1. Resting energy expenditure was measured, by indirect calorimetry, in 12 patients with Parkinson's disease and in eight healthy age-matched control subjects. In the patients with Parkinson's disease measurements were made in both the untreated state and after an injection of the dopamine agonist apomorphine (treated state). In each state muscle rigidity was recorded. 2. Resting energy expenditure was higher in patients with Parkinson's disease in both the treated and untreated states than in the control subjects. Of the patients with Parkinson's disease, seven showed no difference in resting energy expenditure between the two treatment states, whereas four showed markedly increased resting energy expenditure in the untreated state. The change in resting energy expenditure in the untreated state, as compared with the treated state, was significantly related to the development of muscle rigidity in the untreated state. 3. In Parkinson's disease, even in optimally treated patients, resting energy expenditure is raised and this may contribute to the weight loss seen in this disease. Severe muscle rigidity occurring during untreated periods results in a further increase in resting energy expenditure.

No abstract

Oxygen consumption and thyroid hormone status have been investigated in relation to dietary protein and energy intake in young growing rats fed a control diet of 18% protein as well as diets containing 9 and 4.5% protein fed ad libitum and an 18% protein diet fed at a restricted intake for up to 14 days. Measurements of growth rate, food intake and oxygen consumption indicated that the rats fed a 4.5% protein diet ad libitum and those fed restricted amounts of an 18% protein diet have behaved similarly with severely arrested growth and reduced rates of oxygen consumption and food intake. However, the rats fed the 9% protein diet ad libitum differed from the control group only in terms of a reduced growth rate. Among all the rats thyroid hormone status was associated with the metabolic rate only in the case of the concentration of free L-3,3',5-triiodothyronine (T3), which was reduced in the groups fed 4.5% protein and 18% protein (restricted). Total T3 was actually increased in the rats fed 9% and 4.5% protein and unchanged in the restricted group. These differences in the concentrations of free and total T3 appeared to reflect the fact that the binding capacity for T3 increased with decreasing levels of dietary protein. It is concluded therefore that measurement of free rather than total T3 is the appropriate index of physiological thyroid status in protein-energy malnutrition, at least in the rat.

Endotoxins induce muscle wasting in part as a result of depressed protein synthesis. To investigate whether these changes reflect impaired energy transduction, blood flow, O2 extraction, and high-energy phosphates in muscle and whole-body O2 consumption (VO2) have been measured. VO2 was measured for 6h after an initial sublethal dose of endotoxin (Escherichia coli lipopolysaccharide 0.3 mg/100 g body wt sc) or saline and during 6h after a second dose 24 h later. In fed or fasted rats, VO2 was either increased or better maintained after endotoxin. In anesthetized fed rats 3-4 after the second dose of endotoxin VO2 was increased, and this was accompanied by increased blood flow to liver (hepatic arterial supply), kidney, and perirenal brown adipose tissue and a 57 and 64% decrease in flow to back and hindlimb muscle, respectively, with no change in any other organ. Hindlimb arteriovenous O2 was unchanged, indicating markedly decreased aerobic metabolism in muscle, and the contribution of the hindlimb to whole-body VO2 decreased by 46%. Adenosine 5'-triphosphate levels in muscle were unchanged in endotoxin-treated rats, and this was confirmed by topical nuclear magnetic resonance spectroscopy, which also showed muscle pH to be unchanged. These results show that although there is decreased blood flow and aerobic oxidation in muscle, adenosine 5'-triphosphate availability does not appear to be compromised so that the endotoxin-induced muscle catabolism and decreased protein synthesis must reflex some other mechanism.