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M L Bonfleur

Publications and source records attributed to M L Bonfleur.

4 recordsLinked to original sources

Parasympathetic activity changes insulin response to glucose and neurotransmitters.

Pancreatic islet isolated from hyperinsulinemic obese rodents showed high glucose sensitivity to stimulation of insulin secretion. Current research evaluates the effect of subdiaphragmatic vagotomy on insulin secretion stimulated by glucose and by a cholinergic agonist carbachol (Cch) in islets isolated from monosodium L-glutamate (MSG)-obese rats. During the first 5 days after birth, MSG was intradermically injected into the cervical area of male Wistar rats (n=26). Control animals were injected with hyperosmotic saline solution (n=26). Vagotomy was performed on 30-day-old rats. On the 90th day, after a 12-h fast, the animals were killed. Pancreatic islets were isolated by collagenase. Batches of islets (n=30) were incubated for 60 min in glucose 2.8-20.0 mM or 0.1-2.0 mM Cch in the presence of glucose 8.3 mM. Released insulin was measured by radioimmunoassay. Insulin secretion stimulated by glucose in islets from MSG-obese rats shifted to the left when compared to that of controls, 63.8+/-3.9 and 42.2+/-2.6 ng/ml/islet/60 min (p<0.001), respectively. Vagotomy decreased by 56% (p<0.001) the secretion induced by all glucose concentrations in islets from MSG-obese rats. In the controls the operation caused a 30% (p<0.01) reduction. Cch stimulated insulin secretion in normal and obese rat islets. Response to obese rat islets was 1/3 less than normal ones (p<0.05). Vagotomy produced a greater potentiation of Cch induced insulin secretion on islets from obese rats. Data suggested that parasympathetic modulation is important to insulin secretion control.

Analysis of Variance↗

Effects of decrease of extracellular sodium in carbachol-evoked catecholamine secretion in isolated adrenal medullae of rats.

The effect of extracellular Na(+) deprivation on the carbachol-evoked catecholamine secretion was evaluated in chromaffin cells. Isolated adrenal medullae of male Wistar rats were incubated in solutions with different sodium concentrations (144,0; 75,0; 25,0 and psi mM). Catecholamine secretions inversely increased as a response to fall of extracellular concentration of sodium. The magnitude of response to cholinergic stimulus (carbachol 100 microM) was decreased in low extracellular sodium concentration. Atropine (100 microM) inhibited secretion of catecholamine induced by carbachol in the presence and in the absence of extracellular sodium. Results suggest that in isolated adrenal medullae of rats (1) decrease in concentration of extracellular sodium increases secretion of catecholamines, perhaps by a greater influx of calcium from the extracellular environment through reversal of Na(+) /Ca(2+) exchanger; (2) intensity of catecholamine secretion induced by cholinergic stimulus seems to depend on extracellular sodium.

Adrenal Medulla↗

Insulin secretion and acetylcholinesterase activity in monosodium l-glutamate-induced obese mice.

OBJECTIVE: Pancreatic islets isolated from mice treated neonatally with monosodium L-glutamate (MSG) were used to study insulin secretion. MATERIALS AND METHODS: Total acetylcholinesterase (AchE) activity of tissue extract was measured as a cholinergic activity marker. Obesity recorded in 90-day-old MSG mice (OM) by Lee index reached 366.40 +/- 1.70, compared to control mice (CM) 324.40 +/- 1.10 (p < 0.0001). Glucose 5.6 mM induced insulin secretion of 36 +/- 5 pg/15 min from islets of CM and 86 +/- 13 from OM (p < 0.001). When glucose was raised to 16.7 mM, islets from OM secreted 1,271 +/- 215 and 1,017 +/- 112 pg/30 min to CM. AchE activity of pancreas from OM was 0.64 +/- 0.02 nmol of substrate hydrolyzed/min/mg of tissue and 0.52 +/- 0.01 to CM (p < 0.0001). Liver of obese animals also presented increase of AchE activity. RESULTS: These indicate that OM insulin oversecretion in low glucose may be attributed, at least in part, to an enhancement of parasympathetic tonus.

Acetylcholinesterase↗

Vagotomy reduces obesity in MSG-treated rats.

In order to study the role of vagus nerve activity at the onset of obesity induced by monosodium glutamate (MSG), 30-day-old MSG-rats were vagotomized or sham operated. Body weight and food intake were recorded until animals were 90 days old and then sacrificed. Naso-anal length was recorded for all animals. Periepididymal and retroperitoneal fat pads were isolated and weighed. Reduction of body weight and naso-anal length were registered in 30-day-old MSG-rats. Obesity could also be observed, as increase of Lee index indicated. Results were most evident in 90-day-old MSG-rats. In both groups neither body weight gain nor food intake was changed by vagotomy. However, fat accumulation on tissues was reduced by vagotomy in MSG-rats. The results showed that MSG-obesity is not related to an increment in food intake behavior. Vagotonia might play a role at the onset of MSG-obesity.

Animals↗