Biomedical subjects

F Rohner-Jeanrenaud

Publications and source records attributed to F Rohner-Jeanrenaud.

95 records · Page 6Linked to original sources

PubMed1981

CNS modulation of pancreatic endocrine function. Multiple modes of expression.

The involvement of the CNS in pancreatic hormone release has been studied. 1.) It has been shown that one source of vagal efferent fibers capable of facilitating insulin secretion originated in the rostral half of the nucleus ambiguus. 2.) Acute lesions of the ventromedial hypothalamus resulted in hyperinsulinaemia that could be abolished by acute vagotomy. 3.) Chronic lesions of the ventromedial hypothalamus increased secretion of insulin and glucagon, and decreased secretion of somatostatin when the pancreas was subsequently isolated and perfused. These changes were attributed to altered cholinergic activity related to previous ventromedial hypothalamic lesions as they could be reversed toward normal by atropine infusion or mimicked by the cholinergic agonist, methacholine. 4.) Electrical stimulation of the lateral hypothalamus in anaesthetized rats produced both an inhibitory component of insulin secretion, probably related to adrenergic stimulation, and a stimulatory component, probably due to the release into the blood of factor(s) that promote insulin secretion. 5.) The anatomical organization of brain of the genetically obese (ob/ob) mice is abnormal. These abnormalities could be involved in the endocrinological disturbances of these animals.

Animals↗

PubMed1980

Nitrogen handling in adult hypothalamic obese rats.

Several aspects of nitrogen metabolism have been studied in adult nonhyperphagic, hyperinsulinemic, ventromedial hypothalamus (VMH)-lesioned rats. Ten days postoperatively, VMH-lesioned rats had high plasma levels of urea and low plasma tyrosine, while plasma alanine, glutamine, total amino acid, and protein levels were unaltered. Urea production and excretion were increased in VMH-lesioned rats. Increased urea synthesis could not be attributed to enhanced peripheral release of amino acids. In vitro, measurements of hepatic amino acid uptake and liver protein synthesis did not reveal any disturbances of these processes in VMH-lesioned rats. However, hepatic transamination and lipogenesis from amino acids were increased following VMH-lesions. In addition to the hyperinsulinemia previously reported to occur in nonhyperphagic VMH-lesioned rats, this study showed an increased glucagon secretion from perfused pancreases of these animals. These data together suggest that the excess of the two hormones at the portal vein of VMH-lesioned rats would favor uptake and deamination of amino acids, their diversion to lipid synthesis and possibly other pathways, with consequent increase in urea production and reduced supply of amino acids to peripheral tissues available for nitrogen retention.

Amino Acids↗

PubMed1980

Consequences of ventromedial hypothalamic lesions upon insulin and glucagon secretion by subsequently isolated perfused pancreases in the rat.

The existence of a relationship between the ventromedial hypothalamic area (VMH) and the activity of the endocrine pancreas has been shown previously. This relationship has been further tested and extended in the present study, using isolated perfused pancreases from rats previously lesioned (4-7 d) in the VMH. It was found that in isolated pancreases obtained from rats fed ad lib. for 4 d after VMH lesions (i.e., that were hyperphagic), the typical biphasic pattern of insulin secretion was observed following glucose stimulation (20 mM) and that the total insulin output was much greater than that of controls. The increased insulin output was not a result of hyperphagia because similar results were obtained using pancreases obtained from VMH-lesioned rats in which a food restriction matching exactly that of control rats was started either immediately of 3 d after the lesions. Pancreases from such food-restricted VMH-lesioned rats oversecreted insulin, when compared with controls fed the same amount, from 7 mM of glucose concentration in perfusion medium onwards. After the addition of arginine (10 mM), the total output of glucagon by pancreases from food-restricted VMH-lesioned rats was twice that of controls. Qualitatively, the arginine-induced glucagon secretion by pancreases from food-restricted VMH-lesioned rats retained its biphasic pattern. Similarly, epinephrine (0.1 muM) elicited a greater glucagon release by pancreases from food-restricted VMH-lesioned rats when compared with controls. These data further support the concept of a link (as yet undefined) between the hypothalamus and the endocrine pancreas, as lesions of the VMH area resulted in abnormal secretion not only of insulin, but of glucagon as well.

Animals↗

PubMedDate not supplied

[Modulation by the central nervous system (CNS) of the activity of the endocrine pancreas].

Electrical stimulation of Nucleus Ambiguus (NA) and of Lateral Hypothalamus (LH) produces a sympathetic response that partly inhibits insulin secretion in anesthetized rats in vivo. This inhibitory component is accompanied by a stimulatory one that can, in both cases, be revealed by the infusion of an alpha-blocker to the rats. The analogy between the stimulatory effect on insulin secretion due to NA or LH electrical stimulation is only partial. Indeed the NA-induced insulin secretion is abolished by vagotomy, while that induced by LH stimulation appears to be mediated by possible release of humoral factor(s). Acute bilateral lesions of the ventromedial hypothalamus (VMH) in anesthetized rats produce, within minutes, an hyperinsulinemia that is abolished by superimposed vagotomy. Semi-chronic (7 d.) lesions of the VMH in rats result in changes in the activity of their subsequently isolated perfused pancreases. Indeed, and compared to controls, pancreases from VMH-lesioned rats oversecrete insulin and glucagon while undersecreting somatostatin. Such alterations due to lesions of the VMH appear to be the result of increased vagal activity and (possibly via a trophic effect of the nerve) of increased cholinergic (muscarinic) receptors. CNS organisation of genetically obese (ob/ob) mice is abnormal when compared to controls. Abnormalities are mainly a relative increase of the size of neurons of the LH and the dorsomotor nucleus of the vagus (DMX), compared to that of other CNS neurons. These abnormalities could conceivably play a role in the genesis of hyperinsulinemia of these animals.

Animals↗

PubMedDate not supplied

Defective diet-induced but normal cold-induced brown adipose tissue adaptation in hypothalamic obesity in rats.

our weeks after bilateral ventromedial hypothalamic (VMH) lesions in the female rat reared at 23 degrees C, the weight of the interscapular brown adipose tissue (IBAT) was doubled as compared to appropriate controls. Tested in vitro, the tissue of the lesioned animals showed, per unit weight, a basal and a noradrenaline--or octanoate--stimulated heat output about half of that of the tissue from the controls. However, basal and stimulated heat outputs as well as beta-oxidative capacity of IBAT from lesioned animals and their appropriate controls were the same when calculated per whole fat pad. The lesioned animals were hyperphagic, with a gross energy intake 70% larger than that of the controls. Cold acclimation at 5 degrees C for 3 weeks was found to restore the basal and stimulated heat outputs per unit weight of IBAT of the lesioned animals to the level of that of their cold acclimated controls. The weight of the tissue did not change significantly in lesioned animals upon cold exposure whereas controls exhibited the expected hypertrophy. Calculated per whole fat pad, the stimulated heat output became 33% larger in lesioned animals than in appropriate controls. The total beta-oxidative capacity increased by 3 fold in controls and 4.8 fold in lesioned animals. Cold exposure was followed by a mean increase of gross energy intake of 43% in the controls and 31% in the lesioned animals as compared to their gross energy intake at 23 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗