Experimental Protein-Calorie Deficiency: Histopathological Changes in the Endocrine Glands of Pigs

Platt, B. S.; Stewart, R. J. C.

doi:10.1677/joe.0.0380121

Cited by 38 publications

(27 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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: 87%

“…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.…”

mentioning

confidence: 99%

See 1 more Smart Citation

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

et al. 1992

View full text Add to dashboard Cite

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...

show abstract

Section: Discussionsupporting

confidence: 87%

mentioning

confidence: 99%

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

et al. 1992

View full text Add to dashboard Cite

show abstract

“…Presumptive abnormalities of both pituitary and gonadal function have been described in vivo (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14). However, the interpretation of these observations is limited by confounding influences of weight loss, protein catabolism, hyperglycemia, gonadal vasculopathy, and homeostatic responses of the pituitary-gonadal and adrenal axes in intact animals (15)(16)(17)(18)(19)(20)(21)(22). Moreover, precise cellular or biochemical alterations responsible for gonadal dysfunction in diabetes mellitus have not been delineated.…”

mentioning

confidence: 99%

Mechanisms subserving the trophic actions of insulin on ovarian cells. In vitro studies using swine granulosa cells

Veldhuis¹,

Kolp²,

Toaff³

et al. 1983

J. Clin. Invest.

108

View full text Add to dashboard Cite

A B S T R A C T Direct actions of insulin on gonadal tissues have been difficult to demonstrate in vivo. We have developed an in vitro system in which swine ovarian cells remain highly responsive to trophic actions of insulin. Purified porcine insulin significantly augmented the biosynthesis and secretion of progesterone by cultured granulosa cells. These stimulatory actions of insulin were dose-and time-dependent and saturable. Under serum-restricted conditions, insulin also significantly amplified the capacity of estradiol and 8-bromo cyclic AMP to stimulate progesterone production. Inhibitors of protein and RNA synthesis (cycloheximide, actinomycin D, and alpha-amanatin) inhibited insulin action. The stimulation of progesterone production by insulin was attributable to increased biosynthesis of pregnenolone, rather than diminished catabolism of progesterone to its principal metabolite, 20a-hydroxypregn-4-en-3-one. Insulin also enhanced progesterone production in the presence of a soluble sterol substrate, 5-cholesten-3j3,25-diol, which readily gains access to the mitochondrial cholesterol side-chain cleavage system. Moreover, exposure of granulosa cells to insulin produced a three-to sevenfold increase in mitochondrial content of cytochrome P-450 measured by difference spectroscopy, with a corresponding increase in mitochondrial cholesterol side-chain cleavage activity.The capacity of insulin to facilitate progesterone biosynthesis by ovarian cells was mimicked by the insulinlike somatomedin, multiplication stimulating activity, but not by epidermal growth factor, fibroblast growth factor, or porcine relaxin. Insulin's augmentation of progesterone production reflected a selective action on progestin biosynthesis, since insulin significantly suppressed estrogen biosynthesis by granulosa cells.Thus, our investigations indicate that insulin acts on ovarian cells selectively to stimulate pregnenolone (but not estrogen) biosynthesis. The actions of insulin are exerted by processes that require protein and RNA synthesis, and by mechanisms that augment mitochondrial cytochrome P-450 content and facilitate the utilization of cholesterol in the side-chain cleavage 1046 J. Clin. Invest.

show abstract

“…These effects presumably occur as a result of more spermatogenic cells and an increase in testicular fluid secreted by the Sertoli cells in response to FSH and testosterone (Vitale et al, 1973;Courot and Ortavant, 1981 (Tjondronegoro et al, 1990) Platt, 1960;Dickerson et al, 1964;Platt and Stewart, 1967), which were consistent with there being a reduced storage of, but not necessarily a complete absence of, trophic hormones in this gland.…”

Section: Influence Of Nutrition On Reproductive Function In Mature Malesmentioning

confidence: 78%

“…An Harayama, 1990;Lang et al, 1992;Liu et al, 1992;Wang et al, 1992 (Niwa, 1954). Severe underfeeding of young boars from 2-3 weeks of age for 1 yr (Dickerson et al, 1964) (Platt and Stewart, 1967) …”

Section: Nutritional States In Animalsmentioning

confidence: 99%

A review of nutritional influences on reproduction in boars, bulls and rams

Brown¹

1994

Reprod. Nutr. Dev.

View full text Add to dashboard Cite

Experimental Protein-Calorie Deficiency: Histopathological Changes in the Endocrine Glands of Pigs

Cited by 38 publications

References 34 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

Mechanisms subserving the trophic actions of insulin on ovarian cells. In vitro studies using swine granulosa cells

A review of nutritional influences on reproduction in boars, bulls and rams

Contact Info

Product

Resources

About