Effects of somatostatin on luminal transit and absorption of nutrients in the proximal gut of minipigs

A discrepancy exists on the effects of somatostatin on the absorption of nutrients: in humans, absorption was found to be reduced, whereas in rats no effects were observed. However, intestinal absorption might be influenced by the transit rate of contents. This was not considered in previous studies. Therefore, we investigated simultaneously the effects of somatostatin on the absorption of nutrients and on luminal transit. In five minipigs (44–62 kg), a 150-cm segment of the proximal jejunum was temporarily isolated by two cannulas and perfused with an oligomer diet (60% carbohydrate, 18% protein, and 22% fat). The perfusion rate was 2 kcal/min. Flow rate and mean transit time were determined by markers (Cr-EDTA and Cu-EDTA). Somatostatin was infused intravenously at rates of 0.5, 1.25, 2.5, and 5µg/kg/hr. In control experiments saline was administered intravenously. Somatostatin dose-dependently diminished flow rate of luminal contents and increased the transit time. At the largest dose of somatostatin (5µg/kg/hr) flow rate was reduced by 50% compared with control infusion of saline (1.0±0.4 vs 2.0±0.05 ml/min,P<0.05), and transit time was increased 3.6-fold (39.8±4.7 vs 11.2±4.9 min;P<0.05). Somatostatin also dose-dependently enhanced the absorption of nutrients and energy. However, the increase in absorption was small compared with the effects on flow rate and transit time. At the largest dose (5µg/kg/hr) absorption of energy, carbohydrate, protein, and fat was enhanced only by 9.7%, 7.0%, 5.2%, and 15.3%, respectively (49.9 vs 40.2%, 50.9 vs 43.9%, 67.3 vs 62.1%, and 30.1 vs 14.8% during saline infusion;P<0.05). Results indicate that the major effects of somatostatin consist in a marked reduction of flow rate and a delay of luminal transit. The small increase in absorption was caused by the delay in transit and the prolonged contact of the nutrients with the mucosa. Therefore, in absorption studies, effects on transit need to be considered.     

Effects of enteral infusion of hypertonic saline and nutrients on canine jejunal motor patterns

The aim of the study was to clarify the effects of hypertonic solutions on jejunal motility. The study focused on differential effects of hypertonic saline and nutrients. Motility of the canine proximal jejunum was recorded with closely spaced strain-gauge transducers. During fasting, hyperosmotic solutions (up to 1520 mosmol/liter) of saline or nutrients (1 kcal/ml) were infused into the proximal jejunum (0.5–1.5 ml/min) up to 6 hr. The hyperosmotic solutions stimulated jejunal motility. With both increasing osmolarity of saline or increasing energy load of nutrients, jejunal motility linearly declined. The reduction of motility was associated with a change in motor pattern from a propulsive to a more segmenting one. Hypertonic glucose evoked a significantly smaller level of motor activity compared with both saline (at given osmolarities) and an elemental diet (at given energy loads). Motility parameters were not different between glucose and maltose, although osmolarity of maltose was less than half (760 vs 1520 mosmol/liter). In contrast, a mixture of glucose-fructose exerted a smaller inhibition of jejunal motility than glucose. The hypertonic solutions of saline or nutrients were tolerated over 2 hr; with hypertonic saline retrograde power contractions with or without vomiting occurred, whereas with hypertonic nutrients vomiting was preceded by strong inhibition of jejunal motility. Three conclusions can be derived from the present results: (1) The behavior of jejunal motility suggested that the motor activity was the result of both a local stimulation and an inhibitory feedback mechanism. (2) The different degree of inhibition between glucose and saline indicated that the nutrient itself played a major role in the inhibitory feedback regulation, whereas osmolarity was of minor importance. (3) Comparisons between different nutrients suggested a linkage between inhibitory control of motility and the absorptive capacity of the gut for the single nutrient.     

Effects of psychological stress on small intestinal motility and bacteria and mucosa in mice

AIM: To investigate the effects of psychological stress on small intestinal motility and bacteria and mucosa in mice, and to explore the relationship between small intestinal dysfunction and small intestinal motility and bacteria and mucosa under psychological stress. METHODS: Sixty mice were randomly divided into psychological stress group and control group. Each group were subdivided into small intestinal motility group (n= 10), bacteria group (n = 10), and D-xylose administered to stomach group (n= 10). An animal model with psychological stress was established housing the mice with a hungry cat in separate layers of a two-layer cage. A semi-solid colored marker (carbon-ink) was used for monitoring small intestinal transit. The proximal small intestine was harvested under sterile condition and processed for quantitation for aerobes (Escherichia coli) and anaerobes (Lactobacilli). The quantitation of bacteria was expressed as Iog10(colony forming units/g). D-xylose levels in plasma were measured for estimating trie damage of small intestinal mucosa. RESULTS: Small intestinal transit was inhibited (39.80±9.50% vs 58.79±11.47%,P<0.01) in mice after psychological stress, compared with the controls. Psychological stress resulted in quantitative alterations in the aerobes (E.coli). There was an increase in the number of E coli in the proximal small intestinal flora (1.78±0.30 log10(CFU/g) vs 1.37±0.21 log10(CFU/g), P<0.01), and there was decrease in relative proportion of Lactobacilli and E.coli of stressed mice (0.53±0.63 vs 1.14±1.07,P<0.05), while there was no significant difference in the anaerobes (Lactobacilli) between the two groups (2.31±0.70 log10 (CFU/g) vs 2.44±0.37 log10(CFU/g), P>0.05). D-xylose concentrations in plasma in psychological stress mice were significantly higher than those in the control group (2.90±0.89 mmol/L vs 0.97±0.33 mmol/L, P<0.01). CONCLUSION: Small intestinal dysfunction under psychological stress may be related to the small intestinal motility disorder and dysbacteriosis and the damage of mucosa probably caused by psychological stress.     

Effects of nutrients on gastrointestinal motility and gastric emptying after Billroth-I gastrectomy in dogs

We wanted to clarify the way in which nutrients influence gastrointestinal motility and gastric emptying following distal gastrectomy with Billroth-I gastroduodenostomy. Four gastrectomized dogs were equipped with extraluminal strain gauge transducers. Gastric emptying was measured radiographically. Four intact dogs were used as controls for emptying studies. Following gastrectomy, gastric emptying of both acaloric and nutrient meals was rapid in the initial period of the experiments. Gastric outflow was supported by propagating duodenal contractions. Compared with control dogs, the early emptying of nutrient meals was accelerated. In the following period, nutrients markedly slowed gastric emptying compared with acaloric meals due to a segmenting contractile pattern of the duodenum and a significant diminution of gastrointestinal motility. Results suggest that after Billroth-I gastrectomy (1) the control of gastric emptying by nutrients acts too late to slow the initial enhanced gastric outflow, and (2) the duodenal contractile patterns influence gastric emptying.The study was supported by the Deutsche Forschungsgemeinschaft, grant Eh 64/3-1.     

Integration of canine proximal gastric,antral, pyloric,and proximal duodenal motility during fasting and after a liquid meal

The aim was to investigate the integration of proximal gastric, antral, pyloric, and duodenal motility during fasting and after feeding. Using a proximal gastric barostat and a manometric assembly with an array of side holes astride the gastroduodenal junction, the gastrointestinal interdigestive migrating motor complex was detected in five of seven conscious fasting dogs. During phase III of the complex, which lasted a mean ± SEM of 13 ± 0.5 min, 9.6 ± 0.9 volume waves were present in the proximal stomach. The volume waves were coordinated with clusters of antral waves 64 ± 11% of the time and with inhibition of duodenal waves 91±3% of the time. A 300-ml calorie-dense liquid meal abolished the complex and promptly increased proximal gastric volume in five of six dogs. Volume waves were nearly completely suppressed, while antral waves decreased from 24 ±3.0 waves/10 min to 10±2.8 waves/10 min (P<0.05) and isolated pyloric pressure waves increased from 7.2±2.8 waves/10 min to 22±3.3 waves/10 min (P<0.005). In summary, proximal gastric motility was integrated with antral, pyloric, and duodenal motility under both fasting and fed conditions. The integrated patterns likely account for the efficient clearance of indigestible solids during fasting and the controlled emptying of nutrients with feeding.Supported in part by USPHS NIH Grants DK 18278, DK34988, and DK07198, the Winthrop Travelling Fellowship of the Royal Australasian College of Physicians, the S.K.F. (Australia) Travelling Fellowship, and the Mayo Foundation.This work was presented in part before the World Congress of Gastroenterology, Sydney, Australia, August 30, 1990     

Nitric oxide synthase inhibition results in immediate postoperative recovery of gastric, small intestinal and colonic motility in awake rats

Background Nitric oxide (NO) is known to inhibit gastrointestinal motility. However, no detailed analysis of gastric, small intestinal and colonic motor effects, including effects on contraction frequency, has, as yet, been reported after NO inhibition in awake rats. We therefore investigated the effects of NO synthase inhibition on gastric, small intestinal and colonic motility in awake rats under baseline conditions and in a postoperative ileus model.Methods In Sprague–Dawley rats, strain gauge transducers were sutured either to the gastric corpus, the small intestine or the colon. After 3 days, l-NMMA (NO synthase inhibitor), d-NMMA or vehicle was given i.v., while the motility was recorded continuously. In addition, postoperative gastric, small intestinal or colonic motility was investigated after l-NMMA or vehicle treatment prior to abdominal surgery. The motility index, the contraction amplitude, the area under the contraction amplitude and the contraction frequency were analysed.Results l-NMMA decreased gastric motility to 60±8% for about 15 min, but continuously increased small intestinal motility to 221±22% and colonic motility to 125±7% compared to baseline (baseline=100%; p<0.01 for all comparisons). l-NMMA increased the contraction frequency throughout the gastrointestinal tract (stomach, 13±2%; small intestine, 8±1%; colon, 16±5%; p<0.01 vs. baseline for all comparisons). l-NMMA injection prior to surgery did not prohibit intraoperative inhibition of gastrointestinal motility, but did result in immediate recovery of gastric, small intestinal and colonic motility postoperatively (l-NMMA vs. vehicle, 0–60 min postoperatively; stomach, 90±9% vs. 53±3%; small intestine, 101±5% vs. 57±3%; colon, 134±6% vs. 60±5%; p<0.01 for all comparisons; no significant difference between preoperative baseline motility and l-NMMA treated rats postoperatively).Conclusions Under baseline conditions, endogenous NO inhibits small intestinal and colonic motility and gastric, small intestinal and colonic contraction frequency in awake rats. In the early postoperative period, endogenous NO is a major inhibitory component that seems to constitute the common final pathway of mediators and the neural pathways inhibiting gastrointestinal motility in rats.     

Effect of misoprostol on postprandial intestinal motility and orocecal transit time in humans

We measured the effect of misoprostol (M), a PGE₁ analog, on duodenojejunal postprandial motor activity and orocecal transit in eight healthy volunteers. Intestinal motility was studied by an intraluminal catheter with three strain gauge transducers connected to a solid-state datalogger, and transit time was measured by a hydrogen breath test. Subjects were studied for two consecutive days and fed twice a day with a similar, 600-kcal meal. Misoprostol (M) at 800, 400, or 200 g or placebo were taken orally before every one of the four meals. Transit time was measured after the morning meal on both days, after ingestion of either 800 g of M or placebo. On four occasions, following M, the normal fed pattern was not established and the migrating motor complex (MMC) was not interrupted by the meal. In all other occasions, when the higher doses of M were given, the first 1–2 hr after the meal revealed a hypoactive bowel. This effect was inconsistently seen following 200 g of M. Orocecals transit time was consistently and significantly shorter after M than placebo: 48.3±9.5 min vs 104.4±4.8 min,P<0.0001. Four subjects had diarrhea during the study. We conclude that misoprostol, particularly at higher doses, has a profound effect on intestinal postprandial motility and results in accelerated transit time. The motility changes induced by M may be responsible, in part, for its effect on transit.A preliminary report of this work was given at the annual meeting of the American Gastroenterological Association, May 1991, and was published as an abstract inGastroenterology 100:496, 1990. This study was supported in part by Searle.     

Role of vagal dysfunction in motility and transit disorders of jejunal roux limb after roux-en-Y gastrojejunostomy

After a Roux-en-Y gastrojejunostomy patients frequently complain about abdominal pain, fullness, nausea and vomiting, ie, the Roux-en-Y syndrome. Stasis in the Roux limb due to disordered motility is known to be a cause of these complaints. The aim of the present study was to determine whether vagal denervation contributes to the development of motility disturbances and stasis in the Roux limb. Forty-seven patients with a Roux-en-Y gastrojejunostomy after partial gastrectomy were studied. A truncal vagotomy had been performed in 26 of these 47 patients. Transit through the Roux limb was evaluated by radionuclide studies, motility in the Roux limb was studied by manometry, and vagal function was tested by measuring the pancreatic polypeptide response to an insulin-induced hypoglycemia (PP test). On the basis of the PP test patients were classified as having (1) normal, (2) moderately impaired, and (3) severely impaired vagal function. The PP test showed that two of the 26 patients subjected to vagotomy had a moderately impaired vagal function, the other 24 all had a severely impaired vagal function. In the patients not subjected to a vagotomy, vagal function was disturbed in 11 of the 21 patients. Motility disturbances were not observed more frequently in patients with either moderately or severely impaired vagal function than in patients with normal vagal function. Stasis in the Roux limb was seen even more frequently in patients with a normal vagal function than in patients with a severely impaired vagal function. The results of this study indicate that vagal denervation of the Roux limb is not the cause of motility and transit disorders in the Roux limb.This work was supported by the Jan Kornelis de Cock-Stichting.     

Normal aspects of colorectal motility and abnormalities in slow transit constipation

Human colonic motility is a relatively difficult topic to investigate. However, the refinement of manometric techniques in recent years enabled us to study both the proximal and distal segments of the viscus. The present paper reviews our knowledge about normal aspects of colorectal motility in man and the abnormalities found in slow transit constipation (STC), one of the most frequent and difficult to treat subtypes of constipation. An internetbased search strategy of the Medline and Science Citation Index was performed using the keywords colon, colonic, colorectal, constipation, slow transit, motility, rectal, rectum in various combinations with the Boolean operators AND, OR and NOT. Only articles related to human studies were used, and manual cross-referencing was also performed. Most of colonic motor activity is represented by single nonpropagated contractions, rarely organized in bursts; this activity is maximal during the day, especially after waking and following meals. In addition, a specialized propagated activity with propulsive features is detectable, represented by high-and low-amplitude propagated contractions. In the severe form of constipation represented by the slow transit type, the above motor activity is completely deranged. In fact, both basal segmental activity (especially in response to meals) and propagated activity (especially that of high amplitude) are usually decreased, and this may represent a physiologic marker of this disorder. Human colonic motor activity is quite a complex issue, still only partly understood and investigated, due to anatomic and physiological difficulties. In recent years, however, some more data have been obtained, even in proximal segments. These data have helped in elucidating, although only in part, some pathophysiological mechanisms of chronic constipation, and especially of the STC subtype.     

The effect of acute hyperglycaemia on small intestinal motility in normal subjects

Summary The effects of hyperglycaemia on postprandial small intestinal motor activity are unclear. Duodenal and jejunal pressures and duodeno-caecal transit were measured in eight healthy male volunteers during euglycaemia (blood glucose 4–6 mmol/l) and hyperglycaemia (blood glucose 12–15 mmol/l). Duodenal and jejunal pressures were recorded with a manometric assembly during intraduodenal infusion of 100 ml nutrient liquid comprising 14% protein, 31.5% fat and 54.5% carbohydrate together with 15 g lactulose. Duodeno-caecal transit was determined by a breath hydrogen technique. The number of duodenal (p<0.05) and jejunal (p<0.01) pressure waves, excluding phase III episodes was reduced during hyperglycaemia compared to euglycaemia. Hyperglycaemia was associated with earlier onset of phase III activity (30±12 vs 132±20 min; p<0.05). Duodeno-caecal transit was slower during hyperglycaemia when compared to euglycaemia (114±17 vs 49±6 min, p<0.01). We conclude that induced hyperglycaemia has major effects on postprandial small intestinal motility. The reduction in duodenal and jejunal motor activity is likely to explain the retardation of small intestinal transit during hyperglycaemia.Abbreviations TMPD Transmusocal potential difference - MMC migrating myoelectric complex     

脑外伤大鼠肠运动功能障碍及与血清Ghrelin的关系

目的探讨创伤性脑损伤（TBI）后大鼠肠运动功能异常及其与血清Ghrelin改变的关系。方法雄性Wistar大鼠64只,随机分为两组。TBI组采用改良Feeney自由落体撞击伤法建立TBI模型;对照组只开骨窗,不行落体致伤。两组大鼠分别在致伤后3、6、12、24 h观察血清Ghrelin水平、小肠传输系数及肠黏膜病理改变。结果 TBI后各组大鼠光镜下肠黏膜上皮细胞明显受损,电镜下可见细胞连接较对照组增宽;各时间点的肠道传输系数及血清Ghrelin值均低于对照组,二者呈正相关。结论大鼠在TBI后早期即可出现小肠黏膜损伤和小肠运动功能减低,在此期间血清Ghrelin的变化可能起一定作用。     

Effects of nutrients on gastrointestinal motility and gastric emptying after distal gastrectomy with Roux-Y gastrojejunostomy in dogs

The aim of the study was to clarify whether nutrients are still capable of slowing gastric emptying following Roux-Y gastrectomy, as in normal dogs. Gastrointestinal motility and gastric emptying of acaloric and nutritive meals with different viscosities were measured in normal dogs and after a two-thirds Roux-Y gastrectomy. In gastrectomized dogs low-viscosity nutritive meals emptied unduly rapidly in an initial phase, although the frequency and spread of contractions, ie, the propulsive activity of the jejunal Roux limb were diminished. A slow emptying rate during the following period was due to a long-lasting inhibition of gastric and jejunal motility. Medium-viscosity nutritive meals emptied in gastrectomized dogs as slowly as in normal animals, but this effect was primarily caused by the meal viscosity and only secondarily by the nutrients. It is concluded that following Roux-Y gastrectomy a regulation of gastric emptying is preserved; however, the onset of an effective control is delayed, resulting in a rapid initial emptying of low-viscosity meals.Studies were supported by the Deutsche Forschungsgemeinschaft grant Eh 64/3-1.     

Effects of intestinal mucosal blood flow and motility on intestinal mucosa

AIM:To investigate the role of intestinal mucosal blood flow(IMBF) and motility in the damage of intestinal mucosal barrier in rats with traumatic brain injury.METHODS:Sixty-four healthy male Wistar rats were divided randomly into two groups:traumatic brain injury(TBI) group(n = 32),rats with traumatic brain injury;and control group(n = 32),rats with sham-operation.Each group was divided into four subgroups(n = 8) as 6,12,24 and 48 h after operation.Intestinal motility was measured by the propulsion ratio o...     

创伤性脑损伤大鼠肠黏膜损害及小肠运动功能障碍的关系研究

目的观察创伤性脑损伤（TBI）后大鼠肠黏膜形态学改变及小肠动力变化,探讨二者的关系。方法采用改良Feeney自由落体撞击伤法建立TBI模型。64只雄性健康Wistar大鼠随机分为假手术对照组和TBI组,两组又根据实验终止时间各分为4个亚组,分别于伤后3、6、12、24 h光镜下观察小肠黏膜的病理变化及利用美蓝染色法计算小肠推进比。结果 TBI组小肠推进比均低于对照组（P〈0.05）。光镜下TBI组3 h即可见肠绒毛肿胀、增粗、缩短,12 h见绒毛破损、剥脱。结论 TBI后早期即可出现肠黏膜损伤和肠动力障碍,二者可能互为因果。     

Effect of a model of canine jejunoileal orthotopic autotransplantation on jejunal and ileal transport of water and electrolytes

Canine jejunoileal transplantation induces an early profuse watery diarrhea of uncertain etiology. Our aim was to determine the temporal effects of a canine model of jejunoileal autotransplantation (a model devoid of confounding effects of ischemia-reperfusion or immune rejection) on basal jejunal and ileal absorption of water and electrolytes to determine if impaired absorption is responsible for the diarrhea. Our hypothesis was that net absorption of water and electrolytes in an enterically isolated loop would decrease after jejunoileal transplantation. Four groups of dogs (N 6) were prepared with 80-cm modified Thiry-Vella loops: group I, neurally intact jejunum; group II, autotransplanted jejunum; group III, neurally intact ileum; and group IV, autotransplanted ileum. The loops were perfused for 3 hr with 150 mM NaCl at 3 ml/min under fasted conditions; transit time through the loop was determined by bolus of a nonabsorbable marker. Dogs were studied on three separate days at one, two, eight, and nine weeks postoperatively. Net absorptive fluxes of water and electrolytes and transit times were similar (P>0.05) between neurally intact and autotransplant groups (group I vs II and group III vs IV) at each time point. Ileal loops absorbed more than jejunal loops, and transit was slower in ileal loops (eachP<0.05). Our findings suggest that, despite the obligate disruption of extrinsic innervation, enteric (intrinsic) neural continuity, and lymphatic drainage that accompanies this canine model of jejunoileal autotransplantation, net basal absorptive function of water and electrolytes during the fasted state was not decreased nor was transit altered either in jejunum or ileum. These findings have important implications for clinical small intestinal transplantation in man.Supported by NIH RO1 DK39337 (M.G.S.), Ethicon Corporation, and Mayo Foundation.     

针刺对功能性消化不良患者近端胃动力的影响

目的：观察针刺对功能性消化不良患者机械性胃扩张近端胃动力的影响．方法：功能性消化不良患者60例分为针灸组和对照组,分别进行等容机械性胃扩张．观察近端胃动力参数：最小牵张压(MDP),初始容积和压力,最大耐受容积、压力和顺应性(容积和压力的比值)．结果：两组最小牵张压无显著性差异(5．28±2．62mmHg vs 4．98±1．87mmHg,P＞0．05),针灸组的初始压力和容积(8．06±2．95mmHg vs 5．40±2．41mmHg,560．9±119．5mL vs 352．0±139．3mL),最大耐受压力和容积(13．25±2．23mmHg vs 9．82±1．9mmHg,810．7±119．62mL vs 504．1±159．6mL),顺应性(61．2±18．6mL/mmHg vs 51．4±17．8mL/mmHg)均显著高于对照组(P＜0．05)．结论：针灸可以显著提高功能性消化不良患者的近端胃动力,降低内脏敏感性．     

Effects of psychological stress on small intestinal motility and expression of cholecystokinin and vasoactive intestinal polypeptide in plasma and small intestine in mice

AIM: To investigate the effects of psychological stress on small intestinal motility and expression of cholecystokinin (CCK) and vasoactive intestinal polypeptide (VIP) in plasma and small intestine, and to explore the relationship between small intestinal motor disorders and gastrointestinal hormones under psychological stress. METHODS: Thirty-six mice were randomly divided into psychological stress group and control group. A mouse model with psychological stress was established by housing the mice with a hungry cat in separate layers of a two-layer cage. A semi-solid colored marker (carbon-ink) was used for monitoring small intestinal transit. CCK and VIP levels in plasma and small intestine in mice were measured by radioimmunoassay (RIA). RESULTS: Small intestinal transit was inhibited (52.18±19.15% vs70.19±17.79%, P<0.01) in mice after psychological stress, compared to the controls. Small intestinal CCK levels in psychological stress mice were significantly lower than those in the control group (0.75±0.53 μg/g vs1.98±1.17 μg/g, P<0.01), whereas plasma CCK concentrations were not different between the groups. VIP levels in small intestine were significantly higher in psychological stress mice than those in the control group (8.45±1.09 μg/g vs7.03±2.36 μg/g, P<0.01), while there was no significant difference in plasma VIP levels between the two groups. CONCLUSION: Psychological stress inhibits the small intestinal transit, probably by down-regulating CCK and up-regulating VIP expression in small intestine.     

Haem in the gut. I. Fate of haemoproteins and the absorption of haem

Haem (FeII-protoporphyrin-IX) is presented to the gut lumen as haemoproteins derived from exogenous dietary) and endogenous (mucosal cell desquamation and bleeding) sources. Haemoproteins such as haemoglobin, myoglobin and catalase undergo hydrolysis by luminal proteases to release the haem. Released haem is maintained in a soluble form in the gut lumen by the products of haemoprotein digestion. Chelators of elemental iron do not bind haem-iron and so haem-iron is better absorbed than elemental iron. Haem-iron does not exchange with luminal elemental iron. Mucosal uptake of haem is limited. Less than 10% binds to the brush border of the villus cell. Although the mechanisms by which haem binds to the brush border and is transported to the intracellular environment are poorly understood, it is known that some haem is transferred to secondary lysosomes where the porphyrin ring is split to release iron and form bilirubin. Depending upon the composition of the diet, the iron released from haem within the villus cell can be the major physiological source of iron. In iron-deficiency in humans, absorption of haem-iron can increase threefold whereas absorption of elemental-iron can increase tenfold. These observations indicate that haem-iron and elemental-iron are absorbed via different mechanisms which are subject to different regulation. For haem-iron to be absorbed, the haem itself must be taken up by the mucosa.