The effects of added whey protein to a pre-operative carbohydrate drink on glucose and insulin response.

BACKGROUND: Pre-operative complex carbohydrate (CHO) drinks are recommended to attenuate post-operative insulin resistance. However, many institutions use simple CHO drinks, which while convenient, may have less metabolic effects. Whey protein may enhance insulin release when added to complex CHO. The aim of this study was to compare the insulin response to simple CHO vs. simple CHO supplemented with whey protein. METHODS: Twelve healthy volunteers participated in this double-blinded, within subject, cross-over design study investigating insulin response to simple CHO drink vs. simple CHO + whey (CHO + W) drink. The primary outcome was the accumulated insulin response during 180 min after ingestion of the drinks (Area under the curve, AUC). Secondary outcomes included plasma glucose and ghrelin levels, and gastric emptying rate estimated by acetaminophen absorption technique. Data presented as mean (SD). RESULTS: There was no differences in accumulated insulin response after the CHO or CHO + W drinks [AUC: 15 (8) vs. 20 (14) nmol/l, P = 0.27]. Insulin and glucose levels peaked between 30 and 60 min and reached 215 (95) pmol/l and 7 (1) mmol/l after the CHO drink and to 264 (232) pmol/l and 6.5 (1) mmol/l after the CHO + W drink. There were no differences in glucose or ghrelin levels or gastric emptying with the addition of whey. CONCLUSION: The addition of whey protein to a simple CHO drink did not change the insulin response in healthy individuals. The peak insulin responses to simple CHO with or without whey protein were lower than that previously reported with complex CHO drinks. The impact of simple carbohydrate drinks with lower insulin response on peri-operative insulin sensitivity requires further study.

Validation of SmartPill® wireless motility capsule for gastrointestinal transit time: Intra-subject variability, software accuracy and comparison with video capsule endoscopy.

BACKGROUND: There is interest in ultimately combining endoscopy and motility assessments. Gastric emptying (GET), small bowel (SBTT), colon (CTT) and whole gut transit (WGTT) times are conveniently obtained by SmartPill® wireless motility capsule (WMC) that records luminal pH, temperature and pressure. Reproducibility within same subjects and accuracy of software derived times (MotiliGI® ) were investigated for diagnostic application. GET and SBTT were separately measured using video capsule endoscopy (VCE). The aim of this investigation was to assess same subject reproducibility of WMC, accuracy of software derived transit times and relate to Pillcam® SB (small bowel) VCE motility data. METHODS: Seventy three healthy adults ingested a 260 kcal mixed meal followed by WMC tests. Food intake was permitted after 6 hours. Regional transit data was obtained for GET, SBTT and CTT, the sum yielding WGTT. Nineteen subjects repeated WMC tests 2 or 4 weeks later; a separate 70 underwent VCE while fasted. KEY RESULTS: Visually derived data from WMC yielded GET 3.46±0.27, SBTT 5.15±0.21, CTT 20.76±1.19 and WGTT 29.53±1.28 hours (mean±SEM). Pearson's correlation coefficients (r) against software derived results were: GET 0.78 (P<.0001), SBTT 0.28 (P<.05), CTT 0.96 (P<.0001), WGTT 0.99 (P<.0001). VCE yielded lower GET (0.71±0.08 hours) and SBTT (4.15±0.13 hours). CONCLUSIONS AND INFERENCES: GET, SBTT, CTT and WGTT obtained by WMC are commensurate with literature values, including by other methods. Visually and software derived transit times have strongest correlations for CTT and WGTT. WMC yields longer GET and SBTT than VCE, perhaps due to meal related effects on motility.

Capability of different non-nutritive feed additives on improving productive and physiological traits of broiler chicks fed diets with or without aflatoxin during the first 3 weeks of life.

An experiment was conducted to determine whether some non-nutritive feed additives (NNFA) could block the adverse effects of aflatoxin (AF) on growth performance and physiological parameters of Cobb broilers throughout the period from 1 to 21 day of age. There were eight treatments consisting of two levels of AF at 0 and 200 ppb and four NNFA within each AF level. These additives included mannan oligosaccharides (MOS) at 2 g/kg diet, hydrated sodium calcium aluminosilicate (HSCAS) at 2 g/kg diet and Lactobacillus acidophilus (Lac) at 2 g/kg diet. At 21 day of age, five chickens of each treatment were slaughtered to study dressing percentage and relative weight of inner organs and glands. AF had a significant negative effect on body weight gain (BWG), and feed intake, while impairing feed conversion ratio (FCR). Aflatoxin significantly increased percentage liver, lymphocyte (%), monocyte (%), serum triglyceride level, and the aspartate aminotransferase (AST), and alanine aminotransferase (ALT), concentrations while decreasing dressing percentage, intestinal percentage, white blood cells (WBCs), red blood cells (RBCs), haemoglobin (Hgb), packed cell volume (PCV), heterophil (%), heterophil/lymphocyte ratio, total serum protein and serum albumin. Aflatoxin adversely affected the morphology of the liver, bursa and the thymus. There was a significant interaction between AF and NNFA on the relative weights of liver, heart and intestine. Lac completely blocked the negative effects of AF on the percentage liver and the heart and partially on the intestine. In conclusion, Lac was most effective in reversing the adverse effects of AF on growth and FCR and on the percentage, functions and morphology of the liver. Hydrated sodium calcium aluminosilicate also improved the economic traits of broilers but was less effective than Lac and more effective than MOS.

Stunting among primary-school children: a sample from Baghdad, Iraq

The aim of this study was to establish baseline information about the prevalence and distribution of growth deficit [stunting] in a sample of Iraqi schoolchildren from the capital, Baghdad. A cross-sectional descriptive analysis of the growth status of 5286 primary-school children aged 7-12 years [2888 males, 2398 females] was conducted by measuring the prevalence of stunting [height-forage Z-score < -2], and underweight [body mass index-for-age] using the NCHS/WHO and IOTF/WHO cutoff values respectively. The prevalence of stunting only, and concurrent stunting and underweight, were 18.7% and 13.5% respectively, with a slight predominance among girls. The study also demonstrated the progression of height deficit with increasing age

Contractile responses to natural tachykinins and selective tachykinin analogs in normal and inflamed ileal and colonic muscle.

BACKGROUND: Tachykinins and acetylcholine are main physiological motility stimulators in the gut by their effects exerted through neurokinin and muscarinic receptors. METHODS: Longitudinal and circular muscle strips from normal ileum and colon or corresponding tissues from patients with inflammatory bowel disease were studied in organ baths. Contractile responses to the tachykinins substance P, neurokinin A, neurokinin B and neuropeptide gamma and specific analogs for their respective receptors were compared to acetylcholine. RESULTS: Acetylcholine caused concentration-dependent phasic contractions in longitudinal and circular muscle of normal ileum and colon (both P < 0.01). In inflamed tissues, contractile responses were reduced to 17%-33% in ileum (P < 0.05) and 3%-26% in colon (P < 0.01). Both natural tachykinins and their specific analogs caused concentration-dependent phasic, tonic and rhythmic contractions (each P < 0.01). Neuropeptide gamma was most potent in contracting the ileum and colon, followed by neurokinin A, substance P and neurokinin B, let alone longitudinal muscle of the ileum where neuropeptide gamma and neurokinin A were equipotent. Of the tachykinin analogs, Nle10-NKA(4-10) was more potent than substance P methyl ester and senktide, indicating neurokinin 2 receptors are predominant for contractile effects of tachykinins. In inflamed tissues, contractile responses to tachykinins were reduced to 0%-42% in ileum (P < 0.05) and 0%-17% in colon (P < 0.01) compared to controls. CONCLUSION: In humans, tachykinins exert gut contractile effects, of similar strength as acetylcholine, predominantly through activation of neurokinin 2 receptors. These responses are greatly reduced in inflamed tissues of ulcerative colitis and Crohn disease.

Endotoxin actions on myoelectric activity, transit, and neuropeptides in the gut. Role of nitric oxide.

The lipopolysaccharide (endotoxin) of gram-negative bacteria has systemic effects in animals and man. Our aim was to investigate the effects of E. coli lipopolysaccharide on motility and transit through the small intestine in rats and to analyze plasma and tissue concentrations of intestinal neuropeptides. When lipopolysaccharide (20-160 micrograms/kg) was administered intravenously, the migrating myoelectric complex was replaced by spike bursts accompanied by rapid transit. Tissue concentrations of substance P and neurokinin A decreased, while plasma levels of calcitonin gene-related peptide increased N omega-Nitro-L-arginine, N omega-L-arginine methyl ester, dexamethasone, or indomethacin prevented these changes in myoelectric activity and tissue contents of neuropeptides. All of these compounds, except indomethacin, prevented the increased rate of transit. Thus, lipopolysaccharide changes motility through the nitric oxide and arachidonic pathways, resulting in rapid transit through the gut.

Intestinal motility responses to neuropeptide gamma in vitro and in vivo in the rat: comparison with neurokinin 1 and neurokinin 2 receptor agonists.

We have studied the effect of a novel tachykinin, neuropeptide gamma (NP gamma) on small intestinal motility in the rat. Experiments were done in vitro on longitudinal muscle strips of duodenum, and in vivo on the migrating myoelectric complex (MMC) of the small intestine. In vitro, contractile effects of NP gamma were compared with those of a selective neurokinin 1 (NK1) receptor agonist, substance P methyl ester (SPME), and a selective neurokinin 2 (NK2) receptor agonist, Nle10-NKA(4-10)(NleNKA). NP gamma, SPME and NleNKA caused concentration-dependent contractions (P < 0.001). NP gamma was eight-fold more potent than NleNKA, and 118-fold more potent than SPME. Contractile responses to NP gamma were reduced by hexamethonium (P < 0.01) and atropine (P < 0.05). The non-selective NK receptor antagonist spantide I only slightly reduced the contractile response to NP gamma, as did the selective NK1 antagonist GR 82,334, and the selective NK2 antagonist L-659,877 and MEN 10,376. In vivo, effects of NP gamma on the MMC were compared with those of the natural tachykinins substance P (SP) and neurokinin A (NKA). NP gamma disrupted the MMC and induced irregular spiking in a dose-dependent manner from 25 to 100 pmol kg-1 min-1 i.v. (P < 0.05). The effect of NP gamma was more prominent than that of NKA at equal doses, while SP had no effect. Our findings show that NP gamma exerts potent stimulatory effects on small intestinal motility, most likely mediated directly via distinct NK receptors on smooth muscle cells, but also indirectly via a cholinergic link.

Reserpine-induced depletion of neuropeptide Y from cardiovascular nerves and adrenal gland due to enhanced release.

The mechanisms underlying reserpine-induced depletion of neuropeptide Y-like immunoreactivity (NPY-LI) in relation to tissue content of noradrenaline (NA) and cardiovascular impairment were studied in guinea-pigs. Reserpine pretreatment (5 mg/kg SC) caused a 5-fold increase in plasma levels of NPY-LI with a maximum after 4 h. This was associated with a progressive fall in systemic arterial blood pressure and heart rate (to about 50% of basal values). The contents of NPY-LI and NA in nerves of the heart and quadriceps muscle were then reduced by about 75% and 85%, respectively. The adrenal content of NPY-LI was reduced by 40% 8 h after reserpine, while the adrenaline content was uninfluenced. Pretreatment with guanethidine depleted NA in the heart but did not influence plasma levels or tissue content of NPY-LI per se. The reserpine-induced increase in plasma NPY-LI and the depletion of NPY-LI in the heart and skeletal muscle was to a large extent prevented by guanethidine. The reserpine-induced bradycardia and hypotension were reduced after guanethidine pretreatment. Chlorisondamine pretreatment depressed heart rate, blood pressure and plasma levels of NPY-LI. Furthermore, chlorisondamine inhibited the reserpine-induced increase in plasma NPY-LI and prevented the reduction in tissue content of NPY-LI in the heart, skeletal muscle and adrenal.(ABSTRACT TRUNCATED AT 250 WORDS)

Correlation between peptide YY-induced myoelectric activity and transit of small-intestinal contents in rats.

The effect of peptide YY (PYY) on the myoelectric activity of the small intestine was studied in relation to the transit of a 51Cr marker solution in fasted conscious rats. The myoelectric activity was recorded by means of bipolar electrodes implanted at 5, 20, and 35 cm from the pylorus. The marker was administered in the duodenum immediately after an activity front of a migrating myoelectric complex (MMC) had passed the first recording site. Under control conditions, the propagation of one activity front over the three recording levels was accompanied by the propulsion of 90.2 +/- 11.4% of the total radioactivity as one portion distal to the third electrode site. The median peak of the radioactivity was recovered at a distance approximately twice that propagated by an activity front. Intravenous infusion of PYY (50 pmol X kg-1 X min-1) had no effect on the occurrence of the MMC in the duodenum but interrupted its distal propagation and almost totally abolished the spiking activity in the jejunum. In comparison with controls, the transport of the marker was significantly retarded, and the median peak of the radioactivity was recovered proximal to the third electrode site. The results indicate that the small-intestinal contents are propelled as one portion in front of a propagating activity front. The inhibition of the activity front by PYY may account for the delay in the transit of the small-intestinal contents.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of nephrectomy and ureter ligation on plasma neurotensin-like immunoreactivity levels in the conscious rat.

The effect of nephrectomy and ureter ligation on the concentration of endogenous plasma neurotensin-like immunoreactivity (p-NTLI) was studied in conscious rats by means of antiserum 17-8201 which detects NT (1-13) only, and antiserum 0-7709 which detects NT(1-13) and NT(1-8). The unstimulated p-NTLI concentration did not change significantly during a 25-h observation period following nephrectomy in comparison with sham operation. However, stimulation of the release of NTLI by intraduodenal administration of oleic acid (0.2 ml) resulted in significantly higher p-NTLI levels in the nephrectomized rats than in the sham operated rats. Ureter ligation did not significantly affect basal or stimulated p-NTLI. The data indicate that the kidneys play an important part in the elimination of p-NTLI released after fat ingestion.

Nervous control of the release of neurotensin-like immunoreactivity from the small intestine of the rat.

Intraduodenal administration of oleic acid increased plasma neurotensin-like immunoreactivity (p-NTLI). The integrated responses to saline and oleic acid were 5.7 and 9.7 nM0-180 min, respectively. The integrated response was not significantly altered by i.v. administration of atropine, guanethidine, mepyramine, cimetidine, methysergide or a substance P antagonist, but it was abolished by hexamethonium and morphine (5.9 and 6.3 nM0-180 min, respectively). An exogenous supply of bile and pancreatic juice did not alter the integrated response in morphine- and hexamethonium-treated rats. Haloperidol significantly increased the p-NTLI response to oleic acid (13 nM0-180 min). The results suggest that the release of neurotensin is influenced by nervous pathways involving nicotinic and opioid receptors. Catecholamines and 5-HT receptors may exert an inhibitory influence on the release of NTLI.

Somatostatin inhibits bombesin-induced effects on migrating myoelectric complexes in the small intestine of the rat.

The effect of i.v. infusions of bombesin and somatostatin, administered either separately or in combination, on migrating myoelectric complexes (MMCs) in the small intestine were studied in conscious, fasted rats. The myoelectrical activity was recorded by means of three bipolar electrodes chronically implanted into the duodenum and jejunum. Infusion of bombesin (0.5, 0.9 and 3 pmol . kg-1 . min-1) interrupted the MMC and induced irregular spiking activity similar to that observed on feeding. Only after the highest dose a consistent inhibition of the MMCs and a significant increase (P less than 0.05) of the spiking activity were achieved at all recording levels. Somatostatin (90 pmol . kg-1 . min-1) did not interrupt the MMC, but reduced significantly the incidence of the activity fronts and spiking activity of the MMCs (P less than 0.05). The effects of bombesin (3 pmol . kg-1 . min-1) on the MMC pattern were inhibited by simultaneous infusion of somatostatin (P less than 0.05). In a second series of experiments, using anesthetized rats, infusion of bombesin (0.5 and 3 pmol . kg-1 . min-1) increased the plasma concentration of neurotensin- gastrin-like immunoreactivities in a dose-dependent manner. The results show that bombesin alters the myoelectrical activity of the small intestine from a fasting to a fed pattern. Since the effect of bombesin was inhibited by the hormone release inhibitor somatostatin, it is suggested that the effect of bombesin on MMC may be secondary to the release of gastrointestinal peptides, such as neurotensin or gastrin.

Influence of fasting and bombesin-induced myoelectric activity on the transit of small-intestinal contents in the rat.

The relation between the occurrence of the migrating myoelectric complexes (MMC) and the transit of small-intestinal contents was studied in fasted, conscious rats. MMC were monitored by means of three bipolar electrodes implanted along the small intestine 5, 20, and 35 cm distal to the pylorus. In the presence of an MMC, the radioactive marker was transported along the small intestine as one main peak and recovered aboral to the activity front. Intravenous infusion of bombesin, 3 pmol X kg-1 X min-1, disrupted the MMC and induced irregular spiking activity at all recording levels. Furthermore, during bombesin infusion the radioactive marker was propelled a considerable distance, although the transit was significantly retarded in comparison to that in the presence of an MMC (p less than 0.01). The results indicate that the small-intestinal contents are propelled aboral to an activity front. Continuous irregular spiking activity during bombesin infusion contributes less to the transit of the small-intestinal contents than the activity front of MMC observed during fasting.

Analysis of the control of intestinal motility in fasted rats, with special reference to neurotensin.

Migrating myoelectric complexes (MMC) in the small intestine of fasted rats were monitored by means of four bipolar electrodes chronically implanted at 5, 15, 25, and 35 cm distal to the pylorus. In intact rats the MMC occurred at regular intervals. Truncal abdominal vagotomy did not influence the initiation and propagation of the MMC. Administration of atropine, hexamethonium, or somatostatin significantly decreased the spiking activity of the MMC by 30-45% in the duodenum and jejunum. Infusion of neurotensin at two different doses (3.6 or 7 pmol X kg-1 X min-1) interrupted the activity front of the MMC and induced irregular spiking activity at all recording levels in control rats. In vagotomized rats neurotensin interrupted the activity front inconsistently. After atropine or hexamethonium administration, infusion of neurotensin did not interrupt the distal propagation of the activity front in the jejunum. Guanethidine, naloxone, cimetidine, mepyramine, haloperidol, and a substance P antagonist did not change the MMC or alter the normal response to neurotensin. The results suggest that the inhibitory effect of neurotensin on the propagation of the jejunal activity front involves activation of enteric cholinergic mechanisms. Neurotensin seems to induce irregular spiking activity by a direct myogenic action. The enteric cholinergic innervation of the small intestine partially contributes to the occurrence of the spiking activity of the MMC in fasted rats.

The role of neurotensin in gut motility.

The physiological significance of neurotensin, with respect to gut motility in man, may be to mediate postprandial, fat-induced changes in the motility pattern of the gastrointestinal tract. There is strong experimental evidence that this effect of neurotensin is endocrine-mediated. The role of neurotensin as a paracrine hormone, neurotransmitter or neurocrine hormone remains to be determined.

The importance of bile and pancreatic juice for fat-induced release of neurotensin-like immunoreactivity (NTLI) from the small intestine of the rat.

The aim of the present study in the rat was to localize the gastrointestinal site(s) of NTLI release and to investigate the importance of bile and pancreatic juice for fat-induced NTLI release. Administration of Intralipid (2 ml) into the stomach and oleic acid (0.5 ml) into the duodenum increased the plasma concentration of NTLI (p-NTLI). The increase in p-NTLI levels occurred only when the jejunum and ileum were exposed to Intralipid but not when the exposure was limited to the stomach and duodenum. Exclusion of pancreatic juice significantly reduced the p-NTLI response and exclusion of both bile and pancreatic juice completely abolished the p-NTLI response to duodenally-administered oleic acid. The results indicate that neurotension is released by a direct luminal exposure of the neurotensin containing N-cells to fatty acids. It seems probable that fatty acids have to be transformed to a micellar form in order to release NTLI.

Effects of neurotensin and neurotensin analogues on the migrating myoelectrical complexes in the small intestine of rats.

The purpose of the present experiments was to study the effect of neurotensin and neurotensin analogues on the migrating myoelectrical complexes in the small intestine of rats. Four bipolar electrodes were implanted into the muscular wall of the small intestine. The electrodes were placed 5, 15, 25 and 35 cm distal to the pylorus. 7-10 days after the operation the animals were fasted for 48 h with free access to water. Some experiments were performed on conscious rats and in others the rats were anesthetized with pentobarbital, 30 mg/kg. I.v. infusion of either neurotensin (NT) or (Gln4)-neurotensin at doses of 1.8, 3.6 and 7.1 pmol X kg-1 X min-1 abolished the migrating myoelectric complexes, which were replaced by increased spiking activity along the whole length of the small intestine from which activity was recorded. The changes in myoelectrical activity were observed within 2-4 min after commencement of the infusion. The activity returned to control levels within 5-15 min after the end of the infusion period. The neurotensin sequences NT 9-13, NT 8-13, NT 4 -13, NT 1-9 and (Gln4)-NT 1-11 did not induce any changes in the electrical activity in the small intestine. The effects of NT and (Gln4)-neurotensin on the myoelectrical activity in the small intestine were indistinguishable. The changes induced by NT or (Gln4)-NT resemble those found after the ingestion of food. The present data indicate that the intact NT sequence, rather than smaller NT fragments, is necessary to induce changes in myoelectrical activity in the small intestine.