scholarly journals Sporadic Pancreatic Cancer: Glucose Homeostasis and Pancreatogenic Type 3 Diabetes

2018 ◽  
Author(s):  
Jan Škrha ◽  
Přemysl Frič ◽  
Petr Bušek ◽  
Pavel Škrha ◽  
Aleksi Šedo
Keyword(s):  
Pancreatic Cancer ◽  
Glucose Homeostasis ◽  
Type 3 Diabetes ◽  
Type 3 ◽  
Sporadic Pancreatic Cancer

scholarly journals Pin1 Modulation in Physiological Status and Neurodegeneration. Any Contribution to the Pathogenesis of Type 3 Diabetes?

2018 ◽  
Vol 19 (8) ◽  
pp. 2319 ◽  
Author(s):  
Marzia Bianchi ◽  
Melania Manco
Keyword(s):  
Cancer Progression ◽  
Glucose Homeostasis ◽  
Neuronal Degeneration ◽  
Premature Aging ◽  
In Vivo Studies ◽  
Physiological Status ◽  
Type 3 Diabetes ◽  
Type 3

Prolyl isomerases (Peptidylprolyl isomerase, PPIases) are enzymes that catalyze the isomerization between the cis/trans Pro conformations. Three subclasses belong to the class: FKBP (FK506 binding protein family), Cyclophilin and Parvulin family (Pin1 and Par14). Among Prolyl isomerases, Pin1 presents as distinctive feature, the ability of binding to the motif pSer/pThr-Pro that is phosphorylated by kinases. Modulation of Pin1 is implicated in cellular processes such as mitosis, differentiation and metabolism: The enzyme is dysregulated in many diverse pathological conditions, i.e., cancer progression, neurodegenerative (i.e., Alzheimer’s diseases, AD) and metabolic disorders (i.e., type 2 diabetes, T2D). Indeed, Pin1 KO mice develop a complex phenotype of premature aging, cognitive impairment in elderly mice and neuronal degeneration resembling that of the AD in humans. In addition, since the molecule modulates glucose homeostasis in the brain and peripherally, Pin1 KO mice are resistant to diet-induced obesity, insulin resistance, peripheral glucose intolerance and diabetic vascular dysfunction. In this review, we revise first critically the role of Pin1 in neuronal development and differentiation and then focus on the in vivo studies that demonstrate its pivotal role in neurodegenerative processes and glucose homeostasis. We discuss evidence that enables us to speculate about the role of Pin1 as molecular link in the pathogenesis of type 3 diabetes i.e., the clinical association of dementia/AD and T2D.

P4-051: Effect of Analog P165 of APP 5-mer Peptide on Insulin Signaling Protein in Type 3 Diabetes Rats

2010 ◽  
Vol 6 ◽  
pp. e35-e35
Author(s):  
Rong Wang ◽  
Xiang Hong Meng ◽  
Zhi Wei Zhao ◽  
Zhi Juan Ji ◽  
Shu Li Sheng
Keyword(s):  
Insulin Signaling ◽  
Signaling Protein ◽  
Type 3 Diabetes ◽  
Type 3

scholarly journals Correction to: The role of melatonin in the onset and progression of type 3 diabetes

2017 ◽  
Vol 10 (1) ◽  
Author(s):  
Juhyun Song ◽  
Daniel J. Whitcomb ◽  
Byeong C. Kim
Keyword(s):  
Type 3 Diabetes ◽  
Type 3

scholarly journals The Genetic Basis of Sporadic Pancreatic Cancer

2005 ◽  
Vol 27 (1) ◽  
pp. 3-13
Author(s):  
Mario Baumgart ◽  
Ernst Heinmöller ◽  
Olaf Horstmann ◽  
Heinz Becker ◽  
B. Michael Ghadimi
Keyword(s):  
Pancreatic Cancer ◽  
Genetic Basis ◽  
Sporadic Pancreatic Cancer

13. Type 3 Diabetes

Mind Thief ◽  
2021 ◽  
pp. 119-125
Keyword(s):  
Type 3 Diabetes ◽  
Type 3

scholarly journals A133 DEVELOPMENT OF TYPE 3 ACHALASIA WITH DISTANT PANCREATIC MALIGNANCY

2020 ◽  
Vol 3 (Supplement_1) ◽  
pp. 153-155
Author(s):  
K Leung ◽  
F Habal ◽  
M Alrukaibi ◽  
L W Liu
Keyword(s):  
Pancreatic Cancer ◽  
Bile Duct ◽  
Common Bile Duct ◽  
Enteric Neurons ◽  
Thoracic Esophagus ◽  
Residual Pressure ◽  
Type I ◽  
Duodenal Stent ◽  
History Of ◽  
Type 3

Abstract Background Pseudoachalasia is often caused by malignant involvement at the gastroesophageal junction (GEJ) leading to dysphagia. Aims We describe a case of type 3 achalasia presenting in a woman with metastatic pancreatic cancer with no direct involvement at the GEJ, fundus or cardia. Methods A case report and literature review were performed. Results A 53-year-old woman presented with a 2-month-history of progressive abdominal pain, nausea and vomiting with a 30-pound weight loss. She had a remote history of breast cancer in remission after surgery and chemoradiation. On presentation, she denied chest pain, reflux, dysphagia or odynophagia. Abdominal exam revealed focal epigastric tenderness and jaundice. Abdominal CT showed a 6.7 x 5.8 cm conglomerate mass involving the hepatic hilum, pancreatic head, duodenum, common bile duct, and portal vein with gastric outlet and biliary obstruction. This mass was confirmed to be a pancreatic adenocarcinoma on pathology. She then underwent nasogastric tube decompression. Initial esophagogastroduodenoscopy (EGD) confirmed a stenotic area at the distal duodenal cap. A duodenal stent and common bile duct stent were placed during a second EGD. The esophagus and GEJ were unremarkable on both endoscopic exams. She was started on chemotherapy with gemcitabine and abraxane. Two weeks after her stent placement, she rapidly developed severe retrosternal squeezing discomfort and choking occurring with swallowing. CT chest and abdomen were negative for any intrathoracic and diaphragmatic involvement with stability of the mass. A barium swallow study demonstrated tertiary contractions in the thoracic esophagus with marshmallow hold-up in the distal esophagus. She then underwent a high-resolution esophageal manometry study that demonstrated an elevation of integrated residual pressure (IRP) of the lower esophageal sphincter (LES) and absence of peristalsis, with the distal 2/3rds of the esophagus showing a simultaneous and prolonged pressure front consistent with type 3 achalasia, Chicago classification v3.0 [Figure 1]. All contractions had a distal contractile integral (DCI) of >8000 mmHg-cm-s. She experienced significant symptom improvement with pinaverium bromide, a gut-specific calcium channel antagonist. A review of the literature revealed that there have been 4 English-language cases published on pseudoachalasia associated with pancreatic cancer, with all cases describing direct infiltration of pancreatic cancer in the GEJ, cardia or fundus with manometric features of type I achalasia. Conclusions We report the first case of type 3 achalasia with no evidence of direct malignant infiltration at the GEJ on radiographic and endoscopic evaluations. Possible mechanisms to explain this phenomenon include paraneoplastic antibody-mediated impairment of enteric neurons that decrease nitric oxide availability, or microscopic disease involvement at the GEJ. Funding Agencies None

scholarly journals Is Alzheimer's disease a Type 3 Diabetes? A critical appraisal

2017 ◽  
Vol 1863 (5) ◽  
pp. 1078-1089 ◽  
Author(s):  
Ramesh Kandimalla ◽  
Vani Thirumala ◽  
P. Hemachandra Reddy
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Critical Appraisal ◽  
Type 3 Diabetes ◽  
Type 3
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