Effects of Severe Protein-Calorie Deficiency on the Endocrine Control of Carbohydrate Metabolism

Heard, C. R. C.

doi:10.2337/diab.15.2.78

Cited by 42 publications

(23 citation statements)

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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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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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“…Of the remaining cases, the proportions with hyaline membrane disease and cerebral intraventricular hemorrhage were calculated for subgroups of 241 liveborn infants who were less than 36 weeks of gestational age and lived longer than 6 hr but less than 72 hr, 6 hr being chosen because the anatomic features of hyaline membrane disease are usually well developed by this time. Of the other remaining cases, 323 were stillborn or lived less than 1 hr and hence were suitable for a histologic analysis of their lung maturity.…”

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confidence: 99%

“…Hormones might mediate the nutri- tional effects on lung maturation. Turnover rates of corticosteroids and the balance between such corticosteroids and other hormones are abnormal in experimental malnutrition [6]; corticosteroids have been shown to accelerate fetal lung maturation in both human beings and experimental animals [3, g].…”

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Nutrition, Sex, and Fetal Lung Maturation

1974

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Maternal nutrition and the sex of a fetus appear to have important influences on fetal lung maturation and on the neonatal development of hyaline membrane disease. Amniotic fluid lecithin to sphingomyelin ratios and shake test values were greater in undernourished than in overnourished pregnancies after midgestation. There was a similar relation between levels of maternal nutrition and structural variables of fetal lung maturity. Using the same variables, the lungs of female fetuses matured somewhat more rapidly than the lungs of males. Hyaline membrane disease was almost twice as common in infants who died after overnourished gestations as in those who had undernourished mothers. SpeculationT h e study should not be used as the basis for recommendations to restrict food intake during pregnancy. Research is needed to determine whether calories alone or the balance between calories and other specific nutrients are able to influence the rate of fetal lung maturation.

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“…Recent studies on malnourished children (Milner, 1971), adults (Smith et al, 1975) and animals (Heard, 1966;Weinkove et al, 1976) conclusively demonstrate that malnutrition can lead to glucose intolerance. In particular the work on malnourished animals (Weinkove et al, 1976) has implicated protein deficiency as an important precursor of impaired carbohydrate metabolism.…”

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Mechanism of impaired glucose tolerance in patients with neoplasia

Jasani¹,

Donaldson²,

Ratcliffe³

et al. 1978

Br J Cancer

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Summary.-The disappearance rate (k) of i.v. glucose was measured in cachectic and non-cachectic cancer patients and tumour-free controls. The respective k values were found to be 106+027 (mean+s.d.), 164±034 and 163±023. Of the other parameters measured, only plasma albumin level was found to vary significantly amongst the 3 categories, the mean level being the lowest in cachectic cancer patients. The means of total plasma protein, fasting blood glucose and plasma liver enzyme concentrations were similar in the 3 groups. Glucagon, a potent insulin secretogogue, failed to augment the fasting insulin level in cachectic but did so in non-cachectic cancer patients. Taken together, the findings suggest that the reduced glucose tolerance in patients with neoplasia is due to impairment of insulin release exhibited predominantly by ill-nourished advanced cancer patients having a moderate to severe degree of hypoalbuminemia.

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Effects of Severe Protein-Calorie Deficiency on the Endocrine Control of Carbohydrate Metabolism

Cited by 42 publications

References 0 publications

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

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

Nutrition, Sex, and Fetal Lung Maturation

Mechanism of impaired glucose tolerance in patients with neoplasia

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