This study is based on the investigation by light and electron microscopy of hepatic biopsies from 14 rats rendered diabetic by streptozotocin and treated by portal embolization of islets of Langerhans. Macroscopically, voluminous projecting cysts were observed, sometimes occupying a whole lobe. By light microscopy, the cysts were lined with canalicular-type epithelium. Ultrastructural studies confirmed the canalicular nature of these cells and cilia were frequently observed. The presence of identical cysts in rats rendered diabetic by streptozotocin but not treated by embolization proves that this product is the agent responsible for the induction of this adenomatosis.

Download full-text PDF

Source

Publication Analysis

Top Keywords

rendered diabetic
12
diabetic streptozotocin
12
streptozotocin treated
12
islets langerhans
8
rats rendered
8
[multiple hepatic
4
cysts
4
hepatic cysts
4
cysts rat
4
rat rendered
4

Similar Publications

Obesity and type 2 diabetes (T2D) are strongly linked to abnormal adipocyte metabolism and adipose tissue (AT) dysfunction. However, existing adipose tissue models have limitations, particularly in the stable culture of fat cells that maintain physiologically relevant phenotypes, hindering a deeper understanding of adipocyte biology and the molecular mechanisms behind differentiation. Current model systems fail to fully replicate in vivo metabolism, posing challenges in adipose research.

View Article and Find Full Text PDF

The Impact of Modifiable Risk Factors on the Endothelial Cell Methylome and Cardiovascular Disease Development.

Front Biosci (Landmark Ed)

January 2025

School of Cardiovascular and Metabolic Medicine & Sciences, British Heart Foundation Centre of Research Excellence, King's College London, SE5 9NU London, UK.

Cardiovascular disease (CVD) is the most prevalent cause of mortality and morbidity in the Western world. A common underlying hallmark of CVD is the plaque-associated arterial thickening, termed atherosclerosis. Although the molecular mechanisms underlying the aetiology of atherosclerosis remain unknown, it is clear that both its development and progression are associated with significant changes in the pattern of DNA methylation within the vascular cell wall.

View Article and Find Full Text PDF

Diabetes is a metabolic disorder caused by the body's inability to produce or use insulin. Considering the figures projected by the World Health Organization, research on insulin therapy is crucial. Hence, we present a soft biointerface based on a thiol-yne poly(ethylene glycol) (PEG) click-hydrogel as an advanced treatment option to administrate insulin.

View Article and Find Full Text PDF

Here, we retrospectively evaluated the informational yield of 338 post-reperfusion kidney transplant biopsies (including 95 living donations) assessed according to BANFF for the histological characteristics interstitial fibrosis and tubular atrophy (IF/TA), glomerulosclerosis, arteriosclerosis, and acute tubular injury (ATI). Associations with delayed graft function (DGF) and death-censored graft survival were explored through Cox-regression analyses. The maximum follow-up time was 11.

View Article and Find Full Text PDF

Transcriptional regulation of Rankl by Txnip-Ecd in aging and diabetic related osteoporosis.

J Adv Res

January 2025

Shanghai Key Laboratory of Orthopedic Implants, Department of Orthopedic Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China. Electronic address:

Introduction: Bone homeostasis between osteoclast bone resorption and osteoblastic bone formation is tightly regulated by a series of factors such as the receptor activator of nuclear factor-κB ligand (RANKL). Denosumab that neutralizes RANKL is effective and widely applied in the treatment of postmenopausal osteoporosis. However, factors that participated in the RANKL-related bone remodeling process in primary and secondary osteoporosis are less known.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!