scholarly journals Obesity causes PGC-1α deficiency in exocrine pancreas leading to IL-6 upregulation via NF-κB in acute pancreatitis

2021 ◽  
Vol 165 ◽  
pp. 36
Author(s):  
Sergio Rius-Pérez ◽  
Salvador Pérez ◽  
Pablo Martí-Andrés ◽  
Isabela Finamor ◽  
Ignacio Prieto ◽  
...  
Diabetes Care ◽  
2001 ◽  
Vol 24 (12) ◽  
pp. 2156-2157 ◽  
Author(s):  
T. Taniguchi ◽  
J. Tanaka ◽  
S. Seko ◽  
K. Okazaki ◽  
M. Okamoto

2012 ◽  
Vol 303 (9) ◽  
pp. G993-G1003 ◽  
Author(s):  
Anna S. Gukovskaya ◽  
Ilya Gukovsky

Acute pancreatitis is an inflammatory disease of the exocrine pancreas that carries considerable morbidity and mortality; its pathophysiology remains poorly understood. Recent findings from experimental models and genetically altered mice summarized in this review reveal that autophagy, the principal cellular degradative pathway, is impaired in pancreatitis and that one cause of autophagy impairment is defective function of lysosomes. We propose that the lysosomal/autophagic dysfunction is a key initiating event in pancreatitis and a converging point of multiple deranged pathways. There is strong evidence supporting this hypothesis. Investigation of autophagy in pancreatitis has just started, and many questions about the “upstream” mechanisms mediating the lysosomal/autophagic dysfunction and the “downstream” links to pancreatitis pathologies need to be explored. Answers to these questions should provide insight into novel molecular targets and therapeutic strategies for treatment of pancreatitis.


2020 ◽  
Vol 93 (8) ◽  
pp. 149-157
Author(s):  
L. Horalskyi ◽  
◽  
O. Kovalchuk ◽  
I. Sokulskyi ◽  
◽  
...  

From among a great number of digestive system diseases in domestic animals there is pancreatitis which is caused by an early zymogenesis in the acinar cells. The problem of studying the structural organization of a pancreata in sick cats is topical because of a progressive spreading of pancreatitis in domestic animals. Thus, the purpose of the research was to study out the morphological changes of cats pancreata under acute pancreatitis. Working with vertebrate animals we were guided by “European Convention for the Protection of Vertebtate Animals used for Experimental and other Scientific Purposes” (Strasbourg, 1986). The results of the histological examination of cats pancreata under acute pancreatitis show some pathological changes both in endocrine and exocrine pancreas. Such changes were manifested in necrosis of exocrine pancreatitis as well as in spreading and swelling of acinar space, that testified to the infancy of an inflammatory process. Some dystrophic changes, followed by karyolysis, were found in the focus of tissue nicrosis. Pancreatocyte cytoplasm was cloudy, its basal and apical zones were obscure, clearly defined interstitial tissue swelling was found between the particles and unequal swelling was found inside the particles. Intercellular space was exaggerated. Morphometrically in a group of sick animals was detected an increase in specific weihgt of stromal component (р<0,05),which equalled 22,44±0,24 %, in a control group it equalled 17,78±0,15 %. Some hemorrhage and distrophicvally changed hormone- active cells as well as nonregular distribution of cells were detected under a histological examination of Langerhans islets. In most islets the cells had swelled vacuolar cytoplasm. While analyzing the morphometric indices it was stated that the cats exocrine pancreas under acute pancreatitis was 1.12 as large and occupied 48258,05±135,07 mkm2, (97,88±0,05 %). The cats endocrine pancreas under this pathology occupied 6858,85±315,05 mkm2, (2,12±0,05 %). In cats of a control group this index equalled 6784,71±285,04 mkm2 (1,95±0,06 %). The diameter of sick cats acinus as well as of Langerhans islets equalled respectively 31,85±0,05 and 71,81±2,45 mkm, which reliably (р<0,001) was 1.13 and 1.15 as large. In clinically healhty cats these indices are 28,12±0,11; 70,20±2,48 mkm.


1973 ◽  
Vol 29 (03) ◽  
pp. 603-609
Author(s):  
A Gabryelewicz ◽  
J Prokopowicz ◽  
W Szalaj ◽  
N Wolosowicz ◽  
W Laszewicz ◽  
...  

SummaryThe coagulation and fibrinolytic systems have been investigated in the dogs treated intravenously with secretin, pancreozymin and CCK.There was significant shortening of plastic and glass clotting times, a fall in blood platelet numbers, prolongation of the prothrombin time, and a transitory inhibition of plasma euglobulin fibrinolytic activity. The greatest changes were found after CCK.It should be stressed that the peak changes were earlier and more intense when morphine was given with the hormones.In the authors’ opinion the present findings support the supposition concerning the role of enzymatic toxemia in hemostatic disturbances seen in acute pancreatitis.


2010 ◽  
Vol 177 (6) ◽  
pp. 2827-2836 ◽  
Author(s):  
Risheng Ye ◽  
Olga A. Mareninova ◽  
Ernesto Barron ◽  
Miao Wang ◽  
David R. Hinton ◽  
...  

Autophagy ◽  
2020 ◽  
Vol 16 (11) ◽  
pp. 2084-2097 ◽  
Author(s):  
Olga A. Mareninova ◽  
Wenzhuo Jia ◽  
Sophie R. Gretler ◽  
Conner L. Holthaus ◽  
Diana D. H. Thomas ◽  
...  

Pancreatology ◽  
2014 ◽  
Vol 14 (3) ◽  
pp. S55
Author(s):  
Evelyne Kuster ◽  
Rolf Graf ◽  
François Verrey ◽  
Simone Camargo

Author(s):  
Maxim S Petrov

While most people with diabetes have type 2 disease, a non-negligible minority develops a secondary diabetes. Post-pancreatitis diabetes mellitus (PPDM) is an exemplar secondary diabetes that represents a sequela of pancreatitis - the most common disease of the exocrine pancreas. Although this type of diabetes has been known as a clinical entity since the late 19th century, early 21st century high-quality epidemiological, clinical, and translational studies from around the world have amassed a sizeable body of knowledge that have led to a renewed understanding of PPDM. People have at least two-fold higher lifetime risk of developing diabetes after an attack of pancreatitis than those in the general population without history of diseases of the exocrine pancreas. PPDM is caused by acute pancreatitis (including non-necrotising pancreatitis, which constitutes the majority of acute pancreatitis) in four-fifth of cases and chronic pancreatitis in one-fifth of cases. Moreover, the frequency of incident diabetes is not considerably lower after acute pancreatitis than after chronic pancreatitis. Recurrent attacks of pancreatitis and exocrine pancreatic dysfunction portend high risk for PPDM, but are not mandatory for its development. Further, young- or middle-aged non-obese men have an increased risk of developing PPDM. In comparison with type 2 diabetes, PPDM is characterised by poorer glycaemic control, higher risk of developing cancer (in particular, pancreatic cancer), younger age at death, and higher risk of mortality. Metformin monotherapy is recommended as first-line therapy for PPDM. Appropriate screening of individuals after an attack of pancreatitis, correct identification of PPDM, and apposite management is crucial with a view to improving the outcomes of this secondary but not inappreciable disease.


1984 ◽  
Vol 246 (3) ◽  
pp. G274-G280 ◽  
Author(s):  
B. E. Stabile ◽  
M. Borzatta ◽  
R. S. Stubbs ◽  
H. T. Debas

We compared the responses of the canine exocrine pancreas to intraduodenal versus intravenous administration of mixed amino acids, fat emulsion, and glucose. Graded doses of amino acid mixture and of fat emulsion gave graded responses in volume, protein, and bicarbonate when administered intraduodenally. In contrast, the same doses of the amino acid mixture and fat emulsion administered by central intravenous infusion caused no significant pancreatic secretion of volume, protein, or bicarbonate. Graded doses of glucose caused no statistically significant pancreatic secretion whether they were given intraduodenally or intravenously. We conclude, contrary to a previously published observation, that amino acids and fats given parenterally do not stimulate pancreatic secretion. As a corollary, it is reasonable to assume that the pancreas is not stimulated during total parenteral nutrition with acute pancreatitis or a pancreatic fistula.


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