Glucose Tolerance and Related Factors in Dogs Fed Diets of Suboptimal Protein Value

Heard, C. R. C.; Turner, M.

doi:10.2337/diab.16.2.96

Cited by 33 publications

(21 citation statements)

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“…Russell (I957), noting similar metabolic responses in starvation and after growth hormone administration, predicted that growth hormone would be raised in starvation, while Heard & Turner (1967) made a similar suggestion to account for the abnormal glucose tolerance in their protein deprived animals. On the other hand, Monckeberg et al (1963), possibly describing a different syndrome, claimed that malnourished children failed to respond to adequate dietary replacement unless growth hormone was concomitantly administered, which suggested growth hormone deficiency.…”

Section: G R O W T H H O R M O N Ementioning

confidence: 99%

“…Protein malnourished rats show a reduction in brain noradrenaline and dopamine (Shoemaker & Wurtman, 1971). Urinary metanephrines are reported as low in a small number of marasmic infants (Bourgeois et al, 1973) while in kwashiorkor, others have found elevated adrenaline and low dopamine excretion (Parra et al, 1973b;Hoeldtke & Wurtman, 1973). Urinary noradrenaline is unaltered while VMA excretion is diminished (Hoeldtke & Wurtman, 1973).…”

Section: P I T U I T a R Y -T H Y R O I D F U N C T I O Nmentioning

confidence: 99%

“…Urinary metanephrines are reported as low in a small number of marasmic infants (Bourgeois et al, 1973) while in kwashiorkor, others have found elevated adrenaline and low dopamine excretion (Parra et al, 1973b;Hoeldtke & Wurtman, 1973). Urinary noradrenaline is unaltered while VMA excretion is diminished (Hoeldtke & Wurtman, 1973). It has been suggested that the increased adrenaline excretion is a non-specific effect of stress.…”

Section: P I T U I T a R Y -T H Y R O I D F U N C T I O Nmentioning

confidence: 99%

“…It has been suggested that the increased adrenaline excretion is a non-specific effect of stress. The low dopamine might reflect a decreased dietary intake of dopa, and decreased VMA in the presence of normal noradrenaline may imply a decrease in noradrenaline catabolism (Hoeldtke & Wurtman, 1973). It will be important to relate these data carefully to other endocrine functions as these substances have important roles in the mechanisms governing the release of many polypeptide hormones as well as in the control of metabolic substrates.…”

Section: P I T U I T a R Y -T H Y R O I D F U N C T I O Nmentioning

confidence: 99%

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Endocrine Function in Protein‐calorie Malnutrition

Pimstone

1976

Clinical Endocrinology

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Undernutrition is widespread. In spite of the research and development being directed towards its prevention and alleviation, the weight of numbers as well as social, cultural, economic and technological considerations make eradication unlikely in the foreseeable future. Ironically, malnutrition is often endemic in areas in which sophisticated medical facilities exist; the problem clearly goes deeper than the mere availability of medical care. But this curious juxtaposition of poverty and medical sophistication has allowed numerous workers to study endocrine function in protein-calorie malnutrition (PCM). As hormones such as glucagon, insulin, growth hormone and cortisol are concerned with the efficient utilization of food, storage and expenditure of energy, and the latter three hormones with synthesis of body protein, it has been suggested that adaptive changes based on alterations in hormone secretion of function might allow for better survival of the threatened individual (Monckeberg, 1968); this conclusion, however, must be regarded as speculative at present; an alternative explanation might be that they are non-specific consequences of severe nutritional deprivation.This review is not primarily concerned with hormonal changes in prolonged fasting, nor will it refer in great depth to animal models of malnutrition which, while they have the advantage of producing more precise quantitation of the deficit, may not always be relevant to the situation in man. For infantile malnutrition is not merely the deprivation of proteins and calories ; it is inevitably associated with variable degrees of vitamin and mineral deficiency, intercurrent infection and electrolyte changes. To what extent hormonal changes are attributable to malnutrition as opposed to associated phenomena is not always apparent, but these might be very relevant in considering the pathogenesis of endocrine dysfunction in the human as opposed to the experimental context.

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Section: G R O W T H H O R M O N Ementioning

confidence: 99%

Section: P I T U I T a R Y -T H Y R O I D F U N C T I O Nmentioning

confidence: 99%

Section: P I T U I T a R Y -T H Y R O I D F U N C T I O Nmentioning

confidence: 99%

Section: P I T U I T a R Y -T H Y R O I D F U N C T I O Nmentioning

confidence: 99%

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Endocrine Function in Protein‐calorie Malnutrition

Pimstone

1976

Clinical Endocrinology

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“…However, if dimunition of Beta-cell mass were to be shown, the case for protein deficiency in the aetiology of malnutrition-related diabetes would be strengthened [3]. Histopathological investigations of the endocrine pancreas of children who have died during the acute phase of kwashiorkor are confusing since hypertrophic [24][25][26][27][28] The stunting of growth, the impaired glucose tolerance and blunted insulin secretory response to glucose of kwashiorkor can be reproduced in animal models of proteinenergy malnutrition [36][37][38][39][40][41][42][43]. Following nutritional rehabilitation growth is resumed, glucose tolerance normalized but a lowered capacity for insulin secretion persists [41,42,44].…”

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confidence: 99%

Persistent reduction of pancreatic Beta-cell mass after a limited period of protein-energy malnutrition in the young rat

et al. 1992

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Summary. Kwashiorkor, the human disease of proteinenergy malnutrition, has been implicated in the aetiology of malnutrition-related diabetes mellitus, a form of diabetes not uncommon in developing countries. We have previously demonstrated that temporary protein-energy malnutrition in young rats causes a persisting impairment of insulin secretion. The present study investigates whether this secretory deficiency is accompanied by structural alterations of the endocrine pancreas. Three-week-old rats were weaned onto semi-synthetic diets containing either 15 % or 5 % protein and these diets were maintained for 3 weeks. From 6 weeks of age all rats were fed a commercial chow containing 18 % protein. The endocrine pancreas was investigated by light and electron microscopic morphometry at 3, 6 and 12 weeks of age. In rats not subjected to protein-energy malnutrition there was a progressive increase, with age, of total pancreatic Beta-cell weight and individual Beta-cell size. In 6-week-old rats fed the low protein diet total pancreatic Beta-cell weight and individual Beta-cell size were diminished. In 12-weekold rats previously fed the low protein diet total Beta-cell weight remained lower compared to control rats. It is concluded that protein-energy malnutrition early in life may result in a diminished reserve for insulin production. This may predispose to glucose intolerance or even diabetes in situations with an increased insulin demand.Key words: Malnutrition-related diabetes mellitus, kwashiorkor, protein-calorie malnutrition, rat, pancreatic islets, pancreatic Beta cell, insulin, light microscopy, electron microscopy, morphometry.The relationship between affluent food supply, obesity and diabetes mellitus is well known and has been the subject of numerous studies. The observation made in 1907 [1] that the spectrum of diabetes in tropical regions of the Third World differs from that in western society and that the disease may be related to malnutrition is not as well recognized. However, in recent years the malnutritionrelated diabetic syndromes have been delineated and are now regarded as separate entities [2]. The exact role of malnutrition in the aetiology and pathogenesis of these types of diabetes remains obscure [3].Kwashiorkor, the disease of protein malnutrition in the young, is characterized by, among other symptoms and signs, impaired glucose tolerance and a diminished or even absent insulin secretory response to glucose [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20]. This appears to be a feature typical of protein deficiency, since balanced malnutrition, as in marasmus, has little or * This work was presented in part at the 26th Annual Meeting of the European Association for the Study of Diabetes in Copenhagen, Denmark 10-13 September 1990 no effect on glucose tolerance and insulin secretion [7,9,11,12,15,18]. Following nutritional rehabilitation, patients with kwashiorkor show a rapid improvement of glucose tolerance and insulin secretory response to glucose within weeks but short-term...

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