Ultrastructure of esophageal epithelium of rats fed Zn-deficient diet

Author(s):  
S. Yamashiro ◽  
T. Bast ◽  
T.M. Bray ◽  
W.J. Bettger

It has been shown that animals fed a Zn-deficient diet developed various epithelial lesions. These include parakeratosis of the tongue, larynx and nasal sinuses in the ducks and hypertrophy of esophageal mucosa in the rats and pigs.Twenty-one weanling, male Wistar rats were equally divided into three groups. Seven rats were fed a diet containing less than 1.1 ppm Zn ad libitum for 3 weeks. Control rats were either pair-fed or fed ad libitum a diet supplemented with 100 ppm Zn. The basal diet was composed of 20% egg white, 10% corn oil, 63.55% glucose hydrate, 1% vitamin premix, 4% mineral premix, 0.25% choline chloride, 0.4% sodium phytate and 0.8% calcium carbonate. Minerals and vitamins additions were according to the AIN-76 recommendations (5).

1978 ◽  
Vol 58 (4) ◽  
pp. 597-604
Author(s):  
C. Y. PANG ◽  
L. D. CAMPBELL ◽  
G. D. PHILLIPS

Significantly lower feed intake, higher water intake and depressed growth rate were observed in poults under 30 days of age offered ad libitum a low (0.05%) sodium diet and tap water compared to control poults offered the same basal diet containing 0.25% added sodium. Mortality with dehydration occurred mainly between 2 and 3 wk of age in poults fed the low sodium diet. Significant pathophysiological changes in poults fed low sodium diet compared with the control on days 9–30 were: lower plasma sodium, chloride and osmolal concentrations; higher plasma contents of uric acid and total protein; higher packed cell volume; and lower body sodium and water contents. Indications of extracellular dehydration and intracellular hydration and decreased glomerular filtration rate in sodium-deficient poults are discussed. Plasma and body composition of poults fed the low sodium diet returned to normal 1 wk after the poults were offered a normal (0.25%) sodium diet and tap water ad libitum.


Author(s):  
S. Yamashiro ◽  
T. Bast ◽  
T.M. Bray ◽  
W.J. Bettger

Zinc (Zn) deficiency is thought to cause depressed immune function in both the cell mediated and humoral aspects of the system. Alteration of lymphocyte maturation and migration has been observed in Zn-deficiency and marked reduction of the lymphocyte number was noted in the thymus of the pups fed Zn-deficient diet. Other alterations include parakeratosis of the squamous epithelia of digestive system and skin.Three groups of seven, weanling, male Wistar rats each were fed diets containing either 1.1 ppm Zn (deficient) or supplemented with 100 ppm Zn ad libitum (control) or the Zn supplemented diet limited to the amount consumed by those on the deficient diet (pair-fed) for 3 weeks. Details of the diet compositions have been reported previously (7). The animals were weighed at the onset and end of the experiment. The organ was weighed after it was fixed in Karnovsky's fixative and small pieces of the tissue were post-fixed in 2.0%, OsO4 for electron microscopy.


Author(s):  
Itaru Watanabe ◽  
Dante G. Scarpelli

Acute thiamine deficiency was produced in mice by the administration of oxythiamine, a thiamine analogue, superimposed upon a thiamine deficient diet. Adult male Swiss mice (30 gm. B.W.) were fed with a thiamine deficient diet ad libitumand were injected with oxythiamine (170 mg/Kg B.W.) subcutaneously on days 4 and 10. On day 11, severe lassitude and anorexia developed, followed by death within 48 hours. The animals treated daily with subcutaneous injections of thiamine (300 μg/Kg B.W.) from day 11 through 15 were kept alive. Similarly, feeding with a diet containing thiamine (600 μg/Kg B.W./day) from day 9 through 17 reversed the condition. During this time period, no fatal illness occurred in the controls which were pair-fed with a thiamine deficient diet.The oxythiamine-treated mice showed a significant enlargement of the liver, which weighed approximately 1.5 times as much as that of the pair-fed controls. By light and electron microscopy, the hepatocytes were markedly swollen due to severe fatty change and swelling of the mitochondria.


2006 ◽  
Vol 76 (3) ◽  
pp. 111-116 ◽  
Author(s):  
Hiroshi Matsuzaki ◽  
Misao Miwa

The purpose of this study was to clarify the effects of dietary calcium (Ca) supplementation on bone metabolism of magnesium (Mg)-deficient rats. Male Wistar rats were randomized by weight into three groups, and fed a control diet (control group), a Mg-deficient diet (Mg- group) or a Mg-deficient diet having twice the control Ca concentrations (Mg-2Ca group) for 14 days. Trabecular bone volume was significantly lower in the Mg - and Mg-2Ca groups than in the control group. Trabecular number was also significantly lower in the Mg - and Mg-2Ca groups than in the control group. Mineralizing bone surface, mineral apposition rate (MAR), and surface referent bone formation rate (BFR/BS) were significantly lower in the Mg - and Mg-2Ca groups than in the control group. Furthermore, MAR and BFR/BS were significantly lower in the Mg-2Ca group than in the Mg - group. These results suggest that dietary Ca supplementation suppresses bone formation in Mg-deficient rats.


Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2128
Author(s):  
Marina Martín ◽  
Amaia Rodríguez ◽  
Javier Gómez-Ambrosi ◽  
Beatriz Ramírez ◽  
Sara Becerril ◽  
...  

Energy restriction is a first therapy in the treatment of obesity, but the underlying biological mechanisms have not been completely clarified. We analyzed the effects of restriction of high-fat diet (HFD) on weight loss, circulating gut hormone levels and expression of hypothalamic neuropeptides. Ten-week-old male Wistar rats (n = 40) were randomly distributed into four groups: two fed ad libitum a normal diet (ND) (N group) or a HFD (H group) and two subjected to a 25% caloric restriction of ND (NR group) or HFD (HR group) for 9 weeks. A 25% restriction of HFD over 9 weeks leads to a 36% weight loss with regard to the group fed HFD ad libitum accompanied by normal values in adiposity index and food efficiency ratio (FER). This restriction also carried the normalization of NPY, AgRP and POMC hypothalamic mRNA expression, without changes in CART. Caloric restriction did not succeed in improving glucose homeostasis but reduced HFD-induced hyperinsulinemia. In conclusion, 25% restriction of HFD reduced adiposity and improved metabolism in experimental obesity, without changes in glycemia. Restriction of the HFD triggered the normalization of hypothalamic NPY, AgRP and POMC expression, as well as ghrelin and leptin levels.


2017 ◽  
Vol 68 (1) ◽  
pp. 27-37 ◽  
Author(s):  
Mahmoud M. Said ◽  
Marwa M. Abd Rabo

AbstractAluminium (Al) is a neurotoxic metal that contributes to the progression of several neurodegenerative diseases. The aim of the present study was to evaluate the protective effect of dietary eugenol supplementation against aluminium (Al)- induced cerebral damage in rats. Male Wistar rats were divided into four groups: normal controls, rats fed a diet containing 6,000 μg g-1eugenol, rats intoxicated daily with aluminium chloride (84 mg kg-1body weight) p. o. and fed either a basal diet or a eugenol-containing diet. Daily oral administration of Al for four consecutive weeks to rats significantly reduced brain total antioxidant status (TAS) (11.42±0.31 μmol g-1tissue, p<0.001) with a subsequent significant enhancement of lipid peroxidation (MDA) (32.55±1.68 nmol g-1tissue, p<0.002). In addition, Al enhanced brain acetylcholinesterase activity (AChE) (46.22±4.90 U mg-1protein, p<0.001), tumour necrosis factor alpha (TNF-α) (118.72±11.32 pg mg-1protein, p<0.001), and caspase 3 (Casp-3) (8.77±1.26 ng mg-1protein, p<0.001) levels, and in contrast significantly suppressed brain-derived neurotrophic factor (BDNF) (82.74±14.53 pg mg-1protein, p<0.002) and serotonin (5-HT) (1.54±0.12 ng mg-1tissue, p<0.01) levels. Furthermore, decreased glial fibrillary acidic protein (GFAP) immunostaining was noticed in the striatum of Al-intoxicated rats, compared with untreated controls. On the other hand, co-administration of dietary eugenol with Al intoxication restored brain BDNF (108.76±2.64 pg mg-1protein) and 5-HT (2.13±0.27 ng mg-1tissue) to normal levels, enhanced brain TAS (13.43±0.24 μmol g-1tissue, p<0.05), with a concomitant significant reduction in TNF-α (69.98±4.74 pg mg-1protein) and Casp-3 (3.80±0.37 ng mg-1protein) levels (p<0.001), as well as AChE activity (24.50±3.25 U mg-1protein, p<0.001), and increased striatal GFAP immunoreactivity, compared with Al-treated rats. Histological findings of brain tissues verified biochemical data. In conclusion, eugenol holds potential as a neuroprotective agent through its hydrophobic, antioxidant, and anti-apoptotic properties, as well as its neurotrophic ability against Al-induced brain toxicity in rats.


1973 ◽  
Vol 51 (7) ◽  
pp. 1029-1033 ◽  
Author(s):  
Gregory I. Liou ◽  
W. E. Donaldson

The specific activities of acetyl-CoA carboxylase and fatty acid synthetase were measured in the cytosol fraction of livers from chicks fed various levels of corn oil, cottonseed oil, corn-oil free fatty acids, or crude (79%) oleic acid. Activities of both enzymes were depressed by the addition of fat to a fat-free basal diet. The ratios of synthetase to carboxylase activity were greater than unity when up to 4% fat was fed, but less than unity when 8% or higher levels of fat were fed. The depressions of the activities of these enzymes appeared to be unrelated to the dietary level of linoleate. In in vitro experiments, 2 μM concentrations of palmityl-CoA or oleoyl-CoA depressed acetyl-CoA carboxylase activity. Concentrations of 20 μM of these acyl-CoA esters did not affect the activity of fatty acid synthetase.


1985 ◽  
Vol 36 (6) ◽  
pp. 829 ◽  
Author(s):  
SJ Al-Ali ◽  
NM Malouf ◽  
DM Walker

Preruminant male crossbred lambs, aged 1-2 days at the start of the experiment, were bottle-fed on milk replacers containing casein as the sole source of protein for an experimental period of 15-21 days. Choline-deficient diets were used in experiment 1 to determine the effect on the performance of the lambs of thc dictary protein concentration (10, 15 and 25% protein energy), and in experiment 2 of different sources of fat (butter oil, maize oil or lard), unsupplemented, or with supplements of choline chloride or L-cystine. Supplements of choline chloride decreased liver fat content and decreased urinary creatine excretion, irrespective of dietary protein concentration or source of dietary fat. Ira general, urinary ammonia excretion increased as the sulfur amino acid content of the diets increased, but there were interactions with the source of fat, so that although sulfur intake remained constant ammonia excretion was higher with diets containing lard than with those containing maize oil or butter oil. The effect of the supplements of 1,-cystine on liver fat content and urinary creatine excretion was not significantly different from that of the unsupplemented choline-deficient diets. In experiments 3 and 4 a choline-deficient diet with 25% protein energy and butter oil as the source of fat was supplemented with graded amounts of choline chloride. Energy intake was ad libitum, or restricted to 80% of ad libitum. When the lambs were fed ad libitum there was a significant decrease in liver fat content even with the smallest supplement of choline chloride (c. 9 mg MJ-1 gross energy), but no significant effect when energy intake was restricted. Since liveweight gains and nitrogen balances were unaffected by the presence or absence of the choline supplements it was concluded that in milk replacers containing 25% protein energy from casein, with butter oil as the source of fat, supplementation with choline chloride to provide 9 mg MJ-1 gross energy (233 mg kg-1 dry matter) would be sufficient to prevent the increased deposition of fat in the liver during the 6rst three weeks of life.


2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 107-108
Author(s):  
Andrew D Magnuson ◽  
Xingen Lei

Abstract Enrichment of docosahexaenoic-acid (DHA) into eggs of laying-hens may be limited by the availability phospholipids as a deposition sink. The present study was to determine if dietary supplementations of phospholipid-component molecules or synthesis-enhancers: choline, serine, and ethanolamine could elevate phospholipid and DHA enrichment in the eggs and tissues of hens. A total of 50-White-Leghorn-Shavers (42-wk old) were individually caged and divided into 5 groups (n = 10/group). The 5 groups of hens were fed the following diets for 3 wk: Diet-1 = a corn soybean-meal basal-diet, Diet-2 = Diet-1 + 4%-microalgae (Aurantiochytrium, Heliae, Gibert, AZ, 1.81 g-DHA/kg) + choline-chloride (26.3 g/kg diet, 60% purity, DSM-Co., Basel, Switzerland), Diet-3 = Diet-2 + 1.41% of L-serine (100% purity, Ajinomoto-Co., Inc., Kawasaki, Japan), Diet-4 = Diet-2 + 100 mg of ethanolamine/kg (99% purity, Sigma-Aldirch-Co., St Loius, MO), and Diet-5 = Diet-3 + 100 mg of ethanolamine/kg. At the end of study, eggs, liver, ovary, and adipose samples were collected from 6 hens/group for biochemical analysis. Data were analyzed by one-way ANOVA. Compared with Diet-1, Diet-2 enhanced (P &lt; 0.05) DHA concentrations in egg yolk and liver by 213 mg/egg and 2.98 mg/g tissue, respectively, but decreased (P &lt; 0.05) total phospholipid-concentrations of yolk and liver by 50%, and hepatic-mRNA levels of elongases-2/5 and desaturases-4/6 by 25–50%. Compared with Diet-2, Diet-5 enhanced (P &lt; 0.05) DHA (by 20%) and phospholipid (by 40%) concentrations in the egg yolk, and upregulated (P &lt; 0.05) lipid-metabolism genes involved in the citicoline (CDP, up-to-3-fold) and CDP-ethanolamine (up-to-2.5-fold) pathways in the liver and ovary-tissue. In comparison, Diets-3 and 4 resulted in only 3–11% higher (P &lt; 0.05) DHA-concentrations in the liver over Diet-2. In conclusion, feeding hens a high DHA and choline diet enriched DHA in the egg yolk and down-regulated lipogenesis-gene-expression in the tissues. Supplementing the diet with extra-serine and ethanolamine further-enhanced the DHA enrichment in the egg yolk and restored the high DHA-mediated changes in the gene-expression. (Supported in part by DOE-MAGIC-grant DE-EE0007091, USDA-grant 2019-69012-29905, and Cornell-University-Hatch-grants NYC-127419/127302).


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