Ingestion of potato starch containing high levels of esterified phosphorus reduces calcium and magnesium absorption and their femoral retention in rats

Many studies have shown that esterified phosphorus (P) in diets has a favorable effect on mineral absorption in humans and animals. Phosphorylated oligosaccharides derived from potato starch increase calcium (Ca) absorption from the rat intestine both in situ and in vitro. We hypothesized that the feeding of potato starch has a potential to increase Ca or magnesium (Mg) absorption. Male Sprague-Dawley rats at 7 weeks were fed 4 types of diet containing either 60% sucrose, cornstarch, or 1 of 2 types of potato starch with different P contents for 1, 3, or 5 weeks. A balance test for Ca, Mg, and P was undertaken, and these mineral contents in the femur were determined for the 4 diet groups at each feeding period in vivo. Ingestion of potato starch increased Ca, Mg, and P excretion into feces and decreased the absorption rate of Ca and Mg. Femoral Ca contents were also decreased in the rats fed the potato starch diets compared with those in rats fed the sucrose or cornstarch diet. In vitro experiment in Ca absorption was undertaken using everted jejunal and ileal sacs of the small intestine in male Sprague-Dawley rats (7 weeks old). The potato starch application did not induce significant increase in Ca absorption compared with nonstarch (control) or cornstarch application. In conclusion, the ingestion of potato starch does not increase Ca and Mg absorption and rather accelerates their excretion, inducing the decrease in mineral absorption and retention in growing rats.     

Consumption of raw potato starch alters intestinal function and colonic cell proliferation in the rat

Raw potato starch (RPS) may escape complete digestion to enter the colon and produce alterations in colonic function, while cooked potato starch (CPS) is nearly completely digested in the rat small intestine. Effects of RPS and CPS on colonic function [fecal weight, transmit time and thymidine kinase (TK) activity (a marker for cell proliferation)] were contrasted in a 6-wk feeding study. Male F344 rats consumed either dextrose/sucrose (DS; control), 30% CPS or 30% RPS diet. RPS feeding resulted in a 3-fold increase in fecal weight and a 30% prolongation in transit time, as well as elevated levels of colonic mucosal total protein (50%) and TK activity (4- to 7-fold) compared to DS-fed rats. A second study revealed normal large intestinal histology in rats fed CPS or RPS, with elongated colonic crypts (33% increased over CPS) in group RPS. Large intestinal contents were heavier in group RPS than in group CPS. These studies demonstrate that RPS feeding significantly enhances fecal weight yet prolongs total gastrointestinal transit time. Enhanced colonic TK and elongated colonic crypts suggest that RPS stimulates colonic mucosal growth.     

Glucomannan consumption elevates colonic alkaline phosphatase activity by up-regulating the expression of IAP-I,which is associated with increased production of protective factors for gut epithelial homeostasis in high-fat diet–fed rats

We previously reported that consumption of glucomannan-containing food (lily bulb) modulates gut microbiota and increases gut immunoglobulin A (IgA, index of intestinal immune function), mucins (index of intestinal barrier function), and colonic alkaline phosphatase (ALP) activity in rats fed a high-fat (HF) diet. Small intestinal ALP has an established protective effect in inflammatory diseases, whereas little is known about the function of colonic ALP activity. We hypothesized that dietary glucomannan would increase colonic ALP activity and the gene expression in rats fed an HF diet. To test this hypothesis, male Sprague-Dawley rats were fed a diet containing 30% lard with or without 4% high or low viscous glucomannan (HGM or LGM) for 2 weeks. Dietary HGM and LGM significantly increased colonic ALP activity without affecting ALP activity in the small intestine. The colonic expression of IAP-I, an ALP gene expressed throughout the intestine, was significantly higher in the HGM and LGM groups when compared with the control group. The colonic expression of Akp3 and Alpl, other ALP genes, were not affected by HGM and LGM. Dietary HGM and LGM significantly elevated fecal levels of IgA and mucins and cecal organic acids, including n-butyrate, propionate, and lactate. Colon ALP correlated with fecal IgA, mucins, and cecal organic acids. The present study showed that dietary glucomannan elevates colonic ALP activity by up-regulation of the expression of IAP-I, which might be important for protection of gut epithelial homeostasis.     

The influence of hardly digestive starch granules on sucrase and isomaltase in small intestinal mucosa of rats

The effects of potato-starch granules (PSG) on sucrase and isomaltase activities in the small intestinal mucosa of rats were examined by gel filtration on a Sephacryl S-300 column. Young and adult rats were administered the diet containing 50% of either PSG or pregelatinized potato starch (PPS) as a control for 7 days. Mucosal homogenates were prepared from the small intestine and separated into their component disaccharidases on the column. The sucrase activity, increased by feeding young rats on the PSG diet, was detected in the sucrase-isomaltase complex by changing the activity ratio of the two enzymes. In adult rats, however, the complex seemed to be mature and the increased sucrase moiety was newly combined with a free isomaltase moiety and comprised a portion of the complex. These changes were observed not only in soluble disaccharidases but also in membrane-bound ones. Furthermore, there was a remarkable change of sucrase activity in the distal portion of the small intestine rather than in the proximal.     

Dietary soy protein is associated with reduced intestinal mucosal polyamine concentration in male Wistar rats

Quantitation of polyamine levels has been correlated with biomarkers of proliferation in the colon mucosa where dysregulated epithelial hyperproliferation is associated with colorectal cancer risk. This study was performed to assess the response of polyamine measurements to dietary factors in an animal model. Male Wistar rats were fed purified diet or diets substituted by 20% lard fat, 20% beet fiber and 20% soy protein. After 2 wk, mucosal polyamines were measured along intestinal tracts by HPLC. In rats fed the control diet (n = 10), mucosal polyamines were found at high levels in the duodenum, jejunum and ileum but at low levels in the cecum, colon and rectum. Compared with rats fed the control diet, those fed the 20% lard diet showed greater polyamine levels in the large intestine (P < 0.05, n = 10), but those fed the 20% fiber diet exhibited lower polyamine levels in the small intestine (P < 0.05, n = 9). However, rats fed the 20% soy protein diet had lower polyamine levels in both small and large intestines (P < 0.05, n = 15). Significant linear correlations were observed between rectal polyamine levels and the dietary energy intakes in these four diet groups (r = 0.972-0.991, P < 0.001). Supplementation of 0.1% soy isoflavones to the basal diet or 0.3% DL-methionine to the 20% soy protein diet for 4 wk did not affect polyamine levels. The results indicate that soy protein reduced mucosal polyamine levels, at least in part, through reduction of energy intakes. Further studies are warranted to verify that polyamine levels in intestinal mucosa are useful as an intermediate endpoint of the dietary risk factors.     

The distribution of 3-hydroxy-3-methylglutaryl coenzyme A reductase in the small intestine of rats fed raw or gelatinized starch as a carbohydrate source

The effect of gelatinization of dietary starch (wheat, corn and potato) on the distribution of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase along the small intestine of rats was studied in villus and crypt cell populations isolated by graduated scraping. Gelatinized starch preferentially stimulated jejunal reductase activity in both villus and crypt cells and consequently retained the ileojejunal gradient for the reductase activity which is characteristic for rats fed on a sucrose- or glucose-enriched semi-purified diet. The distribution of the reductase in rats fed the raw starches, however, depended on the degree of gelatinization of the preparations; raw wheat starch maintained the ileojejunal gradient, whereas the corn or potato starch eliminated the gradient, and with the latter in particular, the reductase activity tended to be higher in the ileum than in the jejunum. The digestibility of dietary starches seems to be closely related to the intertissue distribution of the intestinal HMG-CoA reductase activity.     

Effects of medium-chain triglycerides on brush border membrane-bound enzyme activity in rat small intestine

The effects of various types of dietary fat on brush border membrane-bound enzymes in rat intestinal mucosa were examined. Four groups of five rats were pair-fed defined diets for 10 d. The control group was fed a diet containing 57% sucrose and 2% corn oil as a fixed carbohydrate reference; the three experimental groups received diets containing 57% sucrose and 2% corn oil plus 13% fat in the form of medium-chain triglycerides (MCT) or long-chain triglycerides (LCT) (either lard as a highly saturated fat or corn oil as a highly unsaturated fat). Feeding LCT compared to the control diet, decreased sucrase activity in mucosal brush borders of the duodenum and jejunum. In these segments of MCT-fed rats, sucrase activity was similar to that in the control animals. In another experiment, measuring immunoreactive sucrase-isomaltase in jejunal brush border membranes revealed that feeding a high corn oil diet, but not a high MCT diet, led to a reduction in the sucrase catalytic activity per unit weight of enzyme protein, suggesting that the degradation status of sucrase-isomaltase might be altered by the different types of dietary fats. With MCT feeding, jejunal alkaline phosphatase activity was enhanced to a large extent compared to the activity in other groups. Feeding MCT, compared to lard or corn oil, also increased microvillus phospholipids of the jejunal mucosa. These results suggest that MCT, unlike LCT, do not suppress the activity of mucosal microvillus membrane enzymes in rat small intestine.     

Effects of resistant potato starch on cholesterol and bile acid metabolism in the rat

This study examines the effects of two types of resistant starch (RS), raw starch from uncooked potatoes and retrograded starch in the form of cooked and cooled potatoes, on cholesterol and bile acid metabolism in rats. Groups of 8 male Wistar rats were fed a semipurified diet containing 15% cellulose, freeze-dried raw potatoes, or freeze-dried cooked potatoes for four weeks. Serum cholesterol, liver cholesterol, and fecal steroid excretion were determined. Serum cholesterol was significantly higher and liver cholesterol was significantly lower in response to the cooked potato diet compared to the cellulose or raw potato diet. Total steroid excretion was significantly higher in rats fed the cooked potato diet (26.31 mg/d) compared to those fed the cellulose or raw potato diet (14.27 mg/d and 16.81 mg/d, respectively). Daily total bile acid excretion was significantly different among the three groups, with highest excretion seen in rats fed cooked potatoes. High daily excretion of lithocholic acid and hyodeoxycholic acid was observed in rats fed cooked potatoes. These results suggest that changes in the cecal microflora and in the production, pool size, and excretion of chenodeoxycholic acid and its derivatives may be responsible for alterations in cholesterol and bile acid metabolism observed with resistant starch feeding.     

Effect of an amino acid imbalance on intestinal sucrase and leucine aminopeptidase activities in rats.

In order to investigate the relationship between dietary amino acids and protein, as well as the activities of intestinal sucrase and leucine aminopeptidase in rats, the effects of an amino acid imbalance on these enzyme activities were studied. The amino acid imbalance was created by adding 8% of an indispensable amino acid mixture lacking threonine to a 6% casein diet supplemented with 0.3% methionine. The food intake and growth of rats fed the imbalanced diet ad libitum were depressed, and the segmental weights of the small intestine and its sucrase activity were clearly lower than those of rats fed the basal diet. The effect of the imbalanced diet under pair-feeding condition on the sucrase activity was similar to that under an ad libitum feeding condition. The food intake and segmental sucrase activity, that is, sucrase activity per length of the small intestine, of rats injected with cortisol (1 mg/day) and fed the imbalanced diet were not depressed, although administration of insulin (1.5 U/day) had no effect on the food intake or segmental sucrase activity. Force-feeding stimulated growth of rats receiving the imbalanced diet, as well as increasing their segmental sucrase activities. The effects of these different conditions on the leucine aminopeptidase activity of rats receiving the imbalanced diet were obscure. These results suggest that changes in segmental sucrase activity might be mediated by stimulating factors in food intake affected by the composition of ingested amino acids and protein together with sucrose in the gastrointestinal lumen.     

Effect of dietary protein on proteolytic activities in the pancreatic tissue and contents of the small intestine in rats.

The time-courses of proteolytic activities in pancreatic tissue and the contents of the small intestine (the intestinal contents) were determined in rats maintained on a diet containing 30% of various proteins after a switchover from a diet containing 12% casein. 1. The proteolytic activity of the pancreatic tissue quickly responded to change of dietary proteins--within 1 to 6 days--with respect to organ weight, nitrogen content and proteolytic activity, in rats receiving diets containing 30% casein, ovalbumin, lactalbumin, gluten, gelatin or zein. 2. However, the proteolytic activity in the intestinal contents did not necessarily coincide with the pancreatic digestive function; an approximately threefold increase of enzyme activity was demonstrated on the fifth day of feeding in rats receiving gluten. 3. The proteolytic activity in the intestinal contents returned to the initial level on the eighth day in the gluten-fed rats, but those rats maintained on a lysine-supplemented gluten diet exhibited no such elevation of proteolytic activity. 4. No significant difference in pancreatic composition was shown up to the eighth day between the group receiving gluten alone in diet and that receiving the same diet but supplemented with lysine, under the condition of equally restricted food intake. Intestinal trypsin and chymotrypsin levels, however, were higher in the gluten-fed rats, suggesting that the depressed rate of enzyme inactivation in the small intestine might be the principal cause of the finding described under (2) above.     

Enhancement effects of vitamin K1 (phylloquinone) or vitamin K2 (menaquinone-4) on intestinal alkaline phosphatase activity in rats

Alkaline phosphatase (ALP) hydrolyzes a variety of monophosphate esters into inorganic phosphoric acid and alcohol at a high optimal pH, and is thought to play an important role in phosphate metabolism. Intestinal ALP, located at the brush border of intestinal epithelial cells, is known to be affected by several kinds of nutrients, but little is known about the physiological function of intestinal ALP Vitamin K is an essential cofactor for the post-translational carboxylation of glutamate residues into gamma-carboxy glutamate (Gla). Recently, novel functions of vitamin K have been clarified, but no data exist on the relation between vitamin K and intestinal ALP. The aim of this study was to examine the effects of both vitamin Ks (K1: phylloquinone, and K2: menaquinone) on ALP activity. Sprague-Dawley rats (6-wk-old) were divided into three groups: a control, phylloquinone (PK: 600 mg/kg diet), or menaquinone-4 (MK-4: 600 mg/kg diet) diet group. After 3 mo of feeding, we measured intestinal ALP activity by dividing it into five segments. In each segment, both PK and MK-4 increased intestinal ALP activity. The levels of intestinal ALP activity in the duodenum and proximal jejunum from the PK group were significantly higher than in the control group (p < 0.05). Moreover, the levels of intestinal ALP activity from the proximal jejunum and distal ileum of the intestine in the MK group were significantly higher than in the control group (p < 0.05). In this study, we clarified for the first time that both vitamin K1 and K2 as nutritional factors enhance intestinal ALP activity.     

Dietary phytic acid and wheat bran enhance mucosal phytase activity in rat small intestine

The aim of this work was to investigate the influence of dietary phytic acid (PA) on intestinal phytase activity in growing rats by in vitro determination of phytase activity in the three segments of the small intestine (duodenum, jejunum and ileum), and by in vivo intestinal perfusion of a solution rich in PA (diluted soymilk). Using the in vitro method, duodenal and jejunal activities were enhanced significantly by adaptation to purified PA (+44 and +145% respectively, compared with control rats). For the rats adapted to the wheat bran (WB) diet, the induction of intestinal phytase by the substrate compared with the control values (P < 0.001) was observed only in ileum. Using soymilk in perfusions, rats consuming PA or WB diets hydrolyzed more phytate (P < 0.001 and P < 0.05, respectively) than controls. Further, Mg absorption from diluted soymilk was not affected by food adaptation, whereas Ca absorption was greater in the PA and WB groups (P < 0.001 and P < 0.05, respectively) than in the control group. Thus, intake of pure PA by rats enhances phytase in the upper parts of the small intestine (duodenum and jejunum), whereas the WB diet activates ileal phytase. Furthermore, the induction of phytase activity is greater in magnitude in rats fed synthetic PA than that observed in rats fed the WB diet. The enhancement of phytase improves intestinal Ca absorption, thus showing the capacity of the small intestine to adapt to diets rich in PA and poor in Ca.     

Physiological effects of retrograded, alpha-amylase-resistant cornstarch in rats

Retrograded amylose was prepared by gelatinization of high amylose cornstarch, followed by storage at 1 degrees C for 48 h. The insoluble residue, which resisted hydrolysis with porcine amylase, was dried and fed to male Wistar rats for 14 d in powdered semisynthetic diet. Control rats received a similar diet containing sucrose in place of resistant starch. Fecal collections were performed throughout the feeding period. After 14 d the animals were killed. The small intestine and cecum were removed for morphological examination, measurement of small intestinal crypt cell production rate (CCPR) and analysis of luminal carbohydrate content. Blood samples were collected for analysis of cholesterol, glucagon, and enteroglucagon. In the starch-fed rats, fecal bulk and excretion of starch were higher than in the controls, but they declined markedly over the feeding period. Cecal size and contents were also greater in the starch-fed rats, and cecal pH was significantly lower. The CCPR was 66% higher in the ileum of the starch-fed rats (P less than 0.001), but there was no difference in the jejunum. There were no differences in serum cholesterol or enteroglucagon levels. We conclude that retrograded amylose is partially degraded in the alimentary tract of rats, but it contributes significantly to fecal bulk.     

Effect of diets supplemented with amino acids on intestinal sucrase and leucine aminopeptidase activities in rats.

In order to investigate the relationship between dietary amino acids and protein, and activities of intestinal sucrase [EC 3.2.1.26] and leucine aminopeptidase [EC 3.4.11.1, LAPase] in rats, the effect of supplementation of amino acids into a protein-free diet and a low casein diet containing sucrose as the carbohydrate source on these enzyme activities was studied. The segmental weights of the small intestine and its mucosa of rats fed the protein-free diet supplemented with L-methionine or with L-methionine and L-threonine at 0.1 or 0.2% levels were significantly higher than those of rats fed the protein-free diet or one supplemented with L-glutamic acid, but there was no difference in the segmental activities of the sucrase and LAPase among rats fed these diets. On the other hand, the supplementation of methionine or methionine plus threonine to the 5% or 10% casein diet produced remarkable increases in the segmental weights of the small intestine and its mucosa as well as in the segmental activities of the sucrase and LAPase. There was no difference between the segmental sucrase activity of rats fed the 10% casein diet supplemented with 0.2% methionine ad libitum and that of rats fed this diet under restricted feeding conditions, although the segmental LAPase activity was affected by the amount of food consumed.     

Small intestinal mucins are secreted in proportion to the settling volume in water of dietary indigestible components in rats

The aim of this study was to clarify the effect of dietary indigestible components on small intestinal mucin secretion. We prepared polystyrene foam (PSF) with different expansion ratios (PSF-30, -60 and -90) in which powders had different settling volumes in water (SV). Rats were fed a purified diet containing 0, 10, 30, or 90 g of PSF-60/kg for 10 d. After 8 h of food deprivation, rats were refed 3 g of their respective diets within 90 min. Small intestinal mucin fractions were prepared, and periodic acid/Schiff-reactive substances and O-linked oligosaccharide chains were determined as mucin markers. Feeding of PSF-60 increased the small intestinal mucin secretion dose dependently (control vs. 30 or 60 g of PSF-60/kg, P < 0.05). When rats were fed either purified diet or diets containing PSF-30, 60, or 90 at 10 g/kg for 7 d, small intestinal mucins were greatly affected by the SV of the respective PSF tested. Rats fed the diet containing PSF-90 with the highest SV had the highest amount of mucins (vs. control, P < 0.05). In some natural dietary fibers, the small intestinal mucins and SV were correlated (r = 0.967, P = 0.002). Finally, rats were fed a purified diet or that diet containing 50 g of PSF-60/kg for 7 d. Then, each dietary group was further divided into 2 groups. After 8 h of food deprivation, rats were refed 3 g of purified or PSF diet. Greater mucins in the small intestine were manifest only in rats previously fed the PSF diet whether they were refed purified or PSF diet (control vs. PSF, P < 0.05). These results suggest that the small intestinal mucins are secreted in proportion to the SV of dietary indigestible components, and chronic ingestion of indigestible components is required for the appearance of enhanced mucin secretion.     

Ethanol effects on lipid peroxidation and glutathione-mediated defense in rat small intestine: Role of dietary fats

The effect of ethanol feeding for 5 weeks on lipid peroxidation status of small intestine was studied in rats maintained on either a rat pellet (RP) or a semisynthetic diet containing coconut oil (CCO), corn oil (CO), or fish oil (FO). Highest rate of iron/ascorbate-induced lipid peroxidation was observed in intestinal mucosa of FO-fed rats, which was further elevated (p < 0.05) upon ethanol administration. Purified brush borders from all the ethanol-treated dietary groups were more susceptible to iron-induced lipid peroxidation. Level of nonprotein thiols was increased by ethanol feeding to rats given CO or FO. FO-fed rats exhibited increased activities of glutathione reductase (GR), glutathione-S-transferase (GST), and catalase (Cat). Glutathione peroxidase (GPx) was the lowest in the CCO group. Ethanol-treated FO group exhibited increased GST and GPx activities compared to controls, whereas in rats fed the RP or CO diet, ethanol feeding significantly decreased GST activity. GR and Cat activities were not affected under these conditions. Thus, ethanol exposes the small intestinal mucosa to oxidative stress. The effects were more pronounced in rats fed n-3 fatty acid-rich (FO) diet. The corresponding rise in GPx and GST levels may reflect the adaptive changes in intestine.     

Fat intake and clofibrate administration have interrelated effects on liver cholesterol concentration and serum butyryl cholinesterase activity in rats.

Rats were fed for 15 d purified diets with different amounts of coconut fat, and with or without clofibrate. Fat was added at the expense of an isoenergetic amount of glucose. The hypolipidemic action of clofibrate was not influenced by the amount of fat in the diet. Clofibrate did not affect liver cholesterol concentration in rats fed the low fat diet, but it counteracted the rise in liver cholesterol seen in rats fed the high fat diet. This could relate to the observed raised intestinal clofibrate-hydrolyzing activity of rats fed the high fat diet, because hydrolysis of clofibrate gives rise to its biologically active form. In rats fed the low fat diet, but not in those fed the high fat diet, clofibrate raised the activity of serum esterase-1, which (unlike esterase-2) does not hydrolyze clofibrate. Possibly, the dramatic stimulatory effect of fat feeding on serum esterase-1 activity had overruled any influence of clofibrate. Clofibrate elevated serum butyryl cholinesterase activity, with this effect being amplified by fat feeding. High levels of dietary fat in the absence of dietary clofibrate did not alter serum butyryl cholinesterase activity. Clofibrate did not change butyryl cholinesterase and esterase-1 activities in small intestine. The high fat diet caused slightly higher levels of butyryl cholinesterase activity in small intestine, but markedly raised intestinal esterase-1 activity. This study shows that certain effects of clofibrate and a high fat diet are interrelated.     

Expression of DNase I in rat parotid gland and small intestine is regulated by starvation and refeeding

DNase I in rats is mainly expressed in the parotid gland and the small intestine and functions as a digestive enzyme. Male Wistar rats were deprived of food for 48 h, refed with nonpurified diet for 2 h and killed at 0, 0.33, 0.67, 1, 2, 6 or 12 h. The activity and mRNA of DNase I in the parotid gland and the small intestine were determined. We found that in rats that were not fed for 48 h there was accumulation of DNase I in the parotid gland but not in the small intestine. In the parotid gland, refeeding decreased DNase I activity (P < 0.05), perhaps due to an increase in secretion. The increase in DNase I mRNA probably resulted from the need for protein synthesis. However, in the small intestine, both the enzyme activity and the amount of mRNA were up-regulated by refeeding (P < 0.05). Exposing rats to food in a sealed transparent flask also caused a 2.5-fold increase in DNase I mRNA within 30 min in the parotid gland. These data suggested that the expression of rat parotid DNase I is up-regulated by feeding and that mastication is not essential for the regulation.     

Dietary zinc deficiency and repletion modulate metallothionein immunolocalization and concentration in small intestine and liver of rats

Metallothionein (MT) functions in zinc (Zn) homeostasis and dietary Zn affects tissue MT concentration. The objective of this study was to investigate the effects of dietary Zn deficiency and 24-h Zn repletion on MT immunolocalization and concentration in the small intestine and liver of growing rats. Three-week-old rats fed Zn-deficient diet (< 1 mg Zn/kg) for 16 d had no MT staining in either small intestine or liver. After 24-h Zn repletion with control diet (30 mg Zn/kg), strong MT staining was observed in intestinal Paneth cells and surface epithelial cells in the proliferative regions of villi. Pair-fed control rats had strong MT staining in liver that was localized around central veins. After 24-h energy repletion, the hepatic MT staining diminished. Furthermore, Zn-deficient rats had significantly reduced intestinal (57%) and hepatic (61%) MT concentrations but unaffected Zn concentrations compared with controls that consumed food ad libitum. Zn repletion for 24 h restored intestinal and hepatic MT concentrations and reduced hepatic Zn concentration. Pair-fed control rats had elevated MT concentration in liver that was normalized by energy repletion. There was a significant positive correlation between tissue Zn and MT concentrations in liver (r = 0.60, P = 0.0001), but not in small intestine. In summary, MT immunolocalization and concentration in rat small intestine and liver were responsive to changes in Zn status, supporting the role of MT in Zn metabolism. Cell-type-specific localization of MT in small intestine after dietary Zn manipulations indicates a function of Zn and MT in gut immunity and intestinal mucosal turnover, and the pattern of hepatic MT distribution with energy restriction may be linked to detoxification processes.     

Estimates of starch digestion in the rat small intestine differ from those obtained using in vitro time-sensitive starch fractionation assays

The objectives of this study were as follows: 1) to determine the rate and extent of starch disappearance from the small intestine of the rat fed selected starch sources, 2) to determine the ratios of the major starch fractions [rapidly digestible starch (RDS), slowly digestible starch (SDS), and resistant starch (RS)] in those starch sources using two in vitro methods and 3) to compare the two data sets to determine the accuracy of the in vitro methods. Diets were prepared using cornstarch, potato starch, amylomaize, maltodextrin, modified maltodextrin or pullulan. Starch sources and diets were analyzed for starch fractions by two in vitro methods. Diets were fed to rats, intestinal contents were collected and the ethanol-induced precipitate from the contents was analyzed to obtain a digestion curve that was mathematically modeled for comparison to results obtained using the two in vitro methods. Only the cornstarch diet had a defined amount of RDS, SDS and RS. The RDS concentration obtained from the intestinal contents of the rats fed the cornstarch diet differed (P < 0.05) from that determined by one in vitro method but was consistent with the value obtained using the other in vitro method. All other digestible starch values obtained differed (P < 0.05) among methods except for that of amylomaize. Starch fractions in starch sources obtained using in vitro procedures differed (P < 0.05) from values obtained for diets. The rate of disappearance differed (P < 0.05) between in vivo and in vitro procedures. There was minimal agreement between in vitro methods tested, and there was also minimal agreement between in vitro and in vivo results. Classification of starch into RDS and SDS components cannot be accomplished for a variety of starch sources, with cornstarch being the major exception.