Regional distribution and localization of zinc and metallothionein in the intestine of rats fed diets differing in zinc content.

BACKGROUND: Zinc (Zn) is protective and enhances epithelial repair in gut diseases. In this study we investigate the localization and distribution of Zn and its binding protein, metallothionein (MT), in the gut of rats fed diets varying in Zn content. METHODS: Male-Sprague Dawley rats were fed low, normal, high, or excess Zn in their diets (10, 100, 400, or 1000 mg Zn/kg, respectively) and killed 7 days later. Blood, liver, and gut tissues were collected. Tissue Zn was determined with atomic absorption spectrophotometery and MT with a Cd/haem affinity assay. Zn and MT were immunohistochemically localized in the small-intestinal wall with zinquin and an anti-MT antibody. RESULTS: Most Zn in the intestinal wall was present in the mucosal scrapings, with 94% membrane-bound and 6% cytosolic, irrespective of dietary Zn. MT levels increased in all gut regions at dietary Zn levels above 100 mg Zn/kg. MT was 40% higher in the ileum than in other gut regions in rats fed low- and normal-Zn diets. The Zn content of the ileum was also 20% higher than that of other gut regions in rats fed low-, normal-, or high-Zn diets. Zn and MT were colocalized in the base of the intestinal crypts, most visibly in the ileum. CONCLUSION: Mucosal cytosolic Zn and MT concentrations are increased only at high or excessive Zn intakes in all gut regions except the ileum, which can respond to a lower Zn intake. As the cytosolic Zn pool most likely influences mucosal protection and repair mechanisms, it is proposed that an increased MT may indicate the adequacy of oral Zn therapy in gut disease.     

Dietary zinc and metallothionein on small intestinal disaccharidases activity in mice

AIM: To examine the effect of increasing dietary zinc (Zn) intake and the lack of metallothionein (MT) expression on activity of small intestinal disaccharidases. METHODS: MT-Ⅰ and Ⅱ knockout (MT-/-) and wild-type (MT+/+) female mice at 3.5 wk of age were randomly fed with a diet containing 2 (2 Zn), 15 (15 Zn) or 50 (50 Zn) mg Zn/kg (n = 8/group/genotype) for 5 wk. Small intestinal segments (duodenum, jejunum and ileum) were collected and either fixed in 10% formalin for histological analysis or snap froze...     

Does the fatty acid profile of dietary fat influence its trophic effect on the small intestinal mucosa?

To compare the enterotrophic effects of different triglycerides, five groups of eight rats were fed mixed diets giving 50% of calories as oils rich in either essential fatty acids (EFA), alpha-linolenic acid, fully saturated fatty acids, oleic acid, or medium chain fatty acids. After 21-24 days there were no significant differences between the groups in overall small intestinal whole gut weight, mucosal weight, or mucosal DNA; overall mucosal protein showed slight variation (p < 0.05) that was compatible with differences in food intake between the groups. However, long chain triglycerides (LCT) and medium chain triglycerides (MCT) differed in their regional effects on cell proliferation; all four LCT rich diets increased mucosal mass and cell proliferation maximally in the mid small intestine, while MCT had their greatest effect proximally. Subsequently, two groups of eight rats were fed diets in which EFA or MCT were given as twice daily boluses (29% of dietary calories) for 20 to 23 days and compared with a third group of eight rats receiving a glucose rich, low fat diet. EFA and MCT boluses increased the overall parameters of small intestinal mucosal mass and for both oils the effects were now maximal in the mid small intestine. Thus different triglycerides have similar effects on overall small intestinal mucosal mass, but MCT differ from LCT in their regional effects on mucosal cell proliferation when they are given in mixed diets, although not when given as boluses.     

Pre-treatment with insulin-like growth factor-I partially ameliorates 5-fluorouracil-induced intestinal mucositis in rats.

Insulin-like growth factor-I (IGF-I) has been demonstrated to enhance mucosal repair following intestinal damage induced by chemotherapeutic agents (intestinal mucositis). However, the potential for prophylactic IGF-I to protect the intestine remains undefined. We investigated the effects of IGF-I pre-treatment on chemotherapy-induced mucositis in rats. Male Sprague Dawley rats were treated for 7 days with 0 or 4.3mg/kg/day IGF-I delivered systemically via osmotic mini-pump. Rats received an intraperitoneal injection of 0 or 150 mg/kg 5-fluorouracil (5-FU) on day 7 and were killed 48 h later for assessment of intestinal damage and repair. Compared to normal controls, 5-FU decreased epithelial proliferation by 86%, concurrently increasing the incidence of apoptosis 87-fold, whilst decreasing small intestinal (SI) length by 14%, SI weight by 30% and total gut weight by 24%. 5-FU decreased villus height in the duodenum (23%), jejunum (20%) and ileum (30%) with crypt depths decreased by 31%, 27% and 33% in these gut regions. These effects were less profound in IGF-I pre-treated rats in which apoptosis was increased 48-fold, with SI length decreased by 7%, SI weight by 18% and total gut weight by 15% accompanied by decreases in villus height of 8% (duodenum), 14% (jejunum) and 21% (ileum), and crypt depth decreases of 23%, 16% and 17% for the same gut regions, compared to normal controls. We conclude that IGF-I pre-treatment only partially attenuates features of intestinal mucositis when assessed 48 h after 5-FU chemotherapy.     

Dietary fructo-oligosaccharides and lactulose inhibit intestinal colonisation but stimulate translocation of salmonella in rats

BACKGROUND AND AIMS: It is frequently assumed that dietary non-digestible carbohydrates improve host resistance to intestinal infections by stimulating the protective gut microflora. However, compelling scientific evidence from in vivo infection studies is lacking. Therefore, we studied the effect of several non-digestible carbohydrates on the resistance of rats to Salmonella enteritidis infection. METHODS: Rats (n=8 per group) were fed "humanised" purified diets containing 4% lactulose, fructo-oligosaccharides (FOS), resistant starch, wheat fibre, or cellulose. After an adaptation period of 2 weeks the animals were orally infected with S enteritidis. Supplement induced changes in faecal biochemical and microbiological parameters were studied before infection. Colonisation of salmonella was determined by studying the faecal excretion of this pathogen and translocation by analysis of urinary nitric oxide metabolites over time and classical organ cultures. Intestinal mucosal myeloperoxidase activity was determined to quantify intestinal inflammation after infection. RESULTS: Despite stimulation of intestinal lactobacilli and bifidobacteria and inhibition of salmonella colonisation, FOS and lactulose significantly enhanced translocation of this pathogen. These supplements also increased cytotoxicity of faecal water and faecal mucin excretion, which may reflect mucosal irritation. In addition, caecal and colonic, but not ileal, mucosal myeloperoxidase activity was increased in infected rats fed FOS and lactulose. In contrast, cellulose, wheat fibre, and resistant starch did not affect the resistance to salmonella. CONCLUSIONS: In contrast to most expectations, FOS and lactulose impair the resistance of rats to intestinal salmonella infection. Obviously, stimulation of the endogenous lactobacilli and bifidobacteria is no guarantee of improved host defence against intestinal infections.     

Regulation by dietary calcium of vitamin D-dependent calcium-binding protein and active calcium transport in the small intestine of lactating rats

To test the hypothesis that vitamin D-dependent calcium-binding protein (CaBP) and active calcium (Ca) transport in the small intestine of vitamin D-replete lactating rats are regulated by dietary Ca intake, pregnant rats were given a high Ca (1.6% Ca and 1.4% phosphorus) or low Ca (0.1% Ca and 0.4% phosphorus) diet starting 3 days before delivery. Toward the end of lactation (days 16-23) the rats were killed, and active Ca transport (using everted gut sacs) and CaBP were determined in duodenum, jejunum, and ileum. The right tibiae were used for bone weight and ash determinations. The Ca transport ratios and CaBP concentrations in jejunum and ileum were significantly increased only in the low Ca group. In contrast, in the duodenum both parameters were equally high regardless of the diet. Nonlactating rats given the two diets for the same length of time had the expected increase in both parameters in the duodenum when fed the low Ca diet. Nonlactating rats, in contrast to lactating rats, had undetectable CaBP in jejunum and ileum regardless of diet. Lactating rats fed the high Ca diet had no net loss of bone at the end of lactation compared with rats on day 1 of lactation. In contrast, lactating rats fed the low Ca diet had a net loss of 44% of bone weight. Plasma 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] concentrations on the 21st day of lactation were (mean +/- SE) 538 +/- 96 and 46 +/- 18 pg/ml in rats consuming the low and high Ca diets, respectively. The comparable values for the nonlactating rats were 140 +/- 4 and 26 +/- 8 pg/ml. In conclusion, dietary Ca restriction during lactation can stimulate CaBP and active Ca transport in both jejunum and ileum, and both parameters appear to be modulated by dietary Ca via the circulating concentration of 1,25-(OH)2D3. In contrast, in the duodenum neither parameter appears to be related to dietary Ca, plasma 1,25-(OH)2D3 concentration, or lactation-associated bone loss.     

Gut decontamination prevents bronchoscopy-induced bacterial translocation. An experimental study in rats

BACKGROUND: Selective gut decontamination is suggested to suppress the gram-negative bacterial overgrowth in the intestine and consequently to reduce bacterial translocation. OBJECTIVE: The purpose of the present study is to examine the effects of gut decontamination on bronchoscopy-induced bacterial translocation, and intestinal mucosal injury. METHODS: Forty-five rats were assigned into three groups. Group 1 served as control (n=15). Group 2 (n=15) and group 3 (n=15) underwent bronchoscopy. In addition, group 3 underwent gut decontamination. Gut decontamination was performed two days prior to bronchoscopy with erythromycin and neomycin. Twenty-four hours after bronchoscopy, blood, mesenteric lymph nodes, spleen, liver, ileum and cecum were harvested for bacterial determination. The ileum was also assessed and graded histologically according to Chiu's injury scale. RESULTS: In the bronchoscopy group, bacterial translocation to the mesenteric lymph nodes was found in 7/15 rats (46.7%), compared to none of the controls (p=0.01). These rats also showed significant evidence of intestinal injury, compared to the controls (mean ranks, 32.7 or 8.5, p<0.0001). On the other hand, gut decontamination prevented bacterial translocation, compared to the bronchoscopy group (p=0.011). However, gut decontamination provided no beneficial effect on the intestinal mucosal injury, compared to the bronchoscopy group. These animals also revealed significant intestinal injury, compared to the controls (mean ranks, 27.8 or 8.5, p<0.0001). CONCLUSIONS: Our data shows that despite no amelioration in bronchoscopy-induced intestinal mucosal injury, gut decontamination has a preventive role for bronchoscopy-induced bacterial translocation.     

Diabetic intestinal growth adaptation and glucagon-like peptide 2 in the rat: effects of dietary fibre

BACKGROUND/AIMS: Dietary fibre influence growth and function of the upper gastrointestinal tract. This study investigates the importance of dietary fibre in intestinal growth in experimental diabetes, and correlates intestinal growth with plasma levels of the intestinotrophic factor, glucagon-like peptide 2 (GLP-2). METHODS: Male Wistar rats were randomised to the following groups: two streptozotocin-diabetic and two control groups fed either a fibre-containing or a fibre-free diet for three weeks. Intestinal weight, length, and morphometric data (villus height, villus area, crypt depth) were measured. Blood samples were obtained after two weeks for measurement of GLP-2 and enteroglucagon (glicentin, oxyntomodulin). RESULTS: The mean daily consumption of food in the two diabetic groups was 40% higher than in controls. In diabetic rats fed fibre, the increase in intestinal weight from day 0 to 20 was sixfold greater than that of the controls and small intestine weight per cm length was increased by 50%. In the diabetic rats fed a fibre-free diet, intestinal growth was 30% less than in diabetic rats fed fibre, and intestinal weight increased only threefold compared with controls. Morphometric data showed that the intestinal increase in diabetic rats fed fibre was due primarily to growth of the mucosal layer. Villus height and crypt depth increased 60% and 40% respectively, but by only 20% in fibre-free diabetic rats. The plasma levels of GLP-2 parallelled diabetic intestinal growth, whereas plasma levels of enteroglucagon increased regardless of the extent of intestinal growth. CONCLUSIONS: Intestinal growth in experimental diabetes is strongly influenced by the presence of dietary fibre. The effect may be mediated by GLP-2.     

Intestinal adaptation and enzymatic changes following reciprocal jejunoileal transposition in rats. Effects of a high-fructose diet

The longitudinal localization of nine enzymes of the carbohydrate metabolism was studied in rats fed standard or high fructose diets, two months after a reciprocal jejuno-ileal transposition. In the ileal segment transposed to jejunal location, an adaptive increase of mucosal mass was observed, but the functional characteristics of enterocytes remained the same in the case of triokinase, aldolase, triose phosphate isomerase, glucose-6-phosphate isomerase and glucose-6-phosphatase activities. In the case of ketohexokinase and hexokinase activities, the functional properties of cells tended to resemble that of jejunum, as revealed by a significant increase in the specific enzyme activity. In the jejunum transposed to the place of the ileum, the fundamental properties of enterocytes and the functional capacity of the gut were maintained except in the case of fructose-1.6-bis phosphatase and of glucose-6-phosphatase. The high fructose diet did not facilitate the re-establishment of the gradient in its normal, aboral, direction. Indeed except for glucose-6-phosphatase, the enzymes of the jejunum transposed to the place of the ileum kept a high sensitivity and the enzymes of transposed ileum a low sensitivity to dietary fructose. Our conclusion is that the response to the diet depends more on the original position of the intestinal segment than on the local nutritional conditions and therefore that the basal activity of the majority of the intracellular enzymes implicated in carbohydrate metabolism and also their regulatory systems, are an intrinsic characteristic of the intestinal cells.     

Enteropathy precedes type 1 diabetes in the BB rat

BACKGROUND AND AIMS: There is increasing evidence implicating intestinal immune responses to dietary proteins in the pathogenesis of type 1 autoimmune diabetes (T1D). Here we investigated the association between intestinal pathology and dietary factors in T1D by examining the mucosal architecture in the BB rat model. METHODS: BB control (BBc) and diabetes prone (BBdp) rats were fed either a diabetes retardant hydrolysed casein based diet or one of two cereal based diets that promote the development of diabetes. Intestinal architecture was assessed in the jejunum by microdissection, histology, and immunohistology, and by measuring peroxidase activity and brush border invertase levels. RESULTS: Enteropathy was present in BBdp rats soon after weaning, as assessed by increases in crypt length and in the proliferative activity of crypt epithelial cells in the jejunum, and this remained constant until 120 days of age. There was also a decrease in invertase activity, as well as increased numbers of intraepithelial lymphocytes, increased levels of mucosal peroxidase activity, and infiltration of the mucosa by CD4(+) T lymphocytes. Equivalent enteropathy was present at all times in BBdp rats and was not influenced by the nature of the diet or by thymectomy at three weeks at age, procedures which prevent the development of diabetes. CONCLUSION: Enteropathy is a consistent feature in the diabetes prone BB rat but it precedes the onset of insulitis and appears to be due to mechanisms distinct from those which cause diabetes. The beneficial effects of the diabetes retardant hydrolysed casein diet on diabetes are not due to an effect on intestinal architecture per se but mucosal damage may be necessary for the development of autoreactivity in the pancreas.     

Hypolipidemic effects of guar gum and its enzyme hydrolysate in rats fed highly saturated fat diets.

The effects of guar gum and its enzyme hydrolysate as well as fructooligosaccharide on lipid metabolism were compared in rats fed high-fat diets employing lard or palm oil as dietary fat (25% in the diets). Guar gum and the enzyme hydrolysate greatly increased cecal volatile fatty acid contents to a similar extent. Fructooligosaccharide also increased the variable but to a lesser extent. Not only guar gum but also the hydrolysate and the oligosaccharide reduced serum cholesterol levels irrespective of dietary fat sources but to a lesser extent. The triglyceride-lowering effects of the hydrolysate and the oligosaccharide were comparable to that of guar gum. Although guar gum enzyme hydrolysate and fructooligosaccharide doubled the biliary bile acid excretion, these materials only slightly increased the activities of hepatic enzymes of cholesterol and bile acid synthesis. Guar gum and its hydrolysate suppressed 3-hydroxy-3-methylglutaryl-coenzyme A reductase activities in the ileum to one half the control value in the experiment where dietary fat was lard. The highly polymeric structure does not appear to be a prerequisite for nonabsorbable carbohydrate to alter lipid metabolism at least in rats fed high-fat diets.     

Neurotensin prevents intestinal mucosal hypoplasia in rats fed an elemental diet

Liquid elemental diets are associated with mucosal hypoplasia of both the small intestine and colon. Neurotensin, a tridecapeptide widely distributed in the gut, is trophic for the small intestine of rats fed a normal chow diet. The purpose of this study was to determine whether neurotensin could reverse the hypoplasia of intestinal mucosa that is associated with feeding a liquid elemental diet. Forty male Sprague-Dawley rats were randomized into five groups. Four groups were fed (for seven days) a glutamine-free liquid elemental diet. Subcutaneuos injection of saline (control) or neurotensin (33, 100, or 300 g/kg) were given to the groups of rats every 8 hr for seven days. Group five (Chow) received rat chowad libitum for seven days. Rats were killed on day 8, and the proximal jejunum, distal ileum, and proximal colon removed. Mucosal weight, DNA, RNA, and protein contents were determined. Neurotensin (300 g/kg) increased the cellularity of the small intestinal mucosa and reversed mucosal hypoplasia due to an elemental diet; a more pronounced effect was noted in the jejunum compared to the ileum. Neurotensin (33 and 100 g/kg) increased mucosal DNA content in the jejunum but was not effective in reversing the hypoplasia. Neurotensin had no effect on growth of colonic mucosa. These results suggest that neurotensin may be an important trophic hormone for the small intestine. Administration of neurotensin may alleviate hypoplasia of the small bowel mucosa and maintain functional integrity of the gut during prolonged feeding of an elemental diet.Supported by grants from the National Institutes of Health (5R37DK 15241-17, P01 DK 35608), the American Cancer Society (PDT-220), and the National Cancer Institute (CA 17701).A preliminary report has appeared inSurgical Forum (1).Dr. Evers is a recipient of an American Surgical Association Foundation Fellowship Award.     

Influence of dietary picolinic acid on mineral metabolism in the rat

Male rats were fed isonitrogenous, isocaloric diets containing different amounts of dietary zinc and picolinic acid (PA) (25, 60, 120 ppm Zn, 0, 20, 40, 60 mmol PA/kg diet) and balance collections of urine and faeces made over a 4-day period. Rats fed 25 ppm Zn were in negative Zn and Cu balance during the experiment. Faecal Zn, but not urinary Zn excretion was elevated with increasing dietary Zn supply. Urinary Zn, Cu and Mg excretion increased with increasing intakes of dietary PA, regardless of Zn intake. Tissue Zn levels were unaffected by dietary Zn or PA. It is concluded that dietary PA forms soluble complexes with metal ions which are rapidly absorbed but are then re-excreted in urine and may not be available for metabolism or incorporation into tissues.     

Feeding rats diets containing cheno- or ursodeoxycholic acid or cholestyramine modifies intestinal uptake of glucose and lipids

We wished to test the hypothesis that variations in the luminal content of bile acid produced by feeding chenodeoxycholic acid (CDC), ursodeoxycholic acid (UDC) or cholestyramine (C) alter intestinal transport properties and morphology. Rats were fed standard chow pellets containing 0.5% CDC, 0.5% UDC or 2% C for a period of 2 weeks, and the in vitro uptake of glucose, cholesterol, bile acids and a homologous series of fatty acids was assessed. The food consumption was similar in animals fed chow, CDC, UDC and C, yet rats fed CDC or UDC gained less weight, and the weight of the jejunal and ileal mucosa was lower in animals fed CDC or C than in those fed chow or UDC. Ileal but not jejunal uptake of glucose was reduced in animals fed UDC, CDC or C. The active ileal uptake of bile acids was enhanced by UDC, CDC or C, whereas the jejunal passive permeability to bile acids was reduced by feeding C. Feeding C inhibited the jejunal and ileal uptake of cholesterol; C, UDC and CDC had a variable effect on the intestinal uptake of the fatty acids 10:0-18:0. The jejunal mucosal surface area was lower in groups fed CDC or UDC as compared with rats fed chow or C, and the ileal mucosal surface area was lower in rats fed CDC. However, the altered intestinal transport could not be explained by the altered morphology. Thus, (1) chronic variations in the intestinal luminal content of bile acids produced by the feeding of CDC, UDC or C resulted in alterations in the active and passive transport properties of the intestine, and (2) these changes differed between the jejunum and the ileum and were not explained simply by alterations in the animals' food intake or mucosal morphology. These studies suggest that chronic variations in the bile acids in the intestinal lumen may be one of the factors independently influencing the transport properties and mucosal surface area of the intestine. The long-term effect of changes in luminal bile acid content on intestinal function in man remains to be established.     

Casein hydrolysate diet controls intestinal T cell activation, free radical production and microbial colonisation in NOD mice

Aims/hypothesis

Dietary and microbial factors and the gut immune system are important in autoimmune diabetes. We evaluated inflammatory activity in the whole gut in prediabetic NOD mice using ex vivo imaging of reactive oxygen and nitrogen species (RONS), and correlated this with the above-mentioned factors.

Methods

NOD mice were fed a normal diet or an anti-diabetogenic casein hydrolysate (CH) diet. RONS activity was detected by chemiluminescence imaging of the whole gut. Proinflammatory and T cell cytokines were studied in the gut and islets, and dietary effects on gut microbiota and short-chain fatty acids were determined.

Results

Prediabetic NOD mice displayed high RONS activity in the epithelial cells of the distal small intestine, in conjunction with a proinflammatory cytokine profile. RONS production was effectively reduced by the CH diet, which also controlled (1) the expression of proinflammatory cytokines and colonisation-dependent RegIIIγ (also known as Reg3g) in ileum; (2) intestinal T cell activation; and (3) islet cytokines. The CH diet diminished microbial colonisation, increased the Bacteroidetes:Firmicutes ratio, and reduced lactic acid and butyric acid production in the gut.

Conclusions/interpretation

Epithelial RONS production and proinflammatory T cell activation appears in the ileum of NOD mice after weaning to normal laboratory chow, but not after weaning to an anti-diabetogenic CH diet. Our data suggest a link between dietary factors, microbial colonisation and mucosal immune activation in NOD mice.     

Effects of starvation and bowel resection on paracellular permeability in rat small-bowel mucosa in vitro

BACKGROUND: Maintenance of intestinal integrity is essential after major abdominal surgery in malnourished subjects. The purpose of this experimental study was to investigate factors affecting small-bowel mucosa permeability in vitro in the immediate postoperative period in starved rats. METHODS: Male Wistar rats were randomly placed in five groups: Controls, Anesthesia, Resection, Starvation, and Starvation + resection. Controls consisted of fed rats. Anesthesia was induced intraperitoneally with xylazine and ketamine. Resection was 5 cm of the mid-jejunum, and the starvation period was 48 h. Two hours after surgery stripped mucosal segments from the jejunum and the ileum were mounted in Ussing chambers, and the transmucosal permeation of 51Cr-labeled ethylenediaminetetraacetic acid (EDTA) and dextran (40,000 Da) was studied for 120 min while electrophysiology was monitored. RESULTS: Starvation increased permeability to 51Cr-EDTA in both the jejunum and ileum. In the jejunum permeability was further increased by starvation + resection. Resection or anesthesia alone did not increase permeability. The villous height in the jejunum was reduced by starvation. Mucosal permeability was correlated to the change in transepithelial resistance during experiments. CONCLUSIONS: Starvation was the main cause of increased mucosal permeability in both intestinal segments of the rat, but surgical trauma had an additive effect, which was most pronounced in the jejunum.     

Zinc deficiency and a high-fat diet during growth: Metabolic and adipocyte alterations in rats

Background and aimsTo evaluate the effects of a high-fat diet during post-weaning growth on intermediate metabolism and retroperitoneal adipose tissue, in adult male rats exposed to adequate or deficient zinc intake during prenatal and postnatal life.Methods and resultsFemale Wistar rats were fed low- or control-zinc diets from pregnancy to offspring weaning. Male offspring born from control mothers were fed either control or high-fat, control-zinc diets for 60 days. Male offspring born from zinc deficient mothers were fed either low-zinc or high-fat, low-zinc diets for 60 days. At 74 days of life, oral glucose tolerance test was performed. In 81-day-old offspring, blood pressure, lipid profile, plasmatic lipid peroxidation and serum adiponectin level were determined. In retroperitoneal adipose tissue, we evaluated oxidative stress, morphology and adipocytokines mRNA expression. Low-zinc diet induced adipocytes hypertrophy, increased oxidative stress, and decreased adiponectin mRNA expression in adipose tissue. Low-zinc diet increased systolic blood pressure, triglyceridemia, plasmatic lipid peroxidation and glycemia at 3 h after glucose overload. Animals fed high-fat or high-fat, low-zinc diets showed adipocytes hypertrophy, decreased adiponectin mRNA expression, and increased leptin mRNA expression and oxidative stress in adipose tissue. They also exhibited decreased serum adiponectin levels, increased triglyceridemia, plasmatic lipid peroxidation and area under the oral glucose tolerance curve. High-fat, low-zinc diet induced greater alterations in adipocyte hypertrophy, leptin mRNA expression and glucose tolerance test than high-fat diet.ConclusionZinc deficiency since early stages of intrauterine life could increase susceptibility to metabolic alterations induced by high-fat diets during postnatal life.     

Effect of dietary fat on the distribution of mucosal mass and cell proliferation along the small intestine.

This study investigated how substitution of long chain triglycerides for glucose in a mixed diet affects the overall small intestinal mucosal mass and the distribution of mucosal mass and cell proliferation along the small intestine. Four groups of eight female Wistar rats (180-200 g) were isocalorically fed mixed diets containing the essential fatty acid rich oil Efamol substituted for glucose at concentrations of 1.2%, 10%, 25%, and 50% total calories for 20 to 23 days. The small intestine was divided into three equal length segments and whole gut weights, mucosal weights, protein and DNA determined. Cell proliferation was estimated from the two hour accumulation of vincristine arrested metaphases in microdissected crypts at points 0%, 17%, 33%, 50%, 66%, and 100% small intestinal length. There were no differences between groups in parameters of overall small intestinal or distal segment mucosal mass. With increasing levels of fat, however, there was a significant trend for the mucosal mass of the proximal segment to fall and that of the middle segment to rise. The pattern of two hour metaphase accumulation reflected these changes. These regional changes in mucosal mass and cell proliferation may reflect differences in the sites of absorption of fat and glucose.     

Changes in Endogenous Lipid Excretion in Rats Fed Diets Containing Non-Heated and Thermally Oxidized Olive Oils

The objective of this study was to determine the effects of diets containing non-heated and thermally oxidized olive oils on fecal endogenous lipids. Male Wistar rats were fed fat-free diets and diets supplemented with 12% non-heated, heated, and a 1: 1 mixture of non-heated/heated olive oils. After a 15-day experimental period two groups of fecal lipids from major endogenous sources were quantitated: neutral sterols and fatty acids associated with intestinal microflora action. Fecal endogenous sterols, particularly cholesterol, were significantly higher when diets contained oil, and excretion increased as the dietary oil alteration increased. Similar results were obtained for endogenous fatty acids. Increments of fecal sterols, dependent on oil alteration, could be explained by impairments in triglyceride hydrolysis and subsequent effect on cholesterol micellar solubilization. Moreover, high concentrations of poorly digestible lipids may have led to intestinal microbial modifications.