The effect of cholesterol administration on lipid biosynthesis by rabbit aortic mitochondria

Whereat, Arthur F.; Orishimo, Margaret W.

doi:10.1016/0014-4800(68)90038-5

Cited by 12 publications

(4 citation statements)

References 24 publications

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“…It has therefore been postulated that the reversal of fatty acid oxidation does not function in the elongation of palmitate or stearate but conserves reducing power (NADPH and NADH) or funnels energy from NADPH into the electron-transport chain (115,129,130). This would only occur when the cell experiences low levels of oxygen or high levels of ATP (115,(129)(130)(131). It seems clear in any case that the ratios of NADPH/NADP+ and of NADH/NAD+, the rate of J3-oxidation, and the reversal of this process in mitochondria are closely interrelated.…”

Section: Mitochondrial Systemsmentioning

confidence: 99%

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Control Mechanisms in the Synthesis of Saturated Fatty Acids

Bloch¹,

Vance²

1977

Annu. Rev. Biochem.

319

140

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Section: Mitochondrial Systemsmentioning

confidence: 99%

“…Reversal of J3-oxidation appears to be the major if not the only mecha nism for fatty acid synthesis in heart muscle and it may be governed only by the NADH/NAD+ ratio since NADPH is not required for this reversal (129,131).…”

Section: Mitochondrial Systemsmentioning

confidence: 99%

Control Mechanisms in the Synthesis of Saturated Fatty Acids

Bloch¹,

Vance²

1977

Annu. Rev. Biochem.

319

140

View full text Add to dashboard Cite

“…This assumption may be true for polyunsaturated fatty acids, because their plaque concentrations are correlated with their serum and adipose content in humans, but such a relationship does not appear to hold for saturated fatty acids (10), suggesting that fatty acids like palmitate may be synthesized in lesions. In fact, a series of studies dating from nearly half a century ago demonstrated the capacity of the vasculature for de novo lipogenesis (11)(12)(13). In rabbit and pigeon models, atherosclerosis accelerates vascular fatty acid synthesis, and the plaque itself appears to be the predominant site of synthesis (14,15).…”

mentioning

confidence: 99%

Macrophage Fatty-acid Synthase Deficiency Decreases Diet-induced Atherosclerosis

Schneider

Yang

Chakravarthy

et al. 2010

Journal of Biological Chemistry

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Fatty acid metabolism is perturbed in atherosclerotic lesions, but whether it affects lesion formation is unknown. To determine whether fatty acid synthesis affects atherosclerosis, we inactivated fatty-acid synthase (FAS) in macrophages of apoEdeficient mice. Serum lipids, body weight, and glucose metabolism were the same in FAS knock-out in macrophages (FASKOM) and control mice, but blood pressure was lower in FASKOM animals. Atherosclerotic extent was decreased 20 -40% in different aortic regions of FASKOM as compared with control mice on Western diets. Foam cell formation was diminished in FASKOM as compared with wild type macrophages due to increased apoAI-specific cholesterol efflux and decreased uptake of oxidized low density lipoprotein. Expression of the anti-atherogenic nuclear receptor liver X receptor ␣ (LXR␣; Nr1h3) and its downstream targets, including Abca1, were increased in FASKOM macrophages, whereas expression of the potentially pro-atherogenic type B scavenger receptor CD36 was decreased. Peroxisome proliferator-activated receptor ␣ (PPAR␣) target gene expression was decreased in FASKOM macrophages. PPAR␣ agonist treatment of FASKOM and wild type macrophages normalized PPAR␣ target gene expression as well as Nr1h3 (LXR␣). Atherosclerotic lesions were more extensive when apoE null mice were transplanted with LXR␣-deficient/FAS-deficient bone marrow as compared with LXR␣-replete/FAS-deficient marrow, consistent with antiatherogenic effects of LXR␣ in the context of FAS deficiency. These results show that macrophage FAS deficiency decreases atherosclerosis through induction of LXR␣ and suggest that FAS, which is induced by LXR␣, may generate regulatory lipids that cause feedback inhibition of LXR␣ in macrophages.

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“…An increased rate of fatty acid synthesis and incorporation of these synthe sized fatty acids into various lipid classes has been demonstrated in the atheroscle rotic arteries of animals (1). The differences in the esterification of fatty acids into phospholipids and glycerides could be due to enzyme specificity toward the fatty acid substrates.…”

mentioning

confidence: 99%