Protein-Calorie Deficiency and Disorders of the Endocrine Glands

Heard, C. R. C.; Stewart, R. J. C.

doi:10.1159/000178223

Cited by 20 publications

(9 citation statements)

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“…In 6-week-old LP rats total islet volume was diminished and the Beta cells showed ultrastructural signs of atrophy confirming previous observations of small Beta cells with hyperchromatic nuclei but lack of degenerative changes and signs of cell death in experimental protein-energy malnutrition [49,[51][52][53]. The measurements of total Betacells mass and individual Beta-cell size indicate that total Beta-cell number had not increased in LP rats between 3 and 6 weeks of age.…”

Section: Discussionsupporting

confidence: 86%

“…Following nutritional rehabilitation growth is resumed, glucose tolerance normalized but a lowered capacity for insulin secretion persists [41,42,44]. Reports on the histopathology of the pancreatic islets during experimental protein-energy malnutrition are again divergent suggesting hypertrophy [45], no change [46,47] or atrophy [48][49][50][51][52][53]. Quantitative morphometry at light and electron microscopic levels was used here to study the structural alterations in the pancreatic Beta cell of the rat during experimental proteinenergy malnutrition and after nutritional rehabilitation.…”

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confidence: 99%

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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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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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Section: Discussionsupporting

confidence: 86%

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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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“…25 ' 26 Similar findings have been reported in most children suffering from various forms of protein-energy malnutrition (PEM) 27 " 39 and in adults with moderate-to severe malnutrition. 40 ' 41 Fasting levels of serum insulin and insulin responses to glucose are markedly reduced in all these groups, 23 ' 31 ' 33 ' 35 ' 38 ' 41 and responses to other insulinotropic stimuli such as glucagon 3536 and amino acids 41 " 43 are also suppressed. Though all these abnormalities can usually be reversed rapidly by refeeding, this is not always so.…”

Section: The Effects Of Undernutrition On the Endocrine Pancreasmentioning

confidence: 97%

“…54 Experimental work in pigs has suggested that protein deficiency leads to reduced beta cell size, degranulation of beta cells, and a lower proportion of beta cells in each islet. 55 In the protein-deprived rat, total islet volume is reduced when corrected for age and weight. 56 By electron microscopy, Weinkove et al found that beta cells from undernourished rats contained a preponderance of abnormal, pale granules.…”

Section: The Effects Of Undernutrition On the Endocrine Pancreasmentioning

confidence: 99%

The Role of Undernutrition in the Pathogenesis of Diabetes Mellitus

Rao

1984

Diabetes Care

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Recent epidemiologic studies show that diabetes mellitus is almost as prevalent in undernourished populations as it is in well-nourished ones, despite the virtual absence of obesity as an etiologic determinant in the former. Undernutrition itself may be the risk factor that replaces obesity in predisposing such populations to diabetes. The glucose intolerance of protein-energy malnutrition is known to be associated with structural changes in the beta cell, and in a significant proportion of undernourished subjects it is irreversible despite prolonged and vigorous nutritional rehabilitation. Chronic undernutrition over a lifetime may, therefore, be an important determinant of diabetes in an individual, either by progressively impairing beta cell function or by increasing the susceptibility of the individual to other genetic and environmental diabetogenic influences.

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“…Protein deficiency leads to reduced β-cell mass due to a decrease in the proliferation rate and an increase in apoptosis (Swenne et al 1992, Petrik et al 1999. Additionally, when the data are corrected for age and weight, a reduction in β-cell size and total islet volume, a lower proportion of β-cells per islet, a degranulation of β-cells and β-cells with a preponderance of abnormal pale granules have been observed (Heard and Stewart 1971, Pimstone 1976, Weinkove et al 1977.…”

Section: Introductionmentioning

confidence: 99%

Short-term low-protein diet during pregnancy alters islet area and protein content of phosphatidylinositol 3-kinase pathway in rats

Salvatierra

Reis

Pessoa

et al. 2015

An. Acad. Bras. Ciênc.

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The phosphatidylinositol 3-kinase and mitogen-activated protein kinase pathways mediate β cell growth, proliferation, survival and death. We investigated whether protein restriction during pregnancy alters islet morphometry or the expression and phosphorylation of several proteins involved in the phosphatidylinositol 3-kinase and mitogen-activated protein kinase pathways. As controls, adult pregnant and non-pregnant rats were fed a normal-protein diet (17%). Pregnant and non-pregnant rats in the experimental groups were fed a low-protein diet (6%) for 15 days. Low protein diet during pregnancy increased serum prolactin level, reduced serum corticosterone concentration and the expression of both protein kinase B/AKT1 (AKT1) and p70 ribosomal protein S6 kinase (p70 S6K ), as well as the islets area, but did not alter the insulin content of pancreatic islets. Pregnancy increased the expression of the Src homology/collagen (SHC) protein and the extracellular signal-regulated kinases 1/2 (ERK1/2) independent of diet. ERK1/2 phosphorylation (pERK1/2) was similar in islets from pregnant and non-pregnant rats fed a low-protein diet, and was higher in islets from pregnant rats than in islets from non-pregnant rats fed a normal-protein diet. Thus, a short-term, low-protein diet during pregnancy was sufficient to reduce the levels of proteins in the phosphatidylinositol 3-kinase pathway and affect islet morphometry.

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Protein-Calorie Deficiency and Disorders of the Endocrine Glands

Cited by 20 publications

References 17 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

The Role of Undernutrition in the Pathogenesis of Diabetes Mellitus

Short-term low-protein diet during pregnancy alters islet area and protein content of phosphatidylinositol 3-kinase pathway in rats

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