Cephalic-phase insulin and glucagon release in normal subjects and in patients receiving pancreas transplantation

Secchi, Antonio; Caldara, Rossana; Caumo, Andrea; Monti, Lucilla D.; Bonfatti, Doretta; Carlo, V. Di; Pozza, G.

doi:10.1016/0026-0495(95)90008-x

Cited by 50 publications

(28 citation statements)

References 31 publications

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“…As it has been demonstrated that the glucagon concentration in peripheral blood showed little diurnal variation in rats [35], it was sufficient in our study to document hyperglucagonemia during fasting. Our finding of hyperglucagonemia after loss of first-pass hepatic drainage is in line with studies reporting basal or stimulated hyperglucagonemia after pancreas transplantation with systemic venous drainage [5,8,9,[37][38][39]. However, there are also a few studies which failed to find hyperglucagonemia although the grafts had systemic venous drainage [6,40].…”

Section: Discussionsupporting

confidence: 77%

The Solution to Hyperglucagonemia after Pancreas Transplantation in Inbred Rats

Kißler

Hennig²,

Gepp³

et al. 2001

Eur Surg Res

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Background: We studied the possible role of the diseased host pancreas and site of venous graft drainage in the development of hyperglucagonemia after pancreas transplantation, to identify the crucial steps of the technique capable of eliminating hyperglucagonemia and its possible diabetogenic effect. Methods: Therefore, we compared 4 groups of inbred rats: (1) heterotopic pancreas transplantation with either systemic (n = 9); or (2) portal (n = 5) venous drainage after prior induction of diabetes with streptozotocin; (3) orthotopic pancreaticoduodenal transplantation with portal venous drainage after prior pancreaticoduodenectomy (n = 7), and (4) sham-operation (Sham; n = 10). The postoperative period was 6 months. Results: Only heterotopic transplantation with systemic venous drainage and loss of glucagon’s first pass hepatic extraction, resulted in arterial hyperglucagonemia, whereas the arterial plasma insulin level was only slightly higher in comparison with the other groups. After either type of heterotopic transplantation the glucagon content of host pancreata remained unchanged, whereas the insulin content was approximately 5% of that in the pancreas of Sham rats. The insulin and glucagon contents of all grafts were similar to those of the control pancreas in Sham rats, and the insulin release was sufficient to normalize fasting plasma glucose and lipids after either type of transplantation. Conclusion: To remove the diseased host pancreas appears unnecessary, as the hyperglucagonemia and the concomitant slight hyperinsulinemia, capable of preventing glucagon’s diabetogenic effects, are due to loss of the first pass hepatic extraction by systemic venous drainage alone. This disadvantage can be eliminated by portal venous graft drainage.

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Section: Discussionsupporting

confidence: 77%

The Solution to Hyperglucagonemia after Pancreas Transplantation in Inbred Rats

Kißler

Hennig²,

Gepp³

et al. 2001

Eur Surg Res

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“…On the other hand, it reveals a close interaction between the parasympathetic and sympathetic motor nuclei, which may provide, in addition to the regulatory mechanisms at the level of the pancreas (Ahren and Taborsky, 1986;Kurose et al, 1992), the anatomic basis at the level of the CNS for the frequently observed cosecretion of insulin and glucagon (Steffens and Strubbe, 1983;Secchi et al, 1995;Taborsky et al, 1998).…”

Section: Discussionmentioning

confidence: 97%

Parasympathetic and sympathetic control of the pancreas: A role for the suprachiasmatic nucleus and other hypothalamic centers that are involved in the regulation of food intake

et al. 2001

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To reveal brain regions and transmitter systems involved in control of pancreatic hormone secretion, specific vagal and sympathetic denervation were combined with injection of a retrograde transsynaptic tracer, pseudorabies virus (PRV), into the pancreas. After sympathetic or vagal transsection first-order neurons were revealed in the dorsal motor nucleus of the vagus (DMV) or in preganglionic spinal cord neurons (SPN), respectively. Careful timing of the survival of the animals allowed the detection of cell groups in immediate control of these DMV or SPN neurons. A far larger number of cell groups is involved in the control of DMV than of SPN neurons. Examples are given of a high level of interaction between the sympathetic and parasympathetic nervous system. Several cell groups project to both branches of the autonomic nervous system, sometimes even the same neurotransmitter is used, e.g., oxytocin neurons in the paraventricular nucleus and melanin-concentrating hormone and orexin neurons in the lateral hypothalamus project to both the DMV and SPN neurons. Moreover, the appearance of third-order neurons located in the sympathetic SPN after complete sympathectomy and in the DMV after complete vagotomy illustrates the possibility that motor neurons of the sympathetic and parasympathetic system may exchange information by means of interneurons. The presence of second-order neurons in prefrontal, gustatory, and piriform cortex may provide an anatomic basis for the involvement of these cortices in the cephalic insulin response. The observation that second-order neurons in both vagal and sympathetic control of the pancreas contain neuropeptides that are known to play a role in food intake indicates a direct association between behavioral and autonomic functions. Finally, the observation of third-order neurons in the suprachiasmatic nucleus and ventromedial hypothalamus shows the modulatory action of the time of the day and metabolic state, respectively.

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“…Basal hyperinsulinemia was observed after pancreas transplantation in humans [34][35][36][37]. Under euglycemic conditions it was postulated that this elevation of insulin was due to an impaired insulin-insulin feedback inhibition that was neurally mediated [35][36][37].…”

Section: Discussionmentioning

confidence: 99%

“…Under euglycemic conditions it was postulated that this elevation of insulin was due to an impaired insulin-insulin feedback inhibition that was neurally mediated [35][36][37]. The most likely mediator in this mechanism was the sympathetic nervous system innervating the pancreas [34].…”

Section: Discussionmentioning

confidence: 99%

Effect of Selective Denervation of the Rat Pancreas on Pancreatic Endocrine Function

Nilsson¹,

Zoucas²,

Lundquist

et al. 2001

Eur Surg Res

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The purpose of this study was to investigate the influence of selective denervation of the rat pancreas on hormone secretion and on peripheral insulin sensitivity. Thirteen rats, 7 denervated and 6 sham operated, received an intravenous glucose challenge for 30 min. The basal plasma levels of insulin, glucagon and glucose did not differ between the two groups. An augmented insulin response to glucose was detected in the denervated group, whereas the glucagon response was unaffected. Glucose tolerance was marginally improved. Twenty-four rats, 12 denervated and 12 sham operated, received a constant infusion of glucose, insulin, epinephrine and propranolol in order to inhibit the endogenous insulin release and thus evaluate insulin sensitivity. No significant change in insulin sensitivity could be detected during our experimental conditions. We conclude that selective denervation brings about an increased insulin response to glucose, probably by interrupting a catecholaminergic negative tone on the β-cell. The sympathectomized animals did not disclose any apparent changes in peripheral insulin sensitivity.

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Cephalic-phase insulin and glucagon release in normal subjects and in patients receiving pancreas transplantation

Cited by 50 publications

References 31 publications

The Solution to Hyperglucagonemia after Pancreas Transplantation in Inbred Rats

The Solution to Hyperglucagonemia after Pancreas Transplantation in Inbred Rats

Parasympathetic and sympathetic control of the pancreas: A role for the suprachiasmatic nucleus and other hypothalamic centers that are involved in the regulation of food intake

Effect of Selective Denervation of the Rat Pancreas on Pancreatic Endocrine Function

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