochemical Journal

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“…This marked decrease in fatty acid synthesis with a modest decrease in cholesterol synthesis has also been noted in the liver after TOFA treatment (17)(18)(19).…”

Section: Discussionsupporting

confidence: 54%

Fatty acids are required for epidermal permeability barrier function.

Man

Elias²,

Feingold³

1993

J. Clin. Invest.

156

117

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The permeability barrier is mediated by a mixture of ceramides, sterols, and free fatty acids arranged as extracellular lamellar bilayers in the stratum corneum. Whereas prior studies have shown that cholesterol and ceramides are required for normal barrier function, definitive evidence for the importance of nonessential fatty acids is not available. To determine whether epidermal fatty acid synthesis also is required for barrier homeostasis, we applied 5-(tetradecyloxy)-2-furancarboxylic acid (TOFA), an inhibitor of acetyl CoA carboxylase, after disruption of the barrier by acetone or tape stripping. TOFA inhibits epidermal fatty acid by -50% and significantly delays barrier recovery. Moreover, coadministration of palmitate with TOFA normalizes barrier recovery, indicating that the delay is due to a deficiency in bulk fatty acids. Furthermore, TOFA treatment also delays the return of lipids to the stratum corneum and results in abnormalities in the structure of lamellar bodies, the organelle which delivers lipid to the stratum corneum. In addition, the organization of secreted lamellar body material into lamellar bilayers within the stratum corneum interstices is disrupted by TOFA treatment. Finally, these abnormalities in lamellar body and stratum corneum membrane structure are corrected by coapplication of palmitate with TOFA. These results demonstrate a requirement for bulk fatty acids in barrier homeostasis. Thus, inhibiting the epidermal synthesis of any of the three key lipids that form the extracellular, lipid-enriched membranes of the stratum corneum results in an impairment in barrier homeostasis. (J. Clin. Invest. 1993. 92:791-798.) Key words: transepidermal water loss . fatty acid synthesis . 5-(tetradecyloxy)-2-furancarboxylic acid * stratum corneum lipids * permeability barrier

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“…*P<0.05 versus G5. by 90% by TOFA, a specific inhibitor of ACC (Panek et al, 1977). Moreover, intracellular lipid accumulation was detected following a 24-hour treatment with either 25 mM glucose or insulin, whereas very few lipid droplets could be detected in myotubes cultured under basal conditions (Fig.…”

Section: Glucose Stimulates Lipogenesis In Contracting Myotubesmentioning

confidence: 86%

Glucose induces de novo lipogenesis in rat muscle satellite cells through a sterol-regulatory-element-binding-protein-1c-dependent pathway

Guillet-Deniau

Pichard

Koné

et al. 2004

Journal of Cell Science

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We previously reported that sterol-regulatory-element-binding-protein-1c (SREBP-1c) mediates insulin upregulation of genes encoding glycolytic and lipogenic enzymes in rat skeletal muscle. Here, we assessed whether glucose could regulate gene expression in contracting myotubes deriving from cultured muscle satellite cells. Glucose uptake increased twofold after a 30 minute treatment with a high glucose concentration, suggesting an acute glucose-stimulated glucose uptake. Time-course experiments showed that, within 3 hours, glucose stimulated the expression of hexokinase II, fatty acid synthase and acetyl-CoA-carboxylase-2 proteins, leading to an increased lipogenic flux and intracellular lipid accumulation in contracting myotubes. Furthermore, kinetic experiments indicated that glucose upregulated SREBP-1c precursor and nuclear proteins within 30 minutes, SREBP-1c nuclear translocation being confirmed using immunocytochemistry. In addition, the knockdown of SREBP-1 mRNA using a RNA-interference technique totally abrogated the glucose-induced upregulation of lipogenic enzymes, indicating that SREBP-1c mediates the action of glucose on these genes in rat skeletal muscle. Finally, we found that glucose rapidly stimulated SREBP-1c maturation through a Jak/STAT dependent pathway. We propose that increased intramuscular lipid accumulation associated with muscle insulin resistance in obesity or type-2 diabetes could arise partly from de novo fatty acid synthesis in skeletal muscle.

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Inhibition by 5‐(tetradecyloxy)‐2‐furoic acid of fatty acid and cholesterol synthesis in isolated rat hepatocytes

Cited by 38 publications

References 18 publications

Evidence for a reciprocal relationship between lipogenesis and ketogenesis in hepatocytes from fed virgin and lactating rats

Evidence for a reciprocal relationship between lipogenesis and ketogenesis in hepatocytes from fed virgin and lactating rats

Fatty acids are required for epidermal permeability barrier function.

Glucose induces de novo lipogenesis in rat muscle satellite cells through a sterol-regulatory-element-binding-protein-1c-dependent pathway

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