Alfons Bonde | Colorado State University (original) (raw)
Papers by Alfons Bonde
PubMed, Nov 1, 1990
Our research has shown that 800 kcal/day sucrose diets, unlike pure protein diets, maintained res... more Our research has shown that 800 kcal/day sucrose diets, unlike pure protein diets, maintained resting metabolic rate (RMR) and triiodothyronine (T3) levels. Concern that thermogenesis from sucrose might reflect protein catabolism led to this study, in which 23 obese women were studied as inpatients for 2 weeks on diets (kcal = 50 percent of RMR) containing either 93 percent sucrose (S, n = 7), sucrose plus protein (75 percent/20 percent, SP, n = 9), or fat plus protein (75 percent/20 percent, FP, n = 7). RMR, leucine kinetics (1-14C)leucine method) and nitrogen balance were measured. RMR fell (P less than 0.03) with SP and FP (-8.4 +/- 2.5 percent, -7.5 +/- 2.5 percent), but was maintained by S (+ 0.3 +/- 2.4 percent, P = 0.05 vs. SP and FP). Plasma leucine decreased (P less than 0.01) with S and SP by 36.6 +/- 4.0 percent and 17.0 +/- 4.7 percent, but increased by +52.8 +/- 9.0 percent (P less than 0.01) with FP (P = 0.0001 vs. S or SP). Leucine turnover, oxidation, and nonoxidative disposal all decreased (P = 0.0001) with S and with SP, in contrast to FP, in which these parameters were unchanged (all P = 0.0001 vs. S or SP). Cumulative (2 week) nitrogen loss was least (P = 0.001) in SP (-2.56 +/- 0.41 mol) compared with S (-4.37 +/- 0.19 mol) and FP (-4.76 +/- 0.12 mol), which did not differ. Since inclusion of sucrose in hypocaloric diets maintained RMR while decreasing leucine turnover, oxidation, and nitrogen loss, we conclude that the thermogenic effects of sucrose do not depend on protein catabolism.
The American Journal of Clinical Nutrition, Nov 1, 1988
Optimal composition of reducing diets remains controversial. Seventeen obese inpatients received ... more Optimal composition of reducing diets remains controversial. Seventeen obese inpatients received 440 kcal/d, either 41% protein plus 55% carbohydrate (CD) or 95% protein (PP), for 3 wk. There were no significant diet effects (all data CD vs PP) in weight loss (8.88 +/- 1.01 vs 8.74 +/- 0.79 kg), loss of lean mass (2.10 +/- 0.35 vs 1.61 +/- 0.39 kg), metabolic rate reduction (15.3 +/- 2.8 vs 13.0 +/- 5.2%), or meal-stimulated thermogenesis (26.6-37.9 vs 29.0-26.1 net kcal/3 h [time NS also]). Triiodothyronine (T3) responses differed (2.35 +/- 0.11 to 1.57 +/- 0.14 vs 2.43 +/- 0.11 to 1.47 +/- 0.12 nmol/L, p less than 0.01) as did free T3 (3.4 +/- 0.2 to 2.6 +/- 0.2 vs 3.2 +/- 0.2 to 2.0 +/- 0.2 pmol/L, (p less than 0.01]; thyroxine declined similarly in both groups. Subjects fed CD gained no advantage over subjects fed PP. Regression analyses revealed no relationship between thyroid hormones, energy deficit, or lean mass with nitrogen losses, suggesting that other or more complex processes govern endogenous protein metabolism during weight loss.
Metabolism-clinical and Experimental, Jun 1, 1987
Although patients with thyrotoxicosis improve clinically after treatment with beta-adrenergic blo... more Although patients with thyrotoxicosis improve clinically after treatment with beta-adrenergic blocking drugs, it has never been established whether the hypermetabolism and body protein wasting caused by thyroid hormone excess are actually mediated by adrenergic mechanisms. To evaluate this issue, we measured basal energy expenditure, epinephrinestimulated calorigenesis, and leucine kinetics ian index of body protein catabolism) in six normal volunteers before and after triiodothyronine IT,) administration (150 pg/d for 1 week). Serum T, rose nearly threefold (P < 0.001) during T, administration, producing significant increases in basal metabolic rate (21%, P < 0.001). nitrogen excretion (45%. P < O.OOl), and leucine flux (45%. P < 0.01). In response to epinephrine infusion, the absolute rise in metabolic rate above basal was 57% greater in the thyrotoxic condition (P < 0.02). Although beta-adrenergic blockade with intravenous propranolol totally abolished the calorigenic response to epinephrine. it had no detectable effect on either the accelerated basal metabolic rate or the augmented body protein catabolism caused by thyroid horomone excess. Our data suggest that in the basal, resting state, the increased metabolic rate and accelerated protein breakdown caused by thyroid hormone are not adrenergically mediated. However, under nonbasal conditions (when sympathetic activity is stimulated). enhanced responsiveness to catecholamine calorigenesis may exaggerate the hypermetabolic state and thereby contribute to weight loss and other clinical manifestations of thyrotoxicosis. This mechanism may explain the clinical efficacy of beta-adrenergic blocking agents in the treatment of thyrotbxicosis.
Comparative Biochemistry and Physiology Part B: Comparative Biochemistry, 1981
Comparative Biochemistry and Physiology Part B: Comparative Biochemistry, 1981
Comparative Biochemistry and Physiology Part B: Comparative Biochemistry, 1981
1. Isolated pig hepatocytes were prepared and the effects of changes in the cytoplasmic [NADH]/[N... more 1. Isolated pig hepatocytes were prepared and the effects of changes in the cytoplasmic [NADH]/[NAD +] ratio on the efficacy of glucagon to alter rates of metabolism were examined.
Metabolism, 1987
Although patients with thyrotoxicosis improve clinically after treatment with beta-adrenergic blo... more Although patients with thyrotoxicosis improve clinically after treatment with beta-adrenergic blocking drugs, it has never been established whether the hypermetabolism and body protein wasting caused by thyroid hormone excess are actually mediated by adrenergic mechanisms.
PubMed, Nov 1, 1990
Our research has shown that 800 kcal/day sucrose diets, unlike pure protein diets, maintained res... more Our research has shown that 800 kcal/day sucrose diets, unlike pure protein diets, maintained resting metabolic rate (RMR) and triiodothyronine (T3) levels. Concern that thermogenesis from sucrose might reflect protein catabolism led to this study, in which 23 obese women were studied as inpatients for 2 weeks on diets (kcal = 50 percent of RMR) containing either 93 percent sucrose (S, n = 7), sucrose plus protein (75 percent/20 percent, SP, n = 9), or fat plus protein (75 percent/20 percent, FP, n = 7). RMR, leucine kinetics (1-14C)leucine method) and nitrogen balance were measured. RMR fell (P less than 0.03) with SP and FP (-8.4 +/- 2.5 percent, -7.5 +/- 2.5 percent), but was maintained by S (+ 0.3 +/- 2.4 percent, P = 0.05 vs. SP and FP). Plasma leucine decreased (P less than 0.01) with S and SP by 36.6 +/- 4.0 percent and 17.0 +/- 4.7 percent, but increased by +52.8 +/- 9.0 percent (P less than 0.01) with FP (P = 0.0001 vs. S or SP). Leucine turnover, oxidation, and nonoxidative disposal all decreased (P = 0.0001) with S and with SP, in contrast to FP, in which these parameters were unchanged (all P = 0.0001 vs. S or SP). Cumulative (2 week) nitrogen loss was least (P = 0.001) in SP (-2.56 +/- 0.41 mol) compared with S (-4.37 +/- 0.19 mol) and FP (-4.76 +/- 0.12 mol), which did not differ. Since inclusion of sucrose in hypocaloric diets maintained RMR while decreasing leucine turnover, oxidation, and nitrogen loss, we conclude that the thermogenic effects of sucrose do not depend on protein catabolism.
The American Journal of Clinical Nutrition, Nov 1, 1988
Optimal composition of reducing diets remains controversial. Seventeen obese inpatients received ... more Optimal composition of reducing diets remains controversial. Seventeen obese inpatients received 440 kcal/d, either 41% protein plus 55% carbohydrate (CD) or 95% protein (PP), for 3 wk. There were no significant diet effects (all data CD vs PP) in weight loss (8.88 +/- 1.01 vs 8.74 +/- 0.79 kg), loss of lean mass (2.10 +/- 0.35 vs 1.61 +/- 0.39 kg), metabolic rate reduction (15.3 +/- 2.8 vs 13.0 +/- 5.2%), or meal-stimulated thermogenesis (26.6-37.9 vs 29.0-26.1 net kcal/3 h [time NS also]). Triiodothyronine (T3) responses differed (2.35 +/- 0.11 to 1.57 +/- 0.14 vs 2.43 +/- 0.11 to 1.47 +/- 0.12 nmol/L, p less than 0.01) as did free T3 (3.4 +/- 0.2 to 2.6 +/- 0.2 vs 3.2 +/- 0.2 to 2.0 +/- 0.2 pmol/L, (p less than 0.01]; thyroxine declined similarly in both groups. Subjects fed CD gained no advantage over subjects fed PP. Regression analyses revealed no relationship between thyroid hormones, energy deficit, or lean mass with nitrogen losses, suggesting that other or more complex processes govern endogenous protein metabolism during weight loss.
Metabolism-clinical and Experimental, Jun 1, 1987
Although patients with thyrotoxicosis improve clinically after treatment with beta-adrenergic blo... more Although patients with thyrotoxicosis improve clinically after treatment with beta-adrenergic blocking drugs, it has never been established whether the hypermetabolism and body protein wasting caused by thyroid hormone excess are actually mediated by adrenergic mechanisms. To evaluate this issue, we measured basal energy expenditure, epinephrinestimulated calorigenesis, and leucine kinetics ian index of body protein catabolism) in six normal volunteers before and after triiodothyronine IT,) administration (150 pg/d for 1 week). Serum T, rose nearly threefold (P < 0.001) during T, administration, producing significant increases in basal metabolic rate (21%, P < 0.001). nitrogen excretion (45%. P < O.OOl), and leucine flux (45%. P < 0.01). In response to epinephrine infusion, the absolute rise in metabolic rate above basal was 57% greater in the thyrotoxic condition (P < 0.02). Although beta-adrenergic blockade with intravenous propranolol totally abolished the calorigenic response to epinephrine. it had no detectable effect on either the accelerated basal metabolic rate or the augmented body protein catabolism caused by thyroid horomone excess. Our data suggest that in the basal, resting state, the increased metabolic rate and accelerated protein breakdown caused by thyroid hormone are not adrenergically mediated. However, under nonbasal conditions (when sympathetic activity is stimulated). enhanced responsiveness to catecholamine calorigenesis may exaggerate the hypermetabolic state and thereby contribute to weight loss and other clinical manifestations of thyrotoxicosis. This mechanism may explain the clinical efficacy of beta-adrenergic blocking agents in the treatment of thyrotbxicosis.
Comparative Biochemistry and Physiology Part B: Comparative Biochemistry, 1981
Comparative Biochemistry and Physiology Part B: Comparative Biochemistry, 1981
Comparative Biochemistry and Physiology Part B: Comparative Biochemistry, 1981
1. Isolated pig hepatocytes were prepared and the effects of changes in the cytoplasmic [NADH]/[N... more 1. Isolated pig hepatocytes were prepared and the effects of changes in the cytoplasmic [NADH]/[NAD +] ratio on the efficacy of glucagon to alter rates of metabolism were examined.
Metabolism, 1987
Although patients with thyrotoxicosis improve clinically after treatment with beta-adrenergic blo... more Although patients with thyrotoxicosis improve clinically after treatment with beta-adrenergic blocking drugs, it has never been established whether the hypermetabolism and body protein wasting caused by thyroid hormone excess are actually mediated by adrenergic mechanisms.