The thermogenic and metabolic effects of food in liver cirrhosis: Consequences on the storage of nutrients and the hormonal counterregulatory response

The thermogenic effect of food and the rates of oxidation and storage of nutrients were evaluated by indirect calorimetry in 10 cirrhotic patients and seven normal controls for a 6-hour period, after they had consumed a standard meal supplying 15 kcal/kg body weight with 15%, 30%, and 55% protein, fat, and carbohydrate calories, respectively. Although the thermogenic response to food was not significantly lower in patients than in controls (51.6 ± 13.5 v 72.2 ± 8.8 kcal6 h), patients exhibited a delayed and blunted increment of energy expenditure after the meal intake (P < .025). The greater part of the glucose load was oxidized in patients (70.2 ± 3.9% v 50.4 ± 3.9% in controls; P < .01), suggesting a defective glucose storage as glycogen. This result could be related to insulin resistance, which was evidenced by a large increase in glucose and insulin levels after the meal intake in patients (P ± .001). Conversely, lipid oxidation was sharply reduced and de novo lipogenesis occurred in patients, so that the rate of lipid storage was increased. The profiles of circulating levels of catecholamines, thyroid hormones (free thyroxine [FT4] and triiodothyronine [T3]), and glucagon were assayed during the test. Norepinephrine and glucagon levels remained higher in patients throughout the test (P < .001), whereas thyroid hormones stayed in the same range in the two groups. After an initial increase, glucose levels decreased sharply, inducing an activation of counterregulatory hormones, glucagon, and notably, epinephrine, for which the increment was correlated with the decrease of glucose (r = −.917; P < .001). The involvement of counterregulatory hormones led to an increase of lipid oxidation; this may explain the preferential use of fat as a fuel substrate that was observed in these patients at fast.