Limits...
Obestatin Accelerates the Recovery in the Course of Ischemia/Reperfusion-Induced Acute Pancreatitis in Rats.

Bukowczan J, Warzecha Z, Ceranowicz P, Kuśnierz-Cabala B, Tomaszewska R - PLoS ONE (2015)

Bottom Line: Several previous studies have shown that obestatin exhibits protective and regenerative effects in some organs including the stomach, kidney, and the brain.Structural changes were accompanied by biochemical and functional improvements manifested by accelerated normalization of interleukin-1β level and activity of myeloperoxidase and lipase, attenuation of the decrease in pancreatic DNA synthesis, and by an improvement of pancreatic blood flow.The involved mechanisms are likely to be multifactorial, and are mediated, at least in part, by anti-inflammatory properties of obestatin.

View Article: PubMed Central - PubMed

Affiliation: Department of Endocrinology and Diabetes Mellitus, Northumbria NHS Foundation Trust, Rake Lane, North Shields, Tyne and Wear, United Kingdom.

ABSTRACT

Objective: Several previous studies have shown that obestatin exhibits protective and regenerative effects in some organs including the stomach, kidney, and the brain. In the pancreas, pretreatment with obestatin inhibits the development of cerulein-induced acute pancreatitis, and promotes survival of pancreatic beta cells and human islets. However, no studies investigated the effect of obestatin administration following the onset of experimental acute pancreatitis.

Aim: The aim of this study was to evaluate the impact of obestatin therapy in the course of ischemia/reperfusion-induced pancreatitis. Moreover, we tested the influence of ischemia/reperfusion-induced acute pancreatitis and administration of obestatin on daily food intake and pancreatic exocrine secretion.

Methods: Acute pancreatitis was induced by pancreatic ischemia followed by reperfusion of the pancreas. Obestatin (8 nmol/kg/dose) was administered intraperitoneally twice a day, starting 24 hours after the beginning of reperfusion. The effect of obestatin in the course of necrotizing pancreatitis was assessed between 2 and 14 days, and included histological, functional, and biochemical analyses. Secretory studies were performed on the third day after sham-operation or induction of acute pancreatitis in conscious rats equipped with chronic pancreatic fistula.

Results: Treatment with obestatin ameliorated morphological signs of pancreatic damage including edema, vacuolization of acinar cells, hemorrhages, acinar necrosis, and leukocyte infiltration of the gland, and led to earlier pancreatic regeneration. Structural changes were accompanied by biochemical and functional improvements manifested by accelerated normalization of interleukin-1β level and activity of myeloperoxidase and lipase, attenuation of the decrease in pancreatic DNA synthesis, and by an improvement of pancreatic blood flow. Induction of acute pancreatitis by pancreatic ischemia followed by reperfusion significantly decreased daily food intake and pancreatic exocrine secretion. Administration of obestatin at doses used was without significant effect with regard to daily food intake or pancreatic exocrine secretion in sham-operated rats, as well as in rats with acute pancreatitis. On the other hand, obestatin abolished a statistical significance of difference in food intake between animals with AP and control animals without pancreatic fistula and induction of AP.

Conclusion: Treatment with the exogenous obestatin reduces severity of ischemia/reperfusion-induced acute pancreatitis and accelerates recovery in this disease. The involved mechanisms are likely to be multifactorial, and are mediated, at least in part, by anti-inflammatory properties of obestatin.

No MeSH data available.


Related in: MedlinePlus

Volume of pancreatic secretion and amylase output under basal conditions in conscious rats without or with ischemia/reperfusion-induced acute pancreatitis and pretreated with saline or obestatin.Key: NaCl = rats pretreated with saline; Obestatin = rats pretreated with obestatin given twice a day i.p. at the dose of 8 nmol/kg/dose; AP = ischemia/reperfusion-induced acute pancreatitis. Values are expressed as mean ± SEM. aP<0.05 compared to control saline-treated rats without induction of AP; bP<0.05 compared to obestatin-treated rats without induction of AP.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4520493&req=5

pone.0134380.g008: Volume of pancreatic secretion and amylase output under basal conditions in conscious rats without or with ischemia/reperfusion-induced acute pancreatitis and pretreated with saline or obestatin.Key: NaCl = rats pretreated with saline; Obestatin = rats pretreated with obestatin given twice a day i.p. at the dose of 8 nmol/kg/dose; AP = ischemia/reperfusion-induced acute pancreatitis. Values are expressed as mean ± SEM. aP<0.05 compared to control saline-treated rats without induction of AP; bP<0.05 compared to obestatin-treated rats without induction of AP.

Mentions: In conscious control rats with chronic pancreatic fistula without induction of AP, a basal volume of pancreatic secretion and amylase output were 510 ± 46μl/30min and 2378 ± 215 U/30min, respectively (Fig 8). Induction of AP significantly reduced a volume of basal pancreatic secretion and amylase output by around 60 and 66%, respectively. Pretreatment with obestatin tended to increase, especially in rats with AP, a basal volume of pancreatic secretion and amylase output, but this effect was statistically insignificant (Fig 8).


Obestatin Accelerates the Recovery in the Course of Ischemia/Reperfusion-Induced Acute Pancreatitis in Rats.

Bukowczan J, Warzecha Z, Ceranowicz P, Kuśnierz-Cabala B, Tomaszewska R - PLoS ONE (2015)

Volume of pancreatic secretion and amylase output under basal conditions in conscious rats without or with ischemia/reperfusion-induced acute pancreatitis and pretreated with saline or obestatin.Key: NaCl = rats pretreated with saline; Obestatin = rats pretreated with obestatin given twice a day i.p. at the dose of 8 nmol/kg/dose; AP = ischemia/reperfusion-induced acute pancreatitis. Values are expressed as mean ± SEM. aP<0.05 compared to control saline-treated rats without induction of AP; bP<0.05 compared to obestatin-treated rats without induction of AP.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4520493&req=5

pone.0134380.g008: Volume of pancreatic secretion and amylase output under basal conditions in conscious rats without or with ischemia/reperfusion-induced acute pancreatitis and pretreated with saline or obestatin.Key: NaCl = rats pretreated with saline; Obestatin = rats pretreated with obestatin given twice a day i.p. at the dose of 8 nmol/kg/dose; AP = ischemia/reperfusion-induced acute pancreatitis. Values are expressed as mean ± SEM. aP<0.05 compared to control saline-treated rats without induction of AP; bP<0.05 compared to obestatin-treated rats without induction of AP.
Mentions: In conscious control rats with chronic pancreatic fistula without induction of AP, a basal volume of pancreatic secretion and amylase output were 510 ± 46μl/30min and 2378 ± 215 U/30min, respectively (Fig 8). Induction of AP significantly reduced a volume of basal pancreatic secretion and amylase output by around 60 and 66%, respectively. Pretreatment with obestatin tended to increase, especially in rats with AP, a basal volume of pancreatic secretion and amylase output, but this effect was statistically insignificant (Fig 8).

Bottom Line: Several previous studies have shown that obestatin exhibits protective and regenerative effects in some organs including the stomach, kidney, and the brain.Structural changes were accompanied by biochemical and functional improvements manifested by accelerated normalization of interleukin-1β level and activity of myeloperoxidase and lipase, attenuation of the decrease in pancreatic DNA synthesis, and by an improvement of pancreatic blood flow.The involved mechanisms are likely to be multifactorial, and are mediated, at least in part, by anti-inflammatory properties of obestatin.

View Article: PubMed Central - PubMed

Affiliation: Department of Endocrinology and Diabetes Mellitus, Northumbria NHS Foundation Trust, Rake Lane, North Shields, Tyne and Wear, United Kingdom.

ABSTRACT

Objective: Several previous studies have shown that obestatin exhibits protective and regenerative effects in some organs including the stomach, kidney, and the brain. In the pancreas, pretreatment with obestatin inhibits the development of cerulein-induced acute pancreatitis, and promotes survival of pancreatic beta cells and human islets. However, no studies investigated the effect of obestatin administration following the onset of experimental acute pancreatitis.

Aim: The aim of this study was to evaluate the impact of obestatin therapy in the course of ischemia/reperfusion-induced pancreatitis. Moreover, we tested the influence of ischemia/reperfusion-induced acute pancreatitis and administration of obestatin on daily food intake and pancreatic exocrine secretion.

Methods: Acute pancreatitis was induced by pancreatic ischemia followed by reperfusion of the pancreas. Obestatin (8 nmol/kg/dose) was administered intraperitoneally twice a day, starting 24 hours after the beginning of reperfusion. The effect of obestatin in the course of necrotizing pancreatitis was assessed between 2 and 14 days, and included histological, functional, and biochemical analyses. Secretory studies were performed on the third day after sham-operation or induction of acute pancreatitis in conscious rats equipped with chronic pancreatic fistula.

Results: Treatment with obestatin ameliorated morphological signs of pancreatic damage including edema, vacuolization of acinar cells, hemorrhages, acinar necrosis, and leukocyte infiltration of the gland, and led to earlier pancreatic regeneration. Structural changes were accompanied by biochemical and functional improvements manifested by accelerated normalization of interleukin-1β level and activity of myeloperoxidase and lipase, attenuation of the decrease in pancreatic DNA synthesis, and by an improvement of pancreatic blood flow. Induction of acute pancreatitis by pancreatic ischemia followed by reperfusion significantly decreased daily food intake and pancreatic exocrine secretion. Administration of obestatin at doses used was without significant effect with regard to daily food intake or pancreatic exocrine secretion in sham-operated rats, as well as in rats with acute pancreatitis. On the other hand, obestatin abolished a statistical significance of difference in food intake between animals with AP and control animals without pancreatic fistula and induction of AP.

Conclusion: Treatment with the exogenous obestatin reduces severity of ischemia/reperfusion-induced acute pancreatitis and accelerates recovery in this disease. The involved mechanisms are likely to be multifactorial, and are mediated, at least in part, by anti-inflammatory properties of obestatin.

No MeSH data available.


Related in: MedlinePlus