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The possibility that dietary-induced thermogenesis may be decreased in obesity has been proposed in recent years. However, the results of human studies so far obtained are conflicting. The present research was undertaken in order to clarify this question. We studied postprandial thermogenesis induced by ingestion of a mixed meal and of a carbohydrate mixture in 15 normal and 12 obese subjects. Blood glucose and plasma insulin levels were measured at the same time. The data obtained have shown that the mean resting metabolic rate (RMR) expressed as a function of body weight3/4, is almost the same in obese as in normal-weight subjects (0.115 +/- 0.018 vs 0.133 +/- 0.021 kj/min/kg3/4, respectively). Moreover, the increment of mixed-meal induced thermogenesis (MM-IT) was 48 +/- 22% in normal and -0.8 +/- 12% in obese subjects, respectively (p less than 0.01). Carbohydrate induced thermogenesis (CHO-IT) appeared slightly higher in normal-weight than in obese subjects (159 +/- 66 vs 98 +/- 46). After carbohydrate ingestion we observed a higher glycemic and insulinemic response in obesity. These results indicate that thermogenesis induced by ingestion of food is reduced in obese subjects; they are also compatible with the idea that insulin resistance could play a role in this phenomenon.

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The effects of prolonged muscular exercise (swim in tepid water for 60 min) on blood glucose, plasma FFA and R-GH were studied in a group of normal rats and the effect on blood glucose and plasma FFA in a group of hypophysectomized rats. The data obtained showed that, whereas in normal rats plasma FFA rose after muscular exercise, plasma R-GH fell sharply. In Hypophysectomized rats, however, muscular exercise did not increase plasma FFA levels.

In many human tissues, fuel is stored for immediate use, as well as for energy exchange between different parts of the body. Fat and glycogen represent, together with proteins, the principal energy storage materials. During energy requirement, e.g. muscular exercise, glycogen as a local reserve, is used first to supply energy needs. Acetyl-carnitine, as an active molecular group, represents an intermediate substrate, usable directly in the working tissue. The present study investigates whether plasma acetyl-carnitine could be a useful biochemical measure for information on fuel exchange in the body, and whether it is a rapidly available energy source exchangeable among tissues with different metabolic functions, such as muscle and liver. The present study investigated control and hepatopathic subjects after maximal and submaximal muscular exercise. Hepatopathic patients may be a useful model, as liver carnitine metabolism is likely to be impaired. Plasma acetyl-carnitine before, during and after maximal exercise in hepatopathic subjects did not differ, while in normal subjects it increased. After submaximal exercise, acetyl-carnitine increased in patients, as well in controls. In the patients (n = 9) with liver metabolism disorders we observed that during maximal exercise plasma acetyl-carnitine varied from 3.26 + 2.18 μηιοΙ/1 (time 0 min) to 4.30 ± 2.02 μιηοΐ/ΐ (time 20 min) and from 1.99 ± 1.36 μηιοΐ/ΐ to 4.83 ± 2.60 μηιοΐ/ΐ (ρ < 0.05) in the controls (n = 7). During submaximal exercise, plasma acetyl-carnitine varied from 1.89 ±1.7 μηιοΙ/1 (time Omin) to 2.92 ± 2.22 μιηοΐ/ΐ (time 30 min) (p < 0.05) and to 4.32 ± 2.22 μηιοΙ/1 (recovery, time 90 min) in controls, while in patients there was a significant variation from 2.98 ± 1.52 μηιοΙ/1 (time Omin) to 5.98 ± 1.43 μηιοΙ/1 (recovery, tim.e 90min). Although plasma acetyl-carnitine concentrations were related to tissue metabolism variations, the relationships of substrate fuel exchange to tissue carnitine metabolism between different parts of the body are still unclear. sential in lipid catabolism (1). Of the different esters Glucose, lipids and amino acids are the principal acetyl-carnitine without doubt holds an important sources of energy during exercise. All metabolic proc-position as a molecule able to subtract acetyl (carniesses depend on an intermediate acetyl group, prin-tine as acceptor for acetyl units) from acetyl-coenzyme cipally bound to coenzyme A to form acetyl-coenzyme A, while maintaining a viable pool of coenzyme A, A. Many researchers have investigated the regulatory as well as storing "active acetate", readily available factors influencing one of the substrates (carbohy-for trans-acetylation back to acetyl-coenzyme A drates, lipids or amino acids) relative to the metabolic (2-4). et Q fpInvestigation of carnitine and acyl-carnitine metabolThe carnitine "shuttle" mechanism, by which fatty ism in different types of tissue has produced very acids are transported across the mitochondria mem-interesting results. Considerable difficulties, however, b...