The effect of bacterial infections on ketone concentrations in rat liver and blood and on free fatty acid concentrations in rat blood

Neufeld, Harold A.; Pace, J.; White, Frost

doi:10.1016/0026-0495(76)90120-7

Cited by 69 publications

(23 citation statements)

References 21 publications

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“…Similar results were obtained when hepatic malonylCoA was measured by the technique of Guynn et al (32). Hepatic mitochondria isolated from fed, fasted or S. pneumoniae-infected rats showed similar rates of state three and state four respiration, respiratory control index, and ADP:O ratio (6,17,34). No significant differences were observed in the ability of isolated mitochondria to convert fatty acids to ketones in livers from fed, fasted or infected rats (Table VII).…”

Section: Resultsmentioning

confidence: 86%

“…This ketonemic adaptation to starvation reduces the need for energy derived from glucose calories, which in turn spares body protein by decreasing the rate of amino acid usage for glucose synthesis. However, there is a general failure of ketonemic adaptation to occur dunrng caloric deprivation associated with severe sepsis in man, monkey, or rodent (2)(3)(4)(5)(6). Because of the lack of alternative fuels during severe sepsis, skeletal muscle breaks down protein and increases the usage of amino acids, especially the branched-chain ones, as a source of energy (7).…”

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confidence: 99%

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Role of the Liver in Regulation of Ketone Body Production during Sepsis

Wannemacher¹,

Pace²,

Beall³

et al. 1979

J. Clin. Invest.

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A B S T R A C T During caloric deprivation, the septic host may fail to develop ketonemia as an adaptation to starvation. Because the plasma ketone body concentration is a function of the ratio of hepatic production and peripheral usage, a pneumococcal sepsis model was used in rats to measure the complex metabolic events that could account for this failure, including the effects of infection on lipolysis and esterification in adipose tissue, fatty acid transport in plasma and the rates of hepatic ketogenesis and whole body oxidation of ketones. Some of the studies were repeated with tularemia as the model infection. From these studies, it was concluded that during pneumococcal sepsis, the failure of rats to become ketonemic during caloric deprivation was the result ofreduced ketogenic capacity of the liver and a possibly decreased hepatic supply of fatty acids. The latter appeared to be a secondary consequence of a severe reduction in circulating plasma albumin, the major transport protein for fatty acids, with no effect on the degree of saturation of the albumin with free fatty acids. Also, the infection had no significant effect on the rate of lipolysis or release of fatty acids from adipose tissue. Ketone body usage (oxidation) was either unaffected or reduced during pneumococcal sepsis in rats. Thus, a reduced rate of ketone production in the infected host was primarily responsible for the failure to develop starvation ketonemia under these conditions.

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Section: Resultsmentioning

confidence: 86%

mentioning

confidence: 99%

Role of the Liver in Regulation of Ketone Body Production during Sepsis

Wannemacher¹,

Pace²,

Beall³

et al. 1979

J. Clin. Invest.

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“…Neufeld et al(1976) have reported that a physiological level of insulin does not reduce ketone body formation in perfused fasted rat livers but that the coinfusion of insulin and glucose does. These results indicate that the present hormonal status of the liver and doses of insulin are important in evaluating the insulin action on ketogenesis in the isolated perfused liver.…”

Section: Resultsmentioning

confidence: 98%

Time course of ketone body production in the isolated perfused rat liver in response to various stimuli.

et al. 1986

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“…2). IP ibuprofen completely abolished rmIL-la anorexia (food intake 99.4% with ibuprofen/IL-l, 56.3% with saline/IL-l).…”

Section: Methodsmentioning

confidence: 92%

Interleukin-1-induced anorexia in the rat. Influence of prostaglandins.

Hellerstein

Meydani²,

Meydani³

et al. 1989

J. Clin. Invest.

306

107

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The anorexia associated with acute and chronic inflammatory or infectious conditions is poorly understood. Our objectives were to explore the anorexigenic effects of interleukin-1 (IL-1) in the rat. Recombinant human (rh) IL-1,6, murine (rm) IL-la and to a lesser extent rhIL-la significantly reduced food intake at 24.0 gg/kg i.p. but not at lower doses, in young (200-250 g) meal-fed rats on chow diets. The anorexic effect appears to be mediated by prostaglandins since pretreatment with ibuprofen completely blocked it, and a fish oil based diet abolished it, in comparison to corn oil or chow diets. Fish oil feeding also decreased basal and IL-1 stimulated prostaglandin E2 production by tissues in vitro (liver, brain, peritoneal macrophages) and in the whole body. Constant intravenous infusions of lower doses of IL-1 also diminished food intake, though intravenous boluses did not (reflecting rapid renal clearance). Chronic daily administration of IL-1 caused persistent inhibition of food intake for 7-17 d in chow and corn oil fed rats, but had no effect in fish oil fed rats. There was an attenuation of the effect (tachyphylaxis) after 7 d in corn oil and chow fed rats, but slowed weight gain and lower final weights were observed after 17-32 d of daily IL-1. Old (18-20 mo Fisher 344) rats showed less sensitivity to IL-1 induced anorexia. In conclusion, IL-1 is anorexigenic in the rat, but this is influenced by the structural form of IL-1, the route and chronicity of administration, the source of dietary fat, and the age of the animal. The ability of prior fat intake to influence the anorexic response to IL-1 represents a novel nutrient-nutrient interaction with potential therapeutic implications.

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The effect of bacterial infections on ketone concentrations in rat liver and blood and on free fatty acid concentrations in rat blood

Cited by 69 publications

References 21 publications

Role of the Liver in Regulation of Ketone Body Production during Sepsis

Role of the Liver in Regulation of Ketone Body Production during Sepsis

Time course of ketone body production in the isolated perfused rat liver in response to various stimuli.

Interleukin-1-induced anorexia in the rat. Influence of prostaglandins.

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