Plasma amylin concentration is related to the severity of intestinal ischemic injury in rats

Phillips, Anthony R.J.; Abu‐Zidan, Fikri M.; Farrant, Glenn; Zwi, Jonathon; Cooper, Garth J. S.; Windsor, John A.

doi:10.1067/msy.2001.113892

Cited by 8 publications

(8 citation statements)

References 21 publications

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“…15) Recently, studies have reported that mesenteric ischaemia induces the release of insulin from pancreas into the blood circulation. 13,14) Therefore, the noted protective eŠect of remote mesenteric ischaemic preconditioning on cerebral injury may be mediated through the endogenous release of insulin, which is further supported by our study with AIS that attenuated the protective eŠect of mesenteric preconditioning on ischaemia-reperfusion induced cerebral injury. Thus, it may be deduced that insulin released as a result of an ischaemic insult to the mesentery may be mediating the resultant protection aŠorded by the remote preconditioning of brain.…”

Section: Discussionsupporting

confidence: 64%

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Possible Involvement of Insulin, Endogenous Opioids and Calcitonin Gene Related Peptide in Remote Ischaemic Preconditioning of Brain

2007

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The present study has been designed to investigate the role of insulin, endogenous opioids and calcitonin gene related peptide (CGRP) on remote mesenteric ischaemic preconditioning induced reversal of global cerebral ischaemiareperfusion injury in mice. Bilateral carotid artery occlusion of 10 min followed by reperfusion for 24 hour was employed in present study to produce ischaemia and reperfusion induced cerebral injury in mice. Cerebral infarct size was measured using triphenyltetrazolium chloride staining. Short-term memory was evaluated using elevated plus maze. Inclined beam walking and resistance to lateral push response, tests were employed to assess motor incoordination. Bilateral carotid artery occlusion followed by reperfusion produced cerebral infarction and impaired short-term memory, motor co-ordination and lateral push response. A preceding episode of mesenteric artery occlusion for 15 min and reperfusion of 15 min (remote mesenteric ischaemic preconditioning) prevented markedly, ischaemia-reperfusion-induced cerebral injury measured in terms of infarct size, loss of short-term memory, motor coordination and lateral push response. Anti-insulin serum, naloxone (an opioid receptor antagonist) and a-CGRP (8 37) (a selective CGRP receptor blocker) attenuated the neuroprotective eŠect of remote mesenteric ischaemic preconditioning. It may be concluded that neuroprotective eŠect of remote mesenteric ischaemic preconditioning probably is mediated through insulin, endogenous opioids and CGRP released as a consequence of mesenteric ischaemia and reperfusion in mice.

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Section: Discussionsupporting

confidence: 64%

“…12) Mesenteric ischaemia has been observed to trigger an abrupt increase in the release of insulin from pancreas. 13,14) Insulin, per se, is documented to attenuate ischaemia-reperfusion injury in brain. 15) Besides, activation of opioid receptors has also been implicated in cardioprotective eŠect of remote ischaemic preconditioning.…”

Section: Introductionmentioning

confidence: 99%

Possible Involvement of Insulin, Endogenous Opioids and Calcitonin Gene Related Peptide in Remote Ischaemic Preconditioning of Brain

2007

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“…Amylin has been shown to be raised in rat intestinal ischaemic injury, 22 and may have a biologic role in sepsis. 9 Future research in the role of amylin in necrotising enterocolitis and sepsis in the neonatal population may benefit from normal values established by our study.…”

Section: Discussionmentioning

confidence: 99%

Amylin peptide levels are raised in infants of diabetic mothers

Kairamkonda

Deorukhkar²,

Coombs³

et al. 2005

Archives of Disease in Childhood

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Background: Amylin is a novel 37 amino acid peptide hormone that is co-secreted with insulin from the pancreas in response to food intake. As a potent inhibitor of gastric emptying it plays an important role in the control of carbohydrate absorption. Feed intolerance is common in infants of diabetic mothers (IDM). Aims: To establish a normal range of amylin levels in healthy neonates, and to determine whether serum amylin levels are raised in IDM. Methods: A serial sample of 221 infants >28 weeks gestation was enrolled prior to delivery over a 12 month period. Blood samples collected immediately after birth (umbilical cord), and at the routine Guthrie test were analysed for amylin and insulin levels. Results: Amylin levels in umbilical cord (n = 181) and Guthrie samples (n = 33) of healthy infants were 5.7 (3.0-9.1) and 6.9 (2.9-9.0) pmol/l respectively. IDM had significantly raised amylin levels in both cord (n = 31; 32.7 pmol/l, 25.9-48.1) and Guthrie samples (n = 8; 18.1 pmol/l, 15.3-23.6). Amylin correlated positively with insulin (n = 42; r = 0.67; 95% CI 0.4 to 0.81), birth weight (r = 0.22; 95% CI 0.08 to 0.36), and gestation (r = 0.18; 95% CI 0.03 to 0.32). Umbilical cord venous amylin levels showed agreement with arterial cord amylin levels (n = 34, mean bias 20.2, 95% CI 3.1 to 23.6). Conclusions: Amylin levels are significantly increased in the umbilical cord and Guthrie blood samples in IDM.

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“…Amylin is raised in infants of diabetic mothers, and may be affected by intestinal ischaemic injury and acute inflammatory conditions,16 31 – 36 influencing our exclusion criteria. Inflammatory markers such as C-reactive protein, white cell count and neutrophil count were comparable between the groups, and therefore not responsible for the observed difference in amylin concentration.…”

Section: Discussionmentioning

confidence: 99%