[Why should Helicobacter pylori be eradicated?].
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Chronic Disease↗
Biomedical subjects
L Picon
Publications and source records attributed to L Picon.
[Simplified measurement of colonic transit time by one radiography of the abdomen and a single type of marker. Normal values in 82 volunteers related to the sexes].
Assessment of total and segmental colonic transit times (CTT) in man using a single type of radiopaque marker and one abdominal X-ray has been validated but not extensively studied. The aims of our prospective study were to establish normal values of this method as a function of age, gender and fiber intake in healthy subjects. Eighty-two healthy volunteers (51 men, 31 women, mean age 38 yr, range 21-61) with normal stool frequency (between 3/day and 3/week) and no history of gastrointestinal disease or medication were enrolled and ingested 10 small (3 mm edge) radiopaque markers every morning for 6 consecutive days. On the 7th day, an abdominal X-ray was performed to calculate total and segmental (right, left, rectosigmoid) CTT according to Arhan's method (CCT = 2.4 N; N = number of markers in the considered zone). During the study the number of stools was recorded and fiber intake estimated on a questionnaire. Stool frequency, total and segmental CTT were evaluated for differences due to age, gender and/or fiber intake. In volunteers, total, left and rectosigmoid CTT were closely related to stool frequency (P = 0.0001) being longer in women than in men (P < 0.02). In contrast, right CTT was independent of gender or stool frequency. Finally, in this group CTT were independent of age and fiber intake. This study confirms the influence of gender on CTT and demonstrate the ability of this simple and non-invasive method (0.08 mrad surface exposure) to assess CTT. Its use as a diagnostic tool in self-defined constipated patients would be of interest in clinical practice.
Adult↗
Fiber type composition and enzyme activities of muscles in two models of obese rats.
1. In oxidative (soleus) and glycolytic (extensor digitorum longus) muscles of obese Zucker rats, a significant decrease in the percentage of relative area occupied by glycolytic fibers was observed. 2. The activity of citrate synthase and beta-hydroxy-acyl-CoA-dehydrogenase was significantly higher in muscles of obese than of lean Zucker rats. 3. In rats, 6 weeks after lesion of the ventromedial hypothalamus, no changes were observed. 4. This indicates that neither the proportion of oxidative fibers, nor the oxidative capacities are decreased in skeletal muscles of obese rats suggesting that insulin resistance cannot be ascribed to a higher glycolytic-oxidative fiber ratio.
Animals↗
[Endoscopic injections of ethanol in the treatment of dysphagia related to esophageal carcinoma: efficacy and tolerance in 16 patients].
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Adenocarcinoma↗
Right and left colonic transit after eating assessed by a dual isotopic technique in healthy humans.
Propulsion of colonic contents after eating in the whole colon was studied in 15 volunteers by scintigraphy with injection of 111In-diethylenetriamine-pentaacetic acid and 99mTc-sulfur colloid into the colon through a nasogastric tube. The radionuclide was injected into the cecoascending colon (n = 7), the hepatic flexure (n = 6), the splenic flexure (n = 9), and the descending colon (n = 4). Changes of activity in the regions distal from and proximal to the injection points were determined before and after a 1000-kcal meal. Isotopic movements were also analyzed when a simultaneous injection of the two markers in the right and left parts of the colon was achieved (n = 11). During fasting, no significant change of activity was seen. After eating, radioactivity injected into the cecoascending and the hepatic flexure was transferred distally (P less than 0.01 and P = 0.07); radioactivity injected into the splenic flexure was transferred both distally (P = 0.07) and proximally (P less than 0.02); and no significant change of activity was seen proximally from or distally to the descending colon. Both antegrade and retrograde isotopic movements increased after eating (P less than 0.01), but the number of antegrade movements was significantly greater (P less than 0.05). This study confirms the colonic propulsive effect of eating and shows that this response is different in the right and left parts of the colon.
Adult↗
Glucose utilization and insulin binding in discrete brain areas of obese rats.
The present study was carried out to determine whether genetically obese Zucker rats present changes in brain glucose utilization and/or insulin binding when compared to their lean counterparts. Glucose utilization in the whole brain, determined by measurement of 2-deoxy(1-3H)glucose-6-phosphate, was significantly lower in obese than in lean Zucker rats. In order to precise the structure involved, we then used quantitative autoradiography methods after either (1-14C) 2-deoxyglucose injection or 125I-insulin incubation. In obese rats, local cerebral glucose utilization (LCGU) was significantly decreased in the external plexiform layer (-37%, p < 0.05), in the lateral hypothalamus (-23%, p < 0.05), and in the basolateral amygdaloid nucleus (-30%, p < 0.05). In contrast, no difference in specific insulin binding was found between the two genotypes in any of the areas studied. These results are consistent with some data showing a decrease of LCGU in hyperinsulinemic rats. All together, these data show perturbations of glucose utilization, particularly in structures linked to the regulation of body weight and food intake in obese Zucker rats.
Amygdala↗
Insulin receptor kinase activity in muscles and white adipose tissue during course of VMH obesity.
Early after lesion of the ventromedial hypothalamus nuclei (VMH), insulin-induced glucose utilization is increased in white adipose tissue (WAT), whereas oxidative and glycolytic muscles are, respectively, normoresponsive or resistant to insulin. Five weeks later, all of the muscles are resistant, whereas WAT returns to normal responsiveness. The aim of this study was to characterize the insulin receptor kinase activity in WAT and muscles 1 and 6 wk after lesion. The number and affinity of insulin receptors were not modified in any of the tissues studied. Autophosphorylation and phosphorylation of an exogenous substrate were similar in oxidative and glycolytic muscles of VMH and control rats both 1 and 6 wk after the lesion. Insulin receptors from WAT of 1-wk VMH rats exhibited a 2.5-fold increase in insulin-stimulated autophosphorylation and phosphorylation. Six weeks after the lesion, both autophosphorylation and phosphorylation returned to normal values. This suggests that insulin receptor tyrosine kinase activity does not play a significant role in the insulin resistance of skeletal muscles but has a crucial role in mediating the variations of insulin action on WAT observed during the development of VMH obesity.
Adipose Tissue↗
Increased islet blood flow in obese rats: role of the autonomic nervous system.
Hyperinsulinemia, a main feature of both human and animal obesity, has been demonstrated to be due to both an increased sensitivity to nutrient secretagogues and an impairment of the nervous regulation of insulin secretion. Recent studies have shown that pancreatic islet blood flow increases under conditions associated with an enhanced insulin secretion. The aim of this study was to determine whether or not changes in islet blood flow are present in hyperinsulinemic obese rats. Using the nonradioactive microsphere technique, we were able to show a significantly higher islet blood flow in obese rats either of the Zucker strain or Wistar rats after lesion of the ventromedial hypothalamus than in their respective lean controls. Subdiaphragmatic vagotomy had no significant effect on basal islet blood flow of lean rats, whereas it decreased significantly that of obese Zucker rats. Conversely, clonidine, an alpha 2-adrenergic agonist, induced a higher decrease of islet blood flow in obese than in lean Zucker rats. The injection of an intravenous bolus of glucose (375 mg/kg iv) increased significantly more islet blood flow in obese than in lean Zucker rats. It is concluded that obese rats present an increased pancreatic islet blood flow, which may result, at least in part, from exaggerated parasympathetic activity and lower than normal sympathetic activity. This could participate in the hyperinsulinemia observed in these rats.
Animals↗
In vivo effect of insulin on the acute proliferative response of the rat aorta to injury.
The objective of our study was to investigate the effect of hyperinsulinemia associated with either euglycemia, hypoglycemia, or hyperglycemia on the short-term mitotic activity of arterial smooth muscle cells (SMCs) after aortic injury. The proliferative reaction of arterial SMCs was provoked by the passage of an embolectomy catheter with a tightly inflated balloon. DNA synthesis was measured as DNA specific activity after incubation of the aorta in a medium containing 3[H]thymidine. Unrestrained rats were rendered hyperinsulinemic (4-7 nM versus 0.3 nM in controls) immediately after aortic injury by insulin infusion (10 units/day) and either euglycemic (about 5.6 mM), hyperglycemic (14-17 mM), or hypoglycemic (about 2.8 mM) by adjusting the flow rate of hypertonic glucose (30% wt/vol) that was infused simultaneously. The infusion was performed via a catheter inserted into the jugular vein and lasted 2 or 4 days after the aortic injury. After the injury, SMC mitotic activity was dramatically increased on day 2 in control rats with deendothelialized aortas and declined between days 2 and 4. In euglycemic-hyperinsulinemic and hyperglycemic-hyperinsulinemic rats, SMC proliferation showed the same pattern as in controls. At no time was a significant difference observed among the three groups of rats. In hypoglycemic-hyperinsulinemic rats, SMC mitotic activity increased to a lesser extent than in controls on day 2 after deendothelialization. These data indicate that hyperinsulinemia with or without hyperglycemia does not stimulate the early stages of arterial SMC proliferation in the rat although a long-lasting effect of hyperinsulinemia cannot be excluded.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Increased gene expression of lipogenic enzymes and glucose transporter in white adipose tissue of suckling and weaned obese Zucker rats.
Previous experiments have shown that insulin-induced glucose utilization is increased in white adipose tissue of young obese Zucker rats. We have investigated the possible role of over-expression of the muscle/fat glucose transporter (Glut 4) and key lipogenic enzymes in this increased insulin-responsiveness. The amount or activity and the mRNA concentrations of Glut 4, fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC) were measured before and after weaning in white adipose tissue of obese and lean Zucker rats. Comparison of the levels of Glut 4 and lipogenic-enzyme expression in 15-day-old suckling and 30-day-old weaned rats on a high-carbohydrate diet shows a marked increase in the latter group. The increase was, in lean and obese rats respectively, 6- and 7-fold for the amount of Glut 4 and 2- and 3-fold for its mRNA concentrations, 40- and 100-fold for the activity of lipogenic enzymes (FAS and ACC) and 30- and 10-fold for their mRNA concentrations. Furthermore, all these parameters, except the amount of Glut 4, were 2-5-fold higher in obese rats, both before and after weaning. Changes at weaning were largely blunted when rats were weaned on to a high-fat diet, although the differences between lean and obese rats persisted, and even became significant for the amount of Glut 4. Whatever the experimental conditions, plasma insulin levels were significantly higher in obese than in lean rats. These results indicate the existence of an enhanced expression of Glut 4, FAS and ACC in white adipose tissue of young obese fa/fa rats which could be related to the increased plasma insulin levels.
Acetyl-CoA Carboxylase↗
Effect of insulin on the properties of liver carnitine palmitoyltransferase in the starved rat: assessment by the euglycemic hyperinsulinemic clamp.
The effect of insulin on the properties of liver carnitine palmitoyltransferase I (CPT I) was assessed in conscious starved rats with the euglycemic hyperinsulinemic clamp. A 24-hour clamp was necessary to fully reverse the effect of starvation on liver malonyl-CoA concentration, CPT I maximal activity, and apparent km and Ki for malonyl-CoA. Since glucagon was not decreased during the clamp, insulin is the major factor involved in the regulation of CPT I.
Animals↗
Effects of fasting and refeeding on the proliferative response of rat aorta to injury.
To explore the interplay between the mitotic activity of arterial smooth muscle cells and the variations of plasma glucose and insulin concentrations, we have studied over 14 days the response of thoracic aorta to injury with a balloon catheter in rats submitted to fasting and refeeding. Animals were fasted from the day before until the third day after injury. The proliferative reaction of intima-media was assessed 2, 3.5, 4, 6, 8, and 14 days after injury, comparing freely fed with fasted-refed rats. Fasting decreased plasma glucose and insulin concentrations and DNA synthesis by intima-media, whereas refeeding increased these three variables transiently. The DNA content of intima-media at any time during the response to injury and the intimal thickening on day 14 were not influenced by the sequence of fasting and refeeding, which suggests that the early decrease in DNA synthesis induced by fasting had been compensated for by the later increase in DNA synthesis induced by refeeding. In conclusion, besides hormonal influences (such as insulin), metabolic influences (such as the availability of energetic fuels) are likely to act on the proliferative response of arteries to injury.
Animals↗
Differential effects of prolonged hyperglycemia on in vivo and in vitro insulin secretion in rats.
The purpose of this study was to investigate the effects of a 48-h glucose (30% wt/vol) infusion in unrestrained catheterized healthy rats (HG) on subsequent in vivo and in vitro insulin response to glucose. High hyperglycemia (400-450 mg/dl) and resulting hyperinsulinemia (1.2 +/- 0.1 mU/ml vs. 0.15 +/- 0.03 mU/ml in controls) were maintained throughout the infusion period. Glucose-induced insulin secretion was examined in vivo 3 h after the end of infusion by performing either a glucose tolerance test or a hyperglycemic clamp (225 mg/dl for 60 min). In addition, in vivo insulin secretion was studied on day 1, 3, 5, and 7 after the end of glucose infusion by performing glucose tolerance tests. Insulin secretion was also investigated in vitro, using the isolated perfused pancreas technique, 3 h and 1 day post glucose infusion. During glucose tolerance tests and hyperglycemic clamps performed at 3 h, insulin secretion was much greater in HG rats than in controls, and remained increased until day 5. By contrast, when studied in vitro 3 h after the end of the infusion, glucose-induced insulin release from isolated perfused pancreases was impaired in HG rats as compared with controls, and the insulin response to arginine was dramatically increased. However, insulin secretion in vitro returned partially to normal after day 1. These data indicate that prolonged hyperglycemia has quite different effects on the subsequent insulin secretion in vivo or in vitro. It impairs, but reversibly, glucose-induced insulin secretion in vitro, whereas it increases it durably in vivo. This suggests that humoral and/or nervous interferences can counterbalance the possible perturbing effects of prolonged hyperglycemia on the normal B cell responsiveness to glucose.
Animals↗
Enhanced insulin secretory response to acetylcholine by perifused pancreas of 5-day-old preobese Zucker rats.
The insulin secretion rate in response to different secretagogues and neurotransmittors was studied in perifused pancreas of 5-day-old lean (Fa/Fa) and preobese (fa/fa) Zucker rats. Glucose (16.6 mM) alone or in combination with 20 mM arginine or 5 mM theophylline induced a net stimulation of insulin secretion. This effect was similar in the two groups. By contrast, the stimulatory effect of acetylcholine on glucose-induced insulin secretion was significantly higher in preobese pups than in lean rats. There was also a tendency toward a higher inhibitory effect of norepinephrine on insulin secretion in preobese than in lean rats, but this difference did not reach statistical significance. Together these results demonstrate a normal insulin secretion in response to nutrient secretagogues in preobese fa/fa rats but an enhanced effect of acetylcholine. This latter effect may be related to the changes in the autonomic nervous system activity, which is usually described in obese fa/fa rats.
Acetylcholine↗
Insulin secretion in adult rats after intrauterine exposure to mild hyperglycemia during late gestation.
We investigated the effects of intrauterine mild hyperglycemia during late fetal life on glucose regulation and insulin secretion in adult rats. Unrestrained pregnant rats were continuously infused with glucose during the last week of pregnancy to induce mild hyperglycemia (6.5-8 mM). Control rats were infused with a glucose-free solution. The offspring were studied, as adults, from 1 to 20 mo by performing glucose tolerance and insulin secretion tests. Young-adult rats from hyperglycemic dams showed mild glucose intolerance and impairment of glucose-induced insulin secretion. This situation gradually evolved to basal hyperglycemia and severe impairment of glucose tolerance and insulin secretion. Insulin secretion was also studied in vitro in 20-mo-old rats with the isolated perfused-pancreas technique. Insulin release in response to glucose stimulation from pancreases of hyperglycemic dams was similar to that of controls, and the response to arginine was increased but not significantly. The possible involvement of enhanced sympathetic nervous system activity in the impairment of insulin secretion in adult rats from hyperglycemic mothers was then investigated by performing glucose tolerance and insulin secretion tests in the presence of the alpha 2-blocker idazoxan in 8-mo-old rats. Under these conditions, rats from hyperglycemic dams recovered almost normal glucose tolerance, and glucose-induced insulin secretion was greatly improved. These data show that mild hyperglycemia induced in the fetus during late pregnancy leads to persistent impairment of glucose regulation and insulin secretion. They suggest that the impairment of insulin secretion in vivo results from a perturbation of the neuroregulation of insulin secretion rather than an intrinsic pancreatic beta-cell defect.
Adrenergic alpha-Antagonists↗
Regulation of glucose homeostasis in pre-obese Zucker rats before and after weaning.
This study was undertaken to determine the changes which could occur in glucose homeostatis during the suckling-weaning transition in the genetically obese Zucker (fa/fa) rat. Glucose kinetics and glucose utilization in individual tissues were determined in 15-day-old suckling and 30-day-old weaned obese Zucker rats either in the post-absorptive state or during a glucose infusion. During suckling, glucose turnover rates in the basal state as well as glucose production and utilization during the glucose infusion were identical in lean and obese rats. Furthermore, individual tissue glucose utilizations were similar in the two groups of rats, except in brown adipose tissue where utilization was lower in obese than in lean rats during the glucose challenge. After weaning, glucose turnover rates and glucose utilization in individual tissues were identical in the two genotypes in the basal state. During the glucose infusion, hepatic glucose production was less suppressed in the obese. Furthermore, glucose utilization was significantly lower in muscles (extensor digitorum longus, tibialis anterior, diaphragm) and higher in white adipose tissue of obese rats. These data show that, before weaning, pre-obese Zucker rats present a perturbation only in the uptake of glucose in brown adipose tissue. Major defects in the regulation of glucose homeostatis occur after weaning.
Animals↗
[Merycism or gastroesophageal reflux: value of antroduodenal manometry].
Decrease in lower esophageal sphincter (LES) pressure and frequent acid reflux were observed in 3 of 5 adult patients with rumination syndrome confirmed by antroduodenal manometry. The role of the LES in the rumination syndrome is unclear but decreased LES pressure could be a determining factor. Antroduodenal manometric studies should therefore be performed during ordinary gastroesophageal reflux in order to determine the diagnostic value of antroduodenal manometry in the rumination syndrome.
Adolescent↗
Hyperinsulinaemia increases insulin action in vivo in white adipose tissue but not in muscles.
The effect of 4 days of stable hyperglycaemia and resulting hyperinsulinaemia on insulin-induced glucose utilization by individual rat tissues was studied in vivo. The treatment produced a net increase in the glucose utilization index under both basal and insulin-stimulated (euglycaemic/hyperinsulinaemic clamp) conditions in white adipose tissue. On the contrary, glucose utilization was unchanged in aerobic muscles but was decreased in glycolytic skeletal muscles during the clamp.
Adipose Tissue↗