A study of endocrine function in protein-energy malnutrition

Olusi, S.O.; Orrell, D. H.; Morris, Peggy; McFarlane, H.

doi:10.1016/0009-8981(77)90293-5

Cited by 9 publications

(4 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The decreased effectiveness of glucocorticoids to increase muscle protein breakdown and net muscle loss in protein-deficient animals, where muscle protein turnover is already depressed (e.g. Millward, 1979;Rikimaru et al 1980; present results, Table 5), indicates that care should be taken in interpreting the physiological significance of the elevated cortisol levels found in human infants suffering from protein-energy malnutrition (Lunn et al 1973;Olusi et al 1977;Whitehead & Lunn, 1979). Our finding, that administered corticosterone can lead to an anabolic response by rats restricted in protein and energy intake, in spite of an apparent increase in myofibrillar protein degradation rate, is a novel one and raises further questions concerning the interactions between nutrient supply and hormonal effects on metabolic processes.…”

Section: Discussionmentioning

confidence: 76%

Modification of glucocorticoid-induced changes in myofibrillar protein turnover in rats by protein and energy deficiency as assessed by urinary excretion ofN^T-methylhistidine

1984

View full text Add to dashboard Cite

1. The effects of differing degrees of experimental protein-energy malnutrition on the response of myofibrillar protein tuniover rates to administration of corticosteroid has been studied in two experiments on rats. The basal control diet, offered ad lib. in each case, contained 40 g protein/kg, and other groups received diets containing 62.5, 95 or 220 g protein/kg at 0.67, 1 or 1.5 times the level of the control energy intake.2. Daily administration of 25 or 30 mg corticosterone/kg body-weight after I8 d pre-feeding caused an increase in plasma protein, glucose and insulin concentrations, but a decrease in the corticosterone: insulin values. Liver size and protein content increased, as did the fractional excretion ofdietary nitrogen as urea-N in all treated groups. However, whereas a fall in food intake and body-weight occurred in one experiment the reverse occurred in the other.3. W-Methylhistidine excretion was 12% lower for rats receiving 40 v. 220 g protein/kg diet and excretion was increased by only 57 v. 90% respectively, when the two groups of rats were given 30mg corticosterone/kg per d. Rats which received 25 mg corticosterone/kg per d and up to 95 g protein/kg diet increased excretion of W-methylhistidine by an average 35%.4. The fractional degradation rate of myofibrillar protein (k,) was reduced by about 10% by the low-protein diet from 3.1 to 2.8%/d. During corticosterone treatment the increment in k , for rats on this diet was only 60% of that for rats receiving the 220 g protein/kg diet, i.e. an increase of 1.8 Y. 3.0%/d. Energy restriction further reduced k, during low-protein intake but did not affect the response to the corticosterone. Variations in dietary protein from 40 to 95g/kg had little effect on the increase in k , during steroid treatment. The effect of corticosterone on calculated synthesis rates (k,) differed markedly between experiments. While k, fell by 5 0 4 5 % in rats which lost weight on treatment, it rose by up to 60% in rats where carcass non-collagen-protein accretion remained unchanged or increased, despite an increase in k,.5. Protein deficiency decreases the catabolic response to glucocorticoid, but the net metabolic response appears crucially dependent on changes in food intake or the stage of growth of the rat or both. A net anabolic response with increased fractional rates of myofibrillar protein breakdown, synthesis and accretion was observed in growing rats fed on relatively-low-protein diets and given 25 mg corticosterone/kg per d. This novel finding indicates that a particular role for cortisol in the adaptation to protein+nergy malnutrition by humans should be ascribed only with caution.

show abstract

Section: Discussionmentioning

confidence: 76%

Modification of glucocorticoid-induced changes in myofibrillar protein turnover in rats by protein and energy deficiency as assessed by urinary excretion ofN^T-methylhistidine

1984

View full text Add to dashboard Cite

show abstract

“…Studies in children with protein-calorie malnutrition demonstrate elevated GH levels and low IGF-I levels with normalization after nutritional recovery (Hintz, et al 1978; Olusi, et al 1977; Robinson and Picou 1977; Soliman, et al 1986). In adults who were fasted and then re-fed a protein-deficient diet, IGF-I levels increased significantly less than in adults fed an iso-caloric, protein-sufficient diet (Isley, et al 1983).…”

Section: States Of Malnutritionmentioning

confidence: 99%

Determinants of GH resistance in malnutrition

Fazeli

Klibanski

2013

Journal of Endocrinology

128

View full text Add to dashboard Cite

States of under-nutrition are characterized by growth hormone resistance. Decreased total energy intake, as well as isolated protein-calorie malnutrition and isolated nutrient deficiencies result in elevated growth hormone levels and low levels of IGF-I. We review various states of malnutrition and a disease state characterized by chronic under-nutrition -- anorexia nervosa -- and discuss possible mechanisms contributing to the state of growth hormone resistance, including FGF-21 and SIRT1. We conclude by examining the hypothesis that growth hormone resistance is an adaptive response to states of under-nutrition, in order to maintain euglycemia and preserve energy.

show abstract

“…It may be that in chronic starvation, a state of neuroglycopenia already exists in the hypothalamic region leading to relative insensitivity to insulin hypoglycemia. Another factor interfering with a normal response may be the high plasma cortisol levels which occur in patients with PEM (21,22).…”

Section: Actcr Pncdintr Sccind 70mentioning

confidence: 99%

Growth Hormone Secretion in Protein Energy Malnutrition

Günöz

Neyzi

et al. 1981

Acta Paediatrica

View full text Add to dashboard Cite

Plasma hGH levels were assessed in 15 infants with protein energy malnutrition following insulin induced hypoglycemia, arginine and L-Dopa provocation tests and intravenous glucose tolerance test. Fasting hGH levels were high in 85.7% of the cases. An adequate hGH response to stimulation was obtained in only 42.8% of the cases with insulin induced hypoglycemia; in 52.5% with arginine; in 30.8% with L-Dopa. Response to at least one type of provocation was obtained in all 5 cases to which all three tests were applied. Exaggerated or delayed response to provocative stimuli was also encountered in a number of the cases. Intravenous glucose tolerance test did not lead to suppression in hGH secretion or to increase in insulin secretion in these subjects. The results indicate that marasmic protein energy malnutrition may lead to defects in the hGH secretory function of the hypothalamopituitary axis.

show abstract

A study of endocrine function in protein-energy malnutrition

Cited by 9 publications

References 9 publications

Modification of glucocorticoid-induced changes in myofibrillar protein turnover in rats by protein and energy deficiency as assessed by urinary excretion ofN^T-methylhistidine

Modification of glucocorticoid-induced changes in myofibrillar protein turnover in rats by protein and energy deficiency as assessed by urinary excretion ofN^T-methylhistidine

Determinants of GH resistance in malnutrition

Growth Hormone Secretion in Protein Energy Malnutrition

Contact Info

Product

Resources

About

A study of endocrine function in protein-energy malnutrition

Cited by 9 publications

References 9 publications

Modification of glucocorticoid-induced changes in myofibrillar protein turnover in rats by protein and energy deficiency as assessed by urinary excretion ofNT-methylhistidine

Modification of glucocorticoid-induced changes in myofibrillar protein turnover in rats by protein and energy deficiency as assessed by urinary excretion ofNT-methylhistidine

Determinants of GH resistance in malnutrition

Growth Hormone Secretion in Protein Energy Malnutrition

Contact Info

Product

Resources

About

Modification of glucocorticoid-induced changes in myofibrillar protein turnover in rats by protein and energy deficiency as assessed by urinary excretion ofN^T-methylhistidine

Modification of glucocorticoid-induced changes in myofibrillar protein turnover in rats by protein and energy deficiency as assessed by urinary excretion ofN^T-methylhistidine