Total and individual free fatty acid concentrations in liver cirrhosis

Riggio, Oliviero; Merli, Manuela; Cantàfora, Alfredo; Biase, Antonella Di; Lalloni, L.; Leonetti, Frida; Miazzo, P.; Rinaldi, Vittorio; Fanelli, Filippo Rossi; Tamburrano, G.; Capocaccia, L.

doi:10.1016/0026-0495(84)90064-7

Cited by 52 publications

(30 citation statements)

References 15 publications

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“…As far as nutritional indices and carnitine plasma level were concerned, the weak direct correlation between triceps skinfold and long chain acylcarnitine that we found is in keeping with the observation that in cirrhotics the amount of free fatty acids coming to the liver is linked to the amount of subcutaneous fat, expressed by triceps skinfold (17). In fact, in cells, free fatty acids must be activated to acyl-CoA to undergo ß-oxidation.…”

Section: Carnitine and Nutritionsupporting

confidence: 89%

Plasma Carnitine Levels in Liver Cirrhosis: Relationship with Nutritional Status and Liver Damage

Amodio¹,

Angeli²,

Merkel³

et al. 1990

Clinical Chemistry and Laboratory Medicine

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Summary:The plasma level of carnitine, a co-factor involved in many metabolic reactions, is high in alcoholic liver cirrhosis, due to an increased amount of esterified carnitine. To determine if this alteration is linked to alcoholic liver disease or to liver cirrhosis per se, total carnitine, free carnitine, total esterified carnitine, short chain acylcarnitine and long chain acylcarnitine were measured in 41 patients suffering from liver cirrhosis of different aetiology and severity. In 19 of these patients, acetylcarnitine was also measured. Moreover, multivariate analysis was performed to assess the association of carnitine plasma levels with nutritional and liver disease indices.Of the nutritional indices (creatinine/height ratio, mid upper arm muscle circumference and triceps skinfold) only triceps skinfold appeared to be weakly correlated with carnitine (with long chain acylcarnitine).Significantly high levels of acetylcarnitine, short chain acylcarnitine, total esterified carnitine and total carnitine were found in cirrhotics independently of the aetiology of cirrhosis, even though a trend towards higher levels of acetylcarnitine was evident in heavy drinkers.Direct correlations of -glutamyltransferase with acetylcarnitine, acetylcarnitine/free carnitine, short chain acylcarnitine/free carnitine and total esterified carnitine/free carnitine were found. Carnitine plasma levels did not differ in the three Pugh-Chiltfs classes; however, a trend towards higher levels of acetylcarnitine was found in Pugh-ChilcTs class C.

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Section: Carnitine and Nutritionsupporting

confidence: 89%

Plasma Carnitine Levels in Liver Cirrhosis: Relationship with Nutritional Status and Liver Damage

Amodio¹,

Angeli²,

Merkel³

et al. 1990

Clinical Chemistry and Laboratory Medicine

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“…Cirrhotic patients manifest glucose intolerance (1, 2), an abnormal plasma lipid profile (13)(14)(15), and impaired insulin-mediated glucose disposal (5)(6)(7)(8). However, none ofthese previous studies attempted to examine whether the disturbances in glucose and lipid metabolism were related, nor did they examine the lower, more physiologic portion ofthe plasma insulin ,uU/ml) dose response curve where the suppressive effect of insulin on hepatic glucose production and FFA turnover are maximal.…”

Section: Discussionmentioning

confidence: 99%

“…Cirrhosis is characterized by a number of abnormalities in circulating substrate and hormone concentrations including FFA (13)(14)(15), glucagon (54), growth hormone (55), norepinephrine (56), and insulin itself(l-8). Moreover, an increase in each of these substrates has been shown to be associated with the development of insulin resistance.…”

Section: Discussionmentioning

confidence: 99%

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Effect of physiologic hyperinsulinemia on glucose and lipid metabolism in cirrhosis.

Petrides¹,

Groop²,

Riely³

et al. 1991

J. Clin. Invest.

140

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Insulin secretion and insulin sensitivity were evaluated in eight clinically stable cirrhotic patients and in 12 controls. OGTT was normal in cirrhotics but plasma insulin response was increased approximately twofold compared with controls. Subjects received a three-step (0.1, 0.5, 1.0 mU/kg -min) euglycemic insulin clamp with indirect calorimetry, 16-311J-glucose, and 11-"CJ-palmitate. During the two highest insulin infusion steps glucose uptake was impaired (333±031 vs. 5.06±0.40 mg/ kg. min, P < 0.01, and 6.09+0.50 vs. 7.95±0.52 mg/kg.m-, P < 0.01). Stimulation of glucose oxidation by insulin was normal; in contrast, nonoxidative glucose disposal (i.e., glycogen synthesis) was markedly reduced. Fasting (r = -0.553, P < 0.01) and glucose-stimulated (r = -0.592, P < 0.01) plasma insulin concentration correlated inversely with the severity of insulin resistance. Basal hepatic glucose production was normal in cirrhotics and suppressed normally with insulin. In postabsorptive state, plasma FFA conc (933±42 vs. 711±44 Mmol/ liter, P < 0.01) and FFA turnover (9.08±1.20 vs. 6. 03±0.53 ,umol/kg min, P < 0.01) were elevated in cirrhotics despite basal hyperinsulinemia; basal FFA oxidation was similar in cirrhotic and control subjects. With low-dose insulin infusion, plasma FFA oxidation and turnover failed to suppress normally in cirrhotics. During the two higher insulin infusion steps, all parameters of FFA metabolism suppressed normally. In summary, stable cirrhotic patients with normal glucose tolerance exhibit marked insulin resistance secondary to the impaired nonoxidative glucose disposal. Our results suggest that chronic hyperinsulinism may be responsible for the insulin resistance observed in cirrhosis. (J. Clin. Invest. 1991. 88:561-570.)

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“…Previous data have shown low IGF-I levels in these patients, even with improving liver function, which may also reflect hepatocyte receptor damage. 38 Plasma NEFAs and lipid oxidation rates are elevated in CLD, 39,40 with increased rates of lipid oxidation, despite high plasma insulin levels. Indirect calorimetry in CLD is consistent with NEFAs providing energy normally derived from carbohydrates, the increased delivery of NEFAs to skeletal muscle inhibiting glycolysis and glucose oxidation in both basal and insulin-stimulated conditions.…”

Section: Discussionmentioning

confidence: 99%

Temporal changes in insulin sensitivity following the development of acute liver failure secondary to acetaminophen

et al. 2001

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Total and individual free fatty acid concentrations in liver cirrhosis

Cited by 52 publications

References 15 publications

Plasma Carnitine Levels in Liver Cirrhosis: Relationship with Nutritional Status and Liver Damage

Plasma Carnitine Levels in Liver Cirrhosis: Relationship with Nutritional Status and Liver Damage

Effect of physiologic hyperinsulinemia on glucose and lipid metabolism in cirrhosis.

Temporal changes in insulin sensitivity following the development of acute liver failure secondary to acetaminophen

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