Carbohydrate sparing of fatty acid oxidation. I. The relation of fatty acid chain length to the degree of sparing. II. The mechanism by which carbohydrate spares the oxidation of palmitic acid

Lossow, W.J.; Chaikoff, I.L.

doi:10.1016/0003-9861(55)90173-9

Cited by 164 publications

(14 citation statements)

References 15 publications

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“…The nature of the "onoff" signal for this reaction, however, is completely unknown. Since it has long been suspected that the regulation of fatty acid oxidation in the liver is intimately related to some facet of carbohydrate metabolism (6)(7)(8), it seemed possible that alterations in the latter might be involved in the control of carnitine acyltransferase and thereby dictate ketogenic potential. Moreover, since hepatic carbohydrate metabolism, which plays a central role in glucose homeostasis, appears to be under bihormonal control by insulin and glucagon (9)(10)(11)(12)(13), the further possibility exists that fluctuation in the relative blood concentrations of these two hormones also represents the key determinant of hepatic ketogenic capacity.…”

Section: Introductionmentioning

confidence: 99%

Hormonal control of ketogenesis. Rapid activation of hepatic ketogenic capacity in fed rats by anti-insulin serum and glucagon.

McGarry¹,

Wright²,

Foster³

1975

J. Clin. Invest.

218

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A B STR A CT The enhanced capacity for long-chain fatty acid oxidation and ketogenesis that develops in the rat liver between 6 and 9 h after the onset of starvation was shown to be inducible much more rapidly by administration of anti-insulin serum or glucagon to fed rats. After only 1 h of treatment with either agent, the liver had clearly switched from a "nonketogenic" to a "ketogenic" profile, as determined by rates of acetoacetate and 1-hydroxybutyrate production on perfusion with oleic acid. As was the case after starvation, the administration of insulin antibodies or glucagon resulted in depletion of hepatic glycogen stores and a proportional increase in the ability of the liver to oxidize long-chain fatty acids and (-)-octanoylcarnitine, suggesting that all three treatment schedules activated the carnitine acyltransferase system of enzymes. In contrast to anti-insulin serum, which produced marked elevations in plasma glucose, free fatty acid, and ketone body concentrations, glucagon treatment had little effect on any of these parameters, presumably due to enhanced insulin secretion after the initial stimulation of glycogenolysis. Thus, after treatment with glucagon alone, it was possible to obtain a "ketogenic" liver from a nonketotic animal. The results are consistent with the possibility that the activity of carnitine acyltransferase, and thus ketogenic capacity, is subject to bihormonal control through the relative blood concentrations of insulin and glucagon, as also appears to be the case with hepatic carbohydrate metabolism.

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Section: Introductionmentioning

confidence: 99%

Hormonal control of ketogenesis. Rapid activation of hepatic ketogenic capacity in fed rats by anti-insulin serum and glucagon.

McGarry¹,

Wright²,

Foster³

1975

J. Clin. Invest.

218

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“…CO 2 from expired gas was measured was first reported by Schwabe et al [5]. Subsequently, many authors [6][7][8] have described the digestion and absorption of fat, using 14 C. However, because 131 I-labeled compounds and 14 Clabeled lipids are radioactive isotopes and may harm patients, their usage has decreased. Since the 1970s, the 13 CO 2 test of expired gas by 13 C-labeled compounds has been adopted [9][10][11].…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, this test cannot be a generally accepted one. There have, so far, been no reports which evaluated reconstructive operations after gastrectomy by direct examinations utilizing 14 C or 13 C compounds.…”

Section: Discussionmentioning

confidence: 99%

“…Conventional methods such as the pancreatic function diagnostic test (PFD) and dxylose absorption test are not direct examinations. Although examinations utilizing 14 C compounds are direct examinations, they have, so far, only been performed in a limited number of patients. In addition, such examinations use radioactive isotopes, and therefore have recently fallen out of favour.…”

Section: Introductionmentioning

confidence: 99%

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Quantitative evaluation of reconstruction methods after gastrectomy using a new type of examination: digestion and absorption test with stable isotope 13 C-labeled lipid compound

2003

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“…Upon refeeding a high-carbohydrate fat-free diet to starved animals, long-chain fatty acid oxidation in both liver and extra hepatic tissue is markedly decreased (Lossow and Chaikoff 1955), with a corresponding decrease in the concentration of plasma free fatty acids (Gordon 1957), but there is a marked and coordinate elevation of the levels of all the key enzymes of lipogenesis (Muto and Gibson 1970). However, it has been observed that under these nutritional conditions lipogenesis does not commence until at least 4 h after the feeding of the high-carbohydrate diet to the starved animal (Baker et al 1968).…”

Section: Introductionmentioning

confidence: 99%

The Acute Biochemical Response of the Starved Rabbit Liver in Situ to Glucose Infusion

Jd¹,

Irving²,

Pf³

et al. 1974

Aust. Jnl. Of Bio. Sci.

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Increasing the blood glucose levels from 88 to 400 mg/IOO ml in rabbit liver in situ during 5-min time intervals resulted in a decrease in the production of C02 from C-I of liver glucose together with a slight increase in the oxidation of C-6 of glucose; this was caused by a high glucose-induced decrease in the activity of the oxidative pentose phosphate pathway. Increasing the glucose concentrations also resulted in a threefold increase in the levels of palmitoyl-and stearoyl-CoA esters at a glucose load of 0·8 g; this is consistent with a specific feed-back inhibition of the production of NADPH by reactions of the oxidative pentose phosphate pathway by long-chain fatty acyl-CoAs. A decrease in plasma free fatty acids occurred when blood glucose levels were raised; this was associated with an increase in the concentration of free fatty acids in liver.There was a decreased glucose output by liver following an increased glucose load. In liver there were increases in AMP levels, decreased ATP levels, a twofold increase in fructose 1,6-diphosphate and a fall in glucose 6-phosphate and fructose 6-phosphate concentrations. These changes are indicative of the decreased gluconeogenic flux caused through inhibition of hexosediphosphatase by AMP, and the elevated levels of the long-chain fatty acyl-CoA esters probably acted to inhibit adenine nucleotide translocation across the mitochondrial membrane. The formation of sn-glycero-3-phosphate appears to be the rate-limiting step for relieving the inhibitions caused by the accumulation of long-chain fatty acyl-CoAs.

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Carbohydrate sparing of fatty acid oxidation. I. The relation of fatty acid chain length to the degree of sparing. II. The mechanism by which carbohydrate spares the oxidation of palmitic acid

Cited by 164 publications

References 15 publications

Hormonal control of ketogenesis. Rapid activation of hepatic ketogenic capacity in fed rats by anti-insulin serum and glucagon.

Hormonal control of ketogenesis. Rapid activation of hepatic ketogenic capacity in fed rats by anti-insulin serum and glucagon.

Quantitative evaluation of reconstruction methods after gastrectomy using a new type of examination: digestion and absorption test with stable isotope 13 C-labeled lipid compound

The Acute Biochemical Response of the Starved Rabbit Liver in Situ to Glucose Infusion

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