Thyrotropin-releasing hormone stimulates intestinal transit in young rats

The effect of intracisternal injection of thyrotropin-releasing hormone (TRH) on small intestinal transit of a charcoal bolus was investigated in 14-, 21-, 28- and 35-day-old and adult rats. Intracisternal TRH (15 micrograms in 2 microliters) was administered, and transit (distance traveled by the charcoal) was measured 120 min later. In all age groups, intracisternal TRH increased charcoal transit significantly (P less than 0.05) as compared to saline-treated controls. This increase in transit was not mimicked by intravascular TRH, and it was blocked in all age groups by prior intraperitoneal injection of atropine (2 micrograms/g body weight). Vagotomy blocked TRH-induced increases in small intestine transit in rats of 28 days and older. Prior intraperitoneal injection of the antiserotonin compound, cyproheptadine (1 microgram/g body weight) reduced TRH-induced increases in small intestine transit in all age groups. These results demonstrate that centrally administered TRH stimulates small intestine transit through both cholinergic and serotonergic mechanisms in rats as early as 14 days of age.     

Small intestinal manometry

Gastrointestinal motility is an integrated process including myoelectrical and contractile activity, tone, compliance and transit. The techniques for the assessment of gastrointestinal motility are multiple and all have their advantages and disadvantages. In the case of suspected abnormal upper gut transit, gastric and small bowel transit scintigraphy followed by small intestinal (antroduodenojejunalileal) manometry is recommended. Small bowel manometry can identify patterns suggestive of myopathy, neuropathy or obstruction. Information on procedures, indications, significance, pitfalls and guidelines for small bowel manometry is provided in this paper. In this context the potentials of small intestinal manometry for scientific experimental study of neurohumoral agents, such as serotonin receptor agonists and antagonists, on small intestinal motility is presented.     

Small intestinal sugar and amino acid transport in semistarvation.

The effect of semistarvation on small intestinal transport of D-glucose, L-valine, and NaCl was studied in an in vitro system of isolated rat brush border membrane vesicles. Whereas semistarvation enhanced the transport rate for L-valine by 19-29%, there was no change in D-glucose transport. When energy in the form of a NaSCN gradient was supplied to the membrane vesicles prepared from semistarved animals, L-valine was concentrated to a greater extent than those from well-fed animals. Strain differences were observed in the manner semistarvation affected NaCl transport across the brush border membrane. Semistarvation increased the NaCl transport rate by a factor of 3.5 in one rat strain and not at all in another. These results provide a partial explanation for the cellular basis of elevated neutral amino acid absorption by the small intestine in semistarvation.     

The effect of atrial natriuretic peptide on small intestinal contractility and transit.

Isometric tension in response to ANF (10(-10) to 10(-4) M) was recorded from longitudinally and circularly oriented rat jejunal smooth muscle strips. Conscious, fasted rats received an IV infusion of 1.25 nmol ANF/100 g body weight in 0.5 ml normal saline and controls received saline alone. Five minutes later 10 muCi Na2 51CrO4 in 0.5 ml saline was instilled through a jejunostomy. Fifteen minutes later animals were sacrificed, and the gut divided into 8 equal segments of small intestine, cecum and remaining colon. The radioactivity of each segment was measured and a geometric center of transit determined for each group. ANF induced relaxation of longitudinally oriented strips (Tm = -72.3 +/- 10.7 mN/g, ED50 7.3 +/- 3.6 x 10(-8) M), and contraction of circularly oriented strips (Tm = 35.0 +/- 5.0 mN/g, ED50 1.3 +/- 1.0 x 10(-8) M). This response was unaffected by 10(-6) M tetrodotoxin. The geometric mean center of transit was significantly (p less than 0.001) further aboral in ANF-treated compared to control animals (intestinal segment 4.2 +/- 0.2 vs. 3.2 +/- 0.2).     

alpha-Lipoic acid ameliorates altered colonic contractility and intestinal transit in STZ-diabetic rats

alpha-Lipoic acid treatment (100 mg/kg/day for 2 weeks after 6 weeks of untreated diabetes) of streptozotocin diabetic rats partially but significantly reversed both reduced contractile response of distal colon to acetylcholine and delayed transit of charcoal meal in small intestine compared to diabetic control. These effects of alpha-Lipoic acid were associated with complete reversal of diabetes induced increased plasma lipid peroxidation level. alpha-Lipoic acid had no effect on any of the parameters measured in non-diabetic rats. These findings demonstrate contribution of oxidative stress in the development of physiological changes of gut in diabetes.     

Small intestinal manifestations of diabetes mellitus

Diabetic diarrhea and steatorrhea occur predominantly in young adult males who have juvenile-onset diabetes mellitus complicated by neuropathy. The presentation is often severe, with nocturnal or postprandial watery diarrhea and tenesmus. Massive malabsorption of fat may occur; however, malabsorption of other nutrients and generalized wasting are quite rare. Because the symptoms are relatively refractory to treatment, it is important to rule out other, more easily treatable causes of this presentation. Bacterial overgrowth, exocrine pancreatic insufficiency, and celiac disease are also associated with diabetes mellitus and can mimic this process. Although the mechanism of diabetic diarrhea and steatorrhea remains unclear, neuropathy, gastrointestinal motor abnormalities, bacterial overgrowth, and bile acid abnormalities have been implicated in the pathogenesis.     

Small intestinal effects of starchy foods

Recent dietary guidelines advocate increased starch intake, but it is not clear as to how the increased intake of starch should be achieved. Recent data suggest that the quality of starch as well as its quantity is important in determining the biological effects of high carbohydrate diets. The quality of starchy foods can be assessed by their rates of digestion, which in turn are related to their glycaemic responses. Many factors affect the rate of digestion of foods and these are probably related to alterations in the chemical structure or nature of the starch. The incorporation of slowly digested, low glycaemic index foods into the diets of healthy subjects and individuals with diabetes and hyperlipidaemia is associated with the predicted reductions in postprandial glycaemic responses and with reductions in insulin secretion and blood lipids. In the past, the aim of starch processing has been to increase digestibility and improve absorption. However, it is now suggested that the use of more slowly digested starchy foods may have positive health benefits.     

Slowing intestinal transit by PYY depends on serotonergic and opioid pathways

Slowing of intestinal transit by fat is abolished by immunoneutralization of peptide YY (PYY), demonstrating a key role for this gut peptide. How PYY slows intestinal transit is not known. We tested the hypothesis that the slowing of intestinal transit by PYY may depend on an ondansetron-sensitive serotonergic pathway and a naloxone-sensitive opioid pathway. In a fistulated dog model, occluding Foley catheters were used to compartmentalize the small intestine into proximal (between fistulas) and distal (beyond midgut fistula) half of gut. Buffer (pH 7.0) was perfused into both proximal and distal gut, and PYY was delivered intravenously. Ondansetron or naloxone was mixed with buffer and delivered into either the proximal or distal half of gut. Intestinal transit was measured across the proximal half of the gut. The slowing of intestinal transit by PYY was abolished when either ondansetron or naloxone was delivered into the proximal, but not the distal gut, to localize the two pathways to the efferent limb of the slowing response. In addition, 5-HT slows intestinal transit with marker recovery decreased from 76.2 +/- 3.6% (control) to 33.5 +/- 2.4% (5-HT) (P < 0.0001) but was reversed by naloxone delivered into the proximal gut with marker recovery increased to 79.9 +/- 7.2% (P < 0.0005). We conclude that the slowing of intestinal transit by PYY depends on serotonergic neurotransmission via an opioid pathway.     

The effect of food protein-induced intestinal anaphylaxis on rate of transit

The aim of this study was to determine if the altered jejunal motility previously demonstrated in this animal model of food protein-induced intestinal anaphylaxis is (a) a localized (the jejunal site of challenge), or a generalized response of the small intestine, and (b) associated with more rapid aboral transit of intraluminal contents. Hooded-Lister rats, 100-150 g in weight, were sensitized by intraperitoneal injection of 10 micrograms egg albumin. Control rats were sham-sensitized. On day 7 rats were surgically prepared with six bipolar electrodes from duodenum to ileum and (or) a jejunostomy tube was positioned at the ligament of Treitz. On day 14, after an 18-h fast, recording of myoelectric activity were obtained from four sensitized animals with electrodes from duodenum to ileum during a control period for 45 min after saline challenge and for 45 min after antigen challenge. Control (n = 25) and sensitized (n = 31) animals with only a jejunostomy had Na2 51CrO4 instilled through the jejunostomy in 0.5 mL of saline, with or without egg albumin, either during a fast or after a standard meal. Propulsion of isotope through the small bowel was allowed to progress for 15 min, the animals were sacrificed, and their gut was removed for division into eight equal segments of small intestine, cecum, and remaining colon. The radioactivity of each segment was determined in a gamma counter.(ABSTRACT TRUNCATED AT 250 WORDS)     

Problems of diabetics in prison.

Providing care for diabetics is difficult in prison. Six diabetic prisoners or former prisoners were seen whose care was difficult or unsatisfactory. Three had multiple admissions to hospital during their sentences with diabetic ketoacidosis that they induced themselves by not taking insulin. The motive seemed to be removal from prison to the fairly pleasant surroundings of the local hospital. A fourth prisoner required admission in a hyperglycaemic, hyperosmolar state that had gone unnoticed as he was thought to be "acting up." The two others had imperfect long term management of diabetes during their sentences. There is clearly room for improvement in diabetic services in British prisons, but manipulative behaviour on the part of some diabetic prisoners may remain a problem.     

Rat small intestinal transit is independent of glucose consumption in the strenuous exercise

The present study was to determine the effect of strenuous exercise on glucose utilization, lactate accumulation and small intestinal transit (SIT). In strenuous exercises, rats would be put on the runway of a moving treadmill for a one-hour compulsive running. Rats first performed running treadmill for 45 min. After orogastric feeding of radiochromium marker, they resumed running for additional 15 min until sacrifice to measure SIT. Saline and various doses of glucose and lactate were infused through previously placed jugular vein during the whole procedure. Blood was finally obtained to measure plasma glucose and lactate levels. Saline infusion had no effect on running rat SIT during strenuous exercise, but plasma glucose level was significantly lowered (P < 0.01). Infusion of various doses of glucose did not alter SIT during strenuous exercise; however, the initially lowered plasma glucose was restored even to a hyperglycemic state. Meanwhile, strenuous running markedly increased plasma lactate level, irrespectively of saline or glucose infusion (P < 0.01). Lactate infusion did not change rat SIT obtained on the quiet runways. In conclusion, rat SIT remained unchanged in the strenuous exercise although obvious hypoglycemia and higher plasma lactate level did exist. Glucose utilization and lactate accumulation after the strenuous exercise may not directly mediate small intestinal motility.