Effects of gastrointestinal polypeptides on hormone content of endocrine pancreas in the rat

1980 ◽  
Vol 238 (6) ◽  
pp. G526-G530 ◽  
Author(s):  
T. Yamada ◽  
T. E. Solomon ◽  
H. Petersen ◽  
S. R. Levin ◽  
K. Lewin ◽  
...  

Although trophic actions of gastrointestinal peptides on exocrine pancreas have been shown, little is known regarding their effects in endocrine pancreas. Therefore, we measured the contents of somatostatin-like immunoreactivity (SLI), insulin and glucagon, in pancreatic extracts from rats that had been treated three times a day for 10 days with saline; 1 microgram/kg caerulein; 5, 25, and 100 microgram/kg secretin; 1 microgram/kg caerulein plus 5, 25, and 100 microgram/kg secretin; 25 microgram/kg pancreatic polypeptide; 15 microgram/kg glicentin; or 15 microgram/kg gastric-inhibitory polypeptide. Pancreatic SLI content was significantly increased in rats treated with glicentin and caerulein plus secretin at the two higher doses. No difference was noted between the control and the caerulein plus 100 microgram/kg secretin groups in delta-cell number per islet when examined by the immunoperoxidase technique. These data suggest that because of their effect on SLI content gastrointestinal polypeptides may modulate pancreatic endocrine function.

2021 ◽  
Vol 12 ◽  
Author(s):  
Eleonóra Gál ◽  
Jurij Dolenšek ◽  
Andraž Stožer ◽  
László Czakó ◽  
Attila Ébert ◽  
...  

Anatomical proximity and functional correlations between the exocrine and endocrine pancreas warrant reciprocal effects between the two parts. Inflammatory diseases of the exocrine pancreas, such as acute or chronic pancreatitis, or the presence of cystic fibrosis disrupt endocrine function, resulting in diabetes of the exocrine pancreas. Although novel mechanisms are being increasingly identified, the intra- and intercellular pathways regulating exocrine–endocrine interactions are still not fully understood, making the development of new and more effective therapies difficult. Therefore, this review sought to accumulate current knowledge regarding the pathogenesis of diabetes in acute and chronic pancreatitis, as well as cystic fibrosis.


1981 ◽  
Vol 15 (4) ◽  
pp. 237-241 ◽  
Author(s):  
Franco Meschi ◽  
Berardo di Natale ◽  
Gian Filippo Rondanini ◽  
Cornelio Uderzo ◽  
Momcilo Jankovic ◽  
...  

2008 ◽  
Vol 197 (2) ◽  
pp. 251-263 ◽  
Author(s):  
J D Bailey ◽  
J G Berardinelli ◽  
T E Rocke ◽  
R A Bessen

Prion diseases are fatal neurodegenerative diseases that can induce endocrinopathies. The basis of altered endocrine function in prion diseases is not well understood, and the purpose of this study was to investigate the spatiotemporal relationship between energy homeostasis and prion infection in hamsters inoculated with either the 139H strain of scrapie agent, which induces preclinical weight gain, or the HY strain of transmissible mink encephalopathy (TME), which induces clinical weight loss. Temporal changes in body weight, feed, and water intake were measured as well as both non-fasted and fasted concentrations of serum glucose, insulin, glucagon, β-ketones, and leptin. In 139H scrapie-infected hamsters, polydipsia, hyperphagia, non-fasted hyperinsulinemia with hyperglycemia, and fasted hyperleptinemia were found at preclinical stages and are consistent with an anabolic syndrome that has similarities to type II diabetes mellitus and/or metabolic syndrome X. In HY TME-infected hamsters, hypodipsia, hypersecretion of glucagon (in both non-fasted and fasted states), increased fasted β-ketones, fasted hypoglycemia, and suppressed non-fasted leptin concentrations were found while feed intake was normal. These findings suggest a severe catabolic syndrome in HY TME infection mediated by chronic increases in glucagon secretion. In both models, alterations of pancreatic endocrine function were not associated with PrPSc deposition in the pancreas. The results indicate that prominent endocrinopathy underlies alterations in body weight, pancreatic endocrine function, and intake of food. The prion-induced alterations of energy homeostasis in 139H scrapie- or HY TME-infected hamsters could occur within areas of the hypothalamus that control food satiety and/or within autonomic centers that provide neural outflow to the pancreas.


1983 ◽  
Vol 36 (3) ◽  
pp. 246-251 ◽  
Author(s):  
MICHAEL BEWICK ◽  
BRENDA H. R. MILLER ◽  
FREDERICK J. COMPTON ◽  
MIGUEL GONZALES-CARILLO ◽  
ALEXANDER AVGOUSTIS ◽  
...  

1981 ◽  
Vol 53 (1) ◽  
pp. 16-20 ◽  
Author(s):  
V. SCHUSDZIARRA ◽  
G. DANGEL ◽  
M. KLIER ◽  
I. HENRICHS ◽  
E. F. PFEIFFER

HPB Surgery ◽  
1990 ◽  
Vol 2 (1) ◽  
pp. 29-39 ◽  
Author(s):  
Bo Ahrén ◽  
Karl-G. Tranberg ◽  
Åke Andrén-Sandberg ◽  
Stig Bengmark

This paper presents a 2-year series of 26 consecutive pancreatectomies for periampullary cancer where the pancreatic tail was closed with a stapler in order to avoid complications related to a pancreatico-digestive anastomosis. The follow-up period was 14 months or more. Seven patients developed operative complications. Pancreatic fistulas developed in 3 patients. The fistulas closed spontaneously in 2 of the patients after 2-4 months, lntraabdominal abscesses developed in 4 patients and required surgical drainage. In 1 of these patients, the abscess eroded a large vessel with a fatal outcome resulting in an operative mortality rate of 3.8%. A transient postoperative gastric stasis was observed in seven patients. Postoperative hospital median stay was 27 days (range 10–83 days). Eighteeen patients have died after 4–30 months in recurrent disease and seven patients are alive after a follow-up period of 15–29 months. Pancreatic endocrine function seemed well preserved; diabetes mellitus has developed in only one patient. In conclusion, it appears that subtotal pancreatectomy with closure of the pancreatic remnant with staples gives a low morbidity and mortality. Although the conclusion should be tempered by the small number of patients, the results justify continued evaluation of this technique with long-term follow-up.


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