Effects of intraduodenal glucose and fructose on antropyloric motility and appetite in healthy humans

Oral fructose empties from the stomach more rapidly and may suppress food intake more than oral glucose. The purpose of the study was to evaluate the effects of intraduodenal infusions of fructose and glucose on antropyloric motility and appetite. Ten healthy volunteers were given intraduodenal infusions of 25% fructose, 25% glucose, or 0.9% saline (2 ml/min for 90 min). Antropyloric pressures, blood glucose, and plasma insulin, gastric inhibitory peptide (GIP), and glucagon-like peptide-1 (GLP-1) were measured concurrently; a buffet meal was offered at the end of the infusion. Intraduodenal fructose and glucose suppressed antral waves (P < 0. 0005 for both), stimulated isolated pyloric pressure waves (P < 0.05 for both), and increased basal pyloric pressure (P = 0.10 and P < 0. 05, respectively) compared with saline, without any significant difference between them. Intraduodenal glucose increased blood glucose (P < 0.0005), as well as plasma insulin (P < 0.0005) and GIP (P < 0.005) more than intraduodenal fructose, whereas there was no difference in the GLP-1 response. Intraduodenal fructose suppressed food intake compared with saline (P < 0.05) and glucose (P = 0.07). We conclude that, when infused intraduodenally at 2 kcal/min for 90 min 1) fructose and glucose have comparable effects on antropyloric pressures, 2) fructose tends to suppress food intake more than glucose, despite similar GLP-1 and less GIP release, and 3) GIP, rather than GLP-1, probably accounts for the greater insulin response to glucose than fructose.     

Intestinal mast cells in gut inflammation and motility disturbances

Mast cells may be regarded as prototypes of innate immune cells that can be controlled by neuronal mediators. Their activation has been implicated in many types of neuro-inflammatory responses, and related disturbances of gut motility, via direct or indirect mechanisms that involve several mechanisms relevant to disease pathogenesis such as changes in epithelial barrier function or activation of adaptive or innate immune responses. Here we review the evidence for the involvement of mast cells in the inflammation of the bowel wall caused by bowel manipulation that leads to motility disturbances such as postoperative gastroparesis and ileus. Also in IBD there is substantial evidence for the involvement of mast cells and a mast cell-mediated neuroimmune interaction showing an increased number and an increased degranulation of mast cells. We discuss the potential of mast cell inhibition as a bona fide drug target to relief postoperative ileus. Further research on mast cell-related therapy either by stabilizing the mast cells or by blocking specific mast cell mediators as adjunctive therapy in IBD is encouraged, bearing in mind that several drugs currently used in the treatment of IBD possess properties affecting mast cell activities. This article is part of a Special Issue entitled: Mast cells in inflammation.     

Plasma fibrinolysis after intraduodenal administration of urokinase in rats

Plasma fibrinolysis in rats rose above the level of physiological fluctuations in a curve with two peaks at 1 and 6 h, following intraduodenal administration of high-molecular-weight urokinase (HMW-UK; MW 53,000; 124,000 IU/mg protein). Activation of plasma fibrinolysis was also confirmed with insolubilized enzyme (glass-coupled UK), but lacked the first activity peak. Plasma fibrinolytic enzyme isolated by affinity chromatography revealed strong fibrinolytic (1,120 IU/dl), pyro-Glu-Gly-Arg-pNA amidolytic (3,200 nmol/dl) and Glu-plasminogen activating (24.5 IU/dl) activities. Using specific UK antibody, it appeared that the first peak originated from the administered UK, while the second one derived from endogenous plasminogen activator. Dose response of UK was not observed, and the maximal effect was at about 5,000 IU/kg body weight.     

Insulin secretion and intestinal motility]

In dogs after feeding increased plasma insulin concentration is positively related in converting the "fasted" pattern of electrical activity into the "fed" pattern. In sheep, the release of insulin induced by a perfusion of volatile fatty acids is accompanied by similar changes in the pattern of electrical activity. The results indicate that insulin release induced by nutrients plays a major role in the control of intestinal motility in both species.     

Intestinal motility during acute Yersinia enterocolitica enteritis in rabbits

To determine if Yersinia enterocolitica (YE) enteritis is associated with an alteration of intestinal myoelectric and motor activity, and with an increased rate of aboral transit, New Zealand white rabbits (500-900 g) were surgically prepared with ileal bipolar electrodes and a manometry catheter adjacent to the distal electrode. One week later animals were inoculated with 10(10) organisms of YE in 10 mL NaHCO3 (infected group) or 10 mL NaHCO3 (sham-infected pair-fed and control groups). Daily food intake, weight gain, YE excretion, and stool pattern were noted. Intestinal myoelectric and motor activity over a 6- to 8-h period before and 3, 6, and 14 days after inoculation was compared in infected (I), pair-fed (PF), and control (C) groups. Intestinal transit was evaluated in I and C animals on days 3 and 6 after inoculation by measuring the distribution in the intestinal lumen of 51Cr 20 min after it was instilled directly into the jejunum. Infected animals exhibited diarrhea, fecal excretion of YE, and significantly decreased food intake, weight gain, and survival (11.4 +/- 0.6 days). Infection was associated with a significant (p less than 0.05) decrease in both the cycle period of the migrating myoelectric complex (MMC) and the total number of single, paired, and (or) clustered contractions per MMC, and a significant (p less than 0.001) increase in duration of phase III of the MMC. There was no change in intestinal slow wave frequency (19 cycles/min), motility index per MMC, or the percentage of contractions that propagated in an orad (7%) or aboral (69%) direction or that appeared stationary (25%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Intestinal motility responses to insulin and glucagon in streptozotocin diabetic rats

Myoelectrical and mechanical activities were chronically recorded by use of nichrome electrodes and miniaturized strain-gage transducers sutured on the serosa of the antrum, the duodenum, and the jejunum. In a first experiment (n = 6 rats) the early (0-6 h) and late (greater than 4 days) effects of streptozotocin (65 mg/kg i.v.) was recorded. In addition, the effect of insulin (1-5 IU/kg) and glucagon (6-200 micrograms/kg) administered intravenously were studied separately each in groups of seven normal and streptozotocin-induced diabetic-fed and fasted rats. The results indicated that within the 30 min following streptozotocin administration there was a significant stimulation of the duodenal and jejunal motility lasting 46 +/- 8 min. When diabetes was established as shown by the basal blood glucose level obtained in those rats (2.30 +/- 0.84 g/L), a progressive decrease of the frequency of the migrating myoelectric complex was observed along with a disorganization of the regular spiking activity phases without disturbing the basal electrical rhythm. Comparing with the basal level, a significant increase in the gastrointestinal motility indexes (MI) appeared both in fasted (p less than 0.01) and fed (p less than 0.05) normal animals, 13.1 +/- 1.6 min after an i.v. injection of 1 IU/kg insulin. Motor effects of glucagon were related to the dose. When used at 25 microgram/kg a disorganization of the spiking activity was observed with a stimulation of the contractile activity in the jejunum. At higher dosages, i.e., 100 micrograms/kg, it induced an immediate and significant decrease of motility at any level tested and lasting up to 20 +/- 7 min. The motility responses to both hormones were lower in diabetic than in normal rats.     

喂养不耐受早产儿肠道菌群的研究

目的 采用实时荧光定量聚合酶链反应（Real-time PCR）技术从微生物生态学的角度分析比较喂养不耐受（feeding intolerance,FI）早产儿与对照组早产儿肠道菌群的变化。方法 以2016年3月至2017年3月于我院儿科新生儿病房确诊的FI早产儿为FI组。选择与FI组胎龄、日龄、出生体重相匹配的非FI早产儿作为对照组。采集出现FI的早产儿和同时段健康早产儿的粪便标本,进行Real-time PCR表达谱分析,比较两组早产儿肠道菌群的差异。结果 临床资料统计分析显示FI组和对照组在性别构成、胎龄、出生体重、生产方式和喂养方式方面差异无统计学意义。Real-time PCR表达谱分析结果显示FI组早产儿肠道大肠埃希菌和肺炎克雷伯菌明显高于对照组,粪肠球菌、乳杆菌和双歧杆菌明显低于对照组。结论 肠道菌群结构的改变参与早产儿FI的发生,该研究结果从微生物学角度为临床儿科医师认识早产儿FI的发生机制和治疗提供了新的思路。     

Effects of prey motility and concentration on feeding in Acartia tonsa and Temora longicornis: the importance of feeding modes

Feeding experiments were conducted with the ambush-feeding copepodAcartia tonsa and the feeding-current-generating copepod Temoralongicornis. The copepods were offered a mixed diet of the dinoflagellateHeterocapsa triquetra and the ciliate Balanion comatum of similarcell size. The dinoflagellate was offered at a constant concentrationof 10–15 cells mL^–1, whereas the ciliate was offeredat a variety of concentrations, ranging from 7 to 57 cells mL^–1.Copepods with different feeding modes possess different mechanismsfor prey detection, suggesting that the two copepods would responddifferently to the two prey types. Both copepods had significantlyhigher clearance rates on the highly motile ciliate than onthe less motile dinoflagellate. In encounters between A. tonsaand its prey, we argue that this is due to the higher hydromechanicalsignal generated by the ciliate. The advection feeding copepodT. longicornis fed on the two prey according to their relativeconcentrations; in this case, we suggest that although B. comatumis capable of detecting feeding-current-generating predators,the feeding current velocity generated by T. longicornis isgreater than the escape velocity of this ciliate.     

Effects of intraduodenal fatty acids on appetite, antropyloroduodenal motility, and plasma CCK and GLP-1 in humans vary with their chain length

The gastrointestinal effects of intraluminal fats may be critically dependent on the chain length of fatty acids released during lipolysis. We postulated that intraduodenal administration of lauric acid (12 carbon atoms; C12) would suppress appetite, modulate antropyloroduodenal pressure waves (PWs), and stimulate the release of cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) more than an identical dose of decanoic acid (10 carbon atoms; C10). Eight healthy males (19-47 yr old) were studied on three occasions in a double-blind, randomized fashion. Appetite perceptions, antropyloroduodenal PWs, and plasma CCK and GLP-1 concentrations were measured during a 90-min intraduodenal infusion of 1) C12, 2) C10, or 3) control (rate: 2 ml/min, 0.375 kcal/min for C12/C10). Energy intake at a buffet meal, immediately after completion of the infusion, was also quantified. C12, but not C10, suppressed appetite perceptions (P < 0.001) and energy intake (control: 4,604 +/- 464 kJ, C10: 4,109 +/- 588 kJ, and C12: 1,747 +/- 632 kJ; P < 0.001, C12 vs. control/C10). C12, but not C10, also induced nausea (P < 0.001). C12 stimulated basal pyloric pressures and isolated pyloric PWs and suppressed antral and duodenal PWs compared with control (P < 0.05 for all). C10 transiently stimulated isolated pyloric PWs (P = 0.001) and had no effect on antral PWs but markedly stimulated duodenal PWs (P = 0.004). C12 and C10 increased plasma CCK (P < 0.001), but the effect of C12 was substantially greater (P = 0.001); C12 stimulated GLP-1 (P < 0.05), whereas C10 did not. In conclusion, there are major differences in the effects of intraduodenal C12 and C10, administered at 0.375 kcal/min, on appetite, energy intake, antropyloroduodenal PWs, and gut hormone release in humans.     

Intestinal inflammation downregulates smooth muscle CPI-17 through induction of TNF-alpha and causes motility disorders

Motility disorders are frequently observed in intestinal inflammation. We previously reported that in vitro treatment of intestinal smooth muscle tissue with IL-1beta decreases the expression of CPI-17, an endogenous inhibitory protein of smooth muscle serine/threonine protein phosphatase, thereby inhibiting contraction. The present study was performed to examine the pathophysiological importance of CPI-17 expression in the motility disorders by using an in vivo model of intestinal inflammation and to define the regulatory mechanism of CPI-17 expression by proinflammatory cytokines. After the induction of acute ileitis with 2,4,6,-trinitrobenzensulfonic acid, CPI-17 expression declined in a time-dependent manner. This decrease in CPI-17 expression was parallel with the reduction of cholinergic agonist-induced contraction of smooth muscle strips and sensitivity of permeabilized smooth muscle fibers to Ca(2+). Among the various proinflammatory cytokines tested, TNF-alpha and IL-1beta were observed to directly inhibit CPI-17 expression and contraction in cultured rat intestinal tissue. Moreover, both TNF-alpha and IL-1beta inhibited CPI-17 expression and contraction of smooth muscle tissue isolated from wild-type and IL-1alpha/beta double-knockout mice. However, IL-1beta treatment failed to inhibit CPI-17 expression and contraction in TNF-alpha knockout mice. In beta-escin-permeabilized ileal tissues, pretreatment with anti-phosphorylated CPI-17 antibody inhibited the carbachol-induced Ca(2+) sensitization in the presence of GTP. These findings suggest that CPI-17 was downregulated during intestinal inflammation and that TNF-alpha plays a central role in this process. Downregulation of CPI-17 may play a role in motility impairments in inflammation.