摘要:

Intestinal absorption of ovalbumin (OVA), a dietary macromolecule, was studied in malnourished and normally nourished suckling mice after experimentally induced infection with rotavirus. All mice developed diarrhea within 24 to 48 h postinoculation. The malnourished animals exhibited more severe symptoms and an increased number of rotavirus-containing enterocytes in intestinal sections as compared to well-nourished mice when examined 3 d postinoculation, at the peak of diarrhea. Histopathologic examination revealed villus atrophy and pronounced vacuolization of villus enterocytes in association with malnutrition and rotavirus infection. The combination of malnutrition and viral infection resulted in more severe mucosal damage, including disruption of microvillus borders. After a single oral dose of 100 µg OVA at 3 d postinoculation, the concentration of OVA in serum, gastric content, intestinal lavage fluid, and intestinal tissue homogenates was measured at different time intervals. The concentrations of OVA in intestinal tissue were significantly higher in malnourished animals, whereas lower values were found in rota virus-infected animals. In all mice, OVA was rapidly absorbed and could be consistently detected in the serum within 5 min. OVA levels peaked at 45 to 60 min and then gradually declined. In malnourished infected animals, the uptake of OVA was rapid and resulted in significantly higher serum levels when compared to well nourished or uninfected controls, respectively. The peak uptake of OVA per g body wt was about 4.5 times more in malnourished infected compared to well-nourished infected mice and 2.5 times higher in normally nourished infected animals when compared to uninfected controls. These results indicate that rotavirus infection in association with malnutrition may cause a significant rise in gut permeability to environmental macromolecules.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

To further document the effect of insulin on intestinal maturation, suckling rats were treated either with exogenous insulin (12.5 mU· g body wt, intraperitoneally, twice daily) or with saline from d 8 to 12 postpartum. Sucrase activity in brush border membrane extracts was precociously induced by insulin, whereas the activities of other brush border membrane enzymes (maltase, aminopeptidase, and neutral lactase) were enhanced (+30 to +131%,p<0.01 versus controls). The lysosomal enzyme, N-acetyl-/3-glucosaminidase, which normally declines at weaning was significantly (p<0.025) decreased in both villus (-51%) and crypt cells (-57%) isolated from the jejunum of insulin-treated rats. The microsomal enzyme, sulfatase C, and the cytosolic enzyme, lactate dehydrogenase, were also sensitive to insulin with decreases in activity ranging from -37 to -63% (p<0.05) compared to salinetreated control rats. Insulin at doses of 0.5 or 12.5 mU did not influence plasma total corticosterone levels, which were about 9-fold lower in suckling than in 25-d-old weaned rats. In weaned rats (from d 25 to 32) insulin treatment (12.5 mU) failed to influence the activity of brush border membrane hydrolases or of lysosomal, microsomal, and cytosolic enzymes. The synthesis rate of mature sucraseisomaltase, measured in weaned rats (32 d) by the incorporation of 14C-leucine into the enzyme precursor protein, was equivalent in both groups. These data demonstrate that the immature enterocyte of the suckling rat is responsive to insulin, whereas the mature enterocyte of the weaned rat is unresponsive. The effect of insulin on the intestinal cell appears not to be mediated via an endogenous stimulation of corticosterone release.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

We wished to characterize the carbohydrate fermentation by intestinal flora in formula-fed infants and in breast-fed infants. We also wished to compare the carbohydrate fermentation process in the two groups to determine whether differences that existed between groups could help explain the observation that breast-fed infants usually have milder forms of acute gastroenteritis. We performed in vitro incubations of fecal samples from nine formula-fed and 14 breast-fed infants and examined the samples for fermentation characteristics, the effect of acid pH on bacterial fermentation, and changes in carbohydrate fermentation in relation to the age of the infant. Fecal samples were incubated, with and without the addition of lactose, at a pH of 6.8 and at a pH of 5.5. Volatile fatty acids and carbohydrates were determined in the incubates. The addition of lactose to the incubate at pH 6.8 resulted in significantly increased volatile fatty acid production and larger amounts of lactose, glucose, and galactose compared with the values observed in 1-h incubates to which no lactose was added. At pH 5.5, volatile fatty acid production was significantly lower in both groups compared with that at pH 6.8, and the accumulation of monosaccharides in the incubate of feces of formula-fed infants increased significantly (p<0.05). In contrast, in stools from breast-fed infants, incubation at pH 5.5 resulted in a greater proportion of saccharides as lactose,i.e.a decrease in the amount of lactose hydrolyzed (p<0.01), accompanied by a nonsignificant increase in the amount of hexose. The decrease in lactose hydrolysis in breast-fed infants results in a lower luminal osmolar load, which may provide a partial explanation for the fact that acute gastroenteritis is milder in this population.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Twenty-four male Guatemalan children, aged 7 to 23 mo, suffering dehydration due to acute diarrhea were studied to assess their fecal endogenous losses of trace minerals zinc, iron, and copper while treated with oral rehydration therapy, either with standard or glycineadded solutions. Sodium and potassium excretions (from endogenous and exogenous sources) were also monitored. No statistically significant effect of glycine was observed on any of the minerals studied, although a tendency to higher output was seen with zinc. Median rates of fecal excretion of zinc, iron, and copper were 6.08, 6.33, and 1.61 µg/ kg/ h, respectively, whereas those for sodium and potassium were 11.2 and 9.7 mg/ kg/ h. All of the minerals' excretion showed significant linear correlations with fecal volume, r values were 0.47 (Zn), 0.64 (Fe), 0.77 (Cu), 0.98 (Na), and 0.97 (K). Mineral-mineral interactions also were evident, with such correlations in fecal excretion rates as: Zn versus Cu,r=0.75; Zn versus Fe,r=0.62; Fe versus Cu,r=0.76.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Iron absorption from human milk and infant formula has received much attention, but experimental design problems have been common. In our study, iron retention from human milk, milk-based infant formula (IF) with and without supplemental ferrous sulfate, and IF supplemented with either human or bovine lactoferrin (Lf) was evaluated in infant rhesus monkeys. The exchange of59Fe (III) Cl3between the whey, casein, and fat fractions required up to 72 h to reach the same distribution as intrinsic iron, depending on the type of diet. Infant monkeys were intubated with labeled human milk or IF and counted in a whole body counter. Each infant received all five diets and was also intubated with a reference dose of55Fe (II) ascorbate. There was no significant difference in iron retention (mean ± SEM) from the experimental diets: human milk 32.5 ± 5.1%; IF 32.1 ± 8.0%; IF + Fe 23.0 ± 3.9%; IF + human Lf 23.5 ± 3.3%; IF + bovine Lf 22.7 ± 4.9%. Therefore, infant monkeys absorb and retain iron similarly from human milk and infant formula. Supplementation of infant formula with human or bovine Lf resulted in similar iron retention to that of ferrous sulfate-supplemented infant formula.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Bilateral lesions of the globus pallidus, ventrolateral thalamus, substantia nigra, or the median raphe produce a generalized learning deficit in rats. Bilateral lesions of the dorsomedial hypothalamic nuclei stunt growth in rats without significantly disturbing endocrine functions and without producing a generalized learning deficit. Globus pallidus, ventrolateral thalamus, substantia nigra, median raphe, and dorsomedial hypothalamic nuclei lesions were produced in weanling Sprague-Dawley rats to compare their effect on physical growth. At approximately 72 d of age, all lesions had resulted in reduced body wt, tail length, and tibial length. The differences lacked significance only in body wt after median raphe lesions and tail length after ventrolateral thalamus lesions. In rats with the generalized learning deficit, body size was most stunted after substantia nigra lesions. Tibial epiphyseal width was modestly increased in rats with the generalized learning deficit. Food intake/ average body wt ratio in substantia nigra and dorsomedial hypothalamic nucleli rats did not differ significantly from control values. Decreases in brain, heart, liver, kidney, and testes tended to occur after all the lesions, but brain and testis organ wt/ body wt ratios were either increased or unchanged. We conclude that brain lesions producing a generalized learning deficit in rats result in impaired physical growth. The results indicated that the stunted animals maintain adequate food intake and have normal growth hormone function. The anatomical substrate for generalized learning impairment may overlap with that of a set point for body size.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Hypoxic injury to differentiating glial cells is a critical event in the development of periventricular leukomalacia, the major hypoxic-ischemic lesion of the premature infant. This study has addressed the effects of hypoxia on differentiating glial cells, primarily astrocytes. Primary cultures of dissociated newborn rat brain, which are composed predominantly of differentiating astroglia, were used. Efflux of lactate dehydrogenase, an enzyme enriched in astroglia, was used to quantitate cellular injury. Three major findings are reported. First, differentiating astrocytes were resistant to hypoxic injury for many hours, although by 24 h of hypoxia severe cellular injury (lactate dehydrogenase efflux of 86% of total and morphologic changes) was obvious. Second, increase of glucose in the culture medium from the approximately physiological concentration of 5.6 to 15 mM had a marked protective effect versus hypoxia, i.e. lactate dehydrogenase efflux was totally prevented during 24 h of hypoxia in 15 mM glucose. Third, the protective effect of high glucose appeared to be related to increased utilization by glycolysis, because there was a direct correlation between the resistance to hypoxic cellular injury and the amount of lactate generated and of glucose consumed by the cells. Thus, the cells with the lowest lactate dehydrogenase efflux (and highest glucose supplementations) had medium lactate concentrations as high as 32-36 mM. These concentrations of lactate are approximately double the reported threshold concentration of lactate considered to produce cellular necrosis in in vivo models of hypoxic injury, primarily in mature animals. The data raise the possibility that hypoxic injury to differentiating glia can be prevented or ameliorated by increase in glucose availability.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

To determine whether neonatal nutrition influences development of CNS noradrenergic systems, litter sizes were manipulated at birth to produce undernutrition (16-17 pups/litter) or overnutrition (five to six pups) and compared to rats reared in normal litter sizes (10-11 pups). Studies were conducted throughout the preweaning period in which nutrition was manipulated, as well as during postweaning nutritional rehabilitation. Sparing of brain growth occurred, evidenced by much smaller changes in brain region wt than in body wt. Similarly, neonatal malnutrition produced major deficits in norepinephrine levels in peripheral sympathetic pathways, but levels in the brain remained within normal limits. Development of [3H]norepinephrine synaptosomal uptake, a biochemical index for presynaptic terminals, was unimpaired by malnutrition; indeed, higher uptake values were seen than in the control population. Nevertheless, norepinephrine turnover was severely attenuated during nutritional restriction and the effect persisted into adulthood; the deficit was greater in the cerebral cortex than in the cerebellum, despite the fact that cerebellar growth showed less sparing. Development of binding capabilities of noradrenergic receptors, particularly theα2- andβ-subtypes, were also adversely affected in cerebral cortex, again suggestive of a deleterious effect on synaptic function. Animals exposed to neonatal overnutrition showed only slight effects on brain region wt or norepinephrine levels, but did display some suppression of [3H]norepinephrine synaptosomal uptake and enhancement of norepinephrine turnover; changes in receptor binding capabilities in the overnourished animals were attributable to the small alterations in brain region wt. These data indicate that neonatal nutrition alters presynaptic and postsynaptic markers of noradrenergic function that remain abnormal even when nutritional rehabilitation occurs.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

We measured body composition, basal metabolic rate (BMR), and total energy expenditure in 28 nonobese and 35 obese adolescents aged 12-18 y using indirect calorimetry and the doubly labeled water method. BMR was highly correlated with fat-free mass in both the nonobese and obese groups (r=0.77 and 0.84, respectively). BMR adjusted for fat-free mass was significantly greater in males than females and in the obese subjects. Total energy expenditure was significantly greater in the obese than nonobese cohort but ratios of total energy expenditure/ BMR were not significantly different in the two groups (1.79 ± 0.2 versus 1.68 ± 0.19, nonobese and obese males and 1.69 ± 0.28 versus 1.74 ± 0.19 nonobese and obese females, respectively). These data indicate that BMR and total energy expenditure are not reduced in the already obese adolescent. Therefore, reduced energy expenditure cannot be responsible for the maintenance of obesity in adolescents.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Twenty-two of 23 consecutive infants with bronchiolitis, 5.5 ± 3.5 mo of age, showed a 1.9 ± 1.4% increase in body weight, increased urinary osmolality of 737 ±193 mmoI/ L with low plasma osmolality of 275 ± 4 mmol/ L, and markedly elevated plasma antidiuretic hormone (ADH) levels of 114 ± 225 pg/ mL. Increased ADH, which usually suppresses plasma renin activity, was associated with increased plasma renin activity of 11-55 ng angiotensin 1/ mL/ h (normal for age < 10 ng angiotensin 1/ mL/ h). Hyperaldosteronism was evident from the low fractional excretion of sodium of 0.27 ± 0.2% and high fractional excretion of potassium of 21 ± 15%. Serum sodium concentrations were normal. All of the pathologic findings returned to normal when the bronchiolitis subsided. A control group of 10 infants with nonrespiratory febrile illness did not show any of the above abnormalities. Thus, bronchiolitis of infancy is characterized by both increased ADH secretion and hyperreninemia with secondary hyperaldosteronism, which induce water retention but counterbalance each other with respect to serum sodium. Increased ADH secretion as well as increased plasma renin activity are not “inappropriate,” but rather suggest a response to the perception of hypovolemia by intrathoracic receptors. We therefore conclude that the clinical management of bronchiolitis requires close monitoring of body wt and plasma osmolality-urinary osmolality relationship; serum sodium levels may be misleading.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID