Increased postprandial energy expenditure in obese women after peroral K- and Mg-phosphate.

Energy expenditure (EE) was studied in 15 obese (BMI > 27.5, median 29.2) and 15 lean (BMI < 22.9, median 21.7) healthy, postmenopausal women before and after peroral orange juice with or without K- and Mg-phosphate supplementation. The women, 56-58 years old, were studied in a double-blind, crossover experiment on two separate days. They received 100 ml of orange juice (10 g of carbohydrates) with or without a supplement of K+ (35 mmol), Mg2+ (17 mmol) and HPO4(2-) (39 mmol). Measurements were made before and 30 and 60 min after the stimuli. Intake of juice only had no effect on EE in either the lean or the obese subjects. When the minerals were added, EE (+6.3%; p < 0.001) increased significantly in the obese group with in a maximum 30 min after stimulus, while no such increase was seen in the lean group. The difference between the groups was significant (p < 0.05) and so was the difference in the obese group with or without minerals (p < 0.01). We conclude that an addition of potassium/magnesium-phosphate to glucose increases the postprandial thermogenesis in obese postmenopausal women, but not in lean ones.

Increased metabolic rate in obese women after ingestion of potassium, magnesium- and phosphate-enriched orange juice or injection of ephedrine.

Thirty-six obese, pre-menopausal women were studied after an overnight fast and randomized to four different regimens of metabolic stimuli: group I (n = 12), 100 ml orange juice with dissolved K- and Mg-phosphates (K, 40 mmol; Mg, 17.5 mmol; HPO4, 35 mmol); group II (n = 8), 100 ml of water with electrolytes as in group I; group III (n = 8), 100 ml of orange juice; group IV (n = 8), injection of ephedrine intravenously, 0.25 mg/kg body weight. The women in groups I, II and III were further stimulated with ephedrine as in group IV and new measurements made. Thirty minutes after the first stimulus VO2, VCO2 and energy expenditure (EE) rose significantly (13.1-16.5 per cent) in groups I and IV only. In groups I and III the blood concentrations of glucose, insulin, and C-peptide rose significantly. After the second stimulus (ephedrine i.v.) no further increase in VO2, VCO2 and EE occurred in group I, but the increases from basal values became significant in group III. In all women at baseline, whole-body potassium was significantly correlated to VO2. Serum-magnesium was negatively correlated to A/I weight (actual/ideal weight). We conclude that the addition of K- and Mg-phosphates to glucose increases the postprandial thermogenesis in obese patients.

The effect of starvation and refeeding with oral versus intravenous glucose on serum 3,5-,3,3'-and 3'-5'-diiodothyronine and 3'-monoiodothyronine.

The effect of complete fasting on the serum concentrations of the iodothyronines 3,5-diiodothyronine (3,5-T2), 3,3'T2, 3', 5'-T2 and 3'-monoiodothyronine (3'-T1) was evaluated. Fourteen obese women underwent a complete fasting for 4 days. Caloric restriction resulted in the following serum hormone levels (before vs 3. day): T4: 103 vs 109 nmol/l (NS), T3: 1.83 vs 1.24 nmol/l (p less than 0.01), rT3: 0.276 vs 0.407 nmol/l (P less than 0.01), 3.5-T2: 70 pmol/l (NS), 3.3'-T2: 42 vs 39 pmol/l (p less than 0.01), 3',5'-T2: 63 vs 93 pmol/l (P less than 0.01), and 3'-T1 60 vs 116 pmol/l (P less than 0.01). All subjects were refed with 200 g (800 kcal, 3350 kJ) d-glucose per day in divided doses for 2 days. Refeeding tended to normalize the changed iodothyronine concentrations and there was no difference whether the glucose was administered by the oral (n = 7) or the intravenous route. In can be concluded that starvation in man is accompanied by profound changes in peripheral metabolism of the T2's and 3'T1. There seems to be no qualitative difference of the effect on the thyroid hormone metabolism of d-glucose administered by the oral or the intravenous route.