F. Schwarz

Metabolic Observations during the Treatment of Obese Patients by Periods of Total Starvation

Ten very obese female patients were treated by periods of total starvation lasting 10 days each. In the interval between these starvation periods, a diet of 600 calories was given. Twenty-one periods were completed, 6 patients went through 3 periods each. The fasting was generally well tolerated; with the appearance of ketone bodies in the urine the feeling of hunger diminished. The average weight loss during total starvation was 447 Gm./day ranging from 290 to 600 Gm. Nitrogen excretion was on the average 4.15 Gm./day (2.6–7.2). There was no significant decrease in BMR neither a lowering of body temperature. During the third starvation period weight loss was less than during the other two, but the BMR did not decrease. There were no changes in serum electrolytes, HCO3-, pH, urea, creatinine or serum proteins. The excretion of 17-OHCS dropped significantly but remained within the normal range. The excretion of 17-KS dropped to subnormal values. Plasma FFA were elevated at the start of the experiment. Generally there was some rise from the first to the seventh day of the starvation periods. In the patients who completed 3 periods the FFA values were lower during the third than during the first period. Serum cholesterol, total fat and phospholipids did not show significant changes. The blood sugar values showed some decrease during starvation which was statistically not significant. The implications of these findings are discussed. We are of the opinion that our patients did not exhibit signs of a disturbance in fat mobilization.

Serum growth hormone and energy supply in fasting obese patients.

Abstract Serum growth hormone (GH) levels, plasma free fatty acids (FFA) and blood glucose were determined during periods of total starvation in 13 severely obese patients, 2 of whom were suffering from hypopituitarism, and in 2 normal volunteers. In all individuals nitrogen excretion was measured and the total caloric expenditure calculated. The percentile contribution of protein to total caloric expenditure (protein ratio = PR) appeared to be lower in the obese than in the normals. GH-values rose steeply in the normals on starvation. In the serum of 4 of the obese no GH could be found, the others showed a slight to moderate response. When these 2 groups of obese were compared with regard to nitrogen excretion, caloric expenditure and PR, no difference was found. Both hypopituitary patients were treated with a small maintenance dose of cortisone. They tolerated starvation well. Their caloric expenditure was lower, but their nitrogen excretion as well as PR-values were in the same range as those of the other obese. From these findings it is concluded that in the obese patients studied, fat mobilization was certainly not impaired but rather more easily accomplished than in the normals. It appeared not to be dependent on demonstrable levels of serum-GH and is probably also independent from other anterior pituitary factors. Plasma-FFA rose less in the obese than in the normals. A slight correlation between GH and FFA but no correlation between blood sugar and GH was found on simultaneous determinations.

Recovery of Adrenocortical Function During Long-term Treatment with Corticosteroids

The recovery of adrenocortical function during long-term corticosteroid treatment in a group of patients with asthmatic bronchitis was compared with that in a group of patients with sarcoidosis. At corresponding dosages of prednisone basal adrenocortical function as well as adrenocortical response to tetracosactrin stimulation was higher in the asthma patients than in those with sarcoidosis. The rate of recovery of adrenocortical function seems mainly to be determined by the dosage of corticosteroids during the initial stages of treatment rather than by the nature of the disease.

Response of growth hormone (GH), FFA, blood sugar and insulin to exercise in obese patients and normal subjects

Ergometer tests with a constant workload of 600 Kg./min. during 30 minutes were done on eight normal subjects, eight severely obese patients, and two women who had formerly been obese. Arterial blood was sampled three times before, four times during and three times after exercise. The incidence and the height of the GH response were the same in the obese as in the normals. The results show that the obese are able to raise their plasma GH to very high levels if subjected to strenuous exercise. It could not be concluded, however, that they can do so to the same extent as normals, because the exercise was more exhausting for the obese, three of whom had to stop prematurely, than for the normal subjects. In eight of the 12 responders, the rise of GH began almost immediately at the start of bicycling. In all of them, GH valves decreased as soon as work was stopped, irrespective of the time it had lasted. There was no correlation between changes in GH and those on the other parameters measured. It is very probable that the elevation of GH was at least in two thirds of the cases triggered by stress rather than by the increase in energy expenditure. FFA levels were throughout the whole test higher in the obese, than in the normal subjects. No correlation with the GH levels could be found. Blood sugar remained stable in the normal subjects and in the majority of the obese. In three obese patients there was a rise of blood sugar during exercise followed by an elevation of plasma insulin. Two of these patients must be viewed as prediabetics on account of their family history.

Influence of exogenous human growth hormone on the metabolism of fasting obese patients.

Three obese female patients were investigated during three courses of starvation. In two of them these periods lasted 12 days; in one 6 days. During the second starvation period HGH was administered on alternate days in a dosage of 10 mg. Plasma values of FFA, hydroxybutyric acid, insulin, electrolytes, glucose, HCO3, and the pH were determined. In addition, a complete balance study of nitrogen, calcium, phosphate, Na, and K was done. In none of these cases HGH led to increased ketoacidosis. The rise of hydroxybutyric acid, as well as the decrease of HCO3 and of the pH, was in one of the patients even less during HGH administration than during control periods. This patient showed an elevation of plasma insulin during HGH administration. The possibility is considered that growth hormone, by virtue of its stimulating action on pancreatic insulin secretion, might counteract the acidosis of starvation. The balance studies showed that during HGH there was less excretion of Na and K, but no other effects were demonstrable.