Effects of a Ganoderma atrum polysaccharide against pancreatic damage in streptozotocin-induced diabetic mice

2019 ◽  
Vol 10 (11) ◽  
pp. 7227-7238 ◽  
Author(s):  
Lu Li ◽  
Rui-Cheng Li ◽  
Ye-Hao Song ◽  
Wen-Ying Wu ◽  
Shu-Hua Yin ◽  
...  

This study aimed at exploring the role of a Ganoderma atrum polysaccharide (PSG-1) in pancreatic damage in streptozotocin (STZ)-induced type 1 diabetes mellitus (T1DM) mice.

2020 ◽  
Vol 9 (2) ◽  
pp. 57-64
Author(s):  
Harem Othman Smail

The main aims of this review were to understand the roles of gene therapy in the treatment and prevention of type 1 diabetes mellitus and I will discuss a brief history, approaches, vector types with the future of diabetes following clinical use. Type 1 diabetes mellitus is a metabolic condition that is identified by insufficient insulin development due to pancreatic damage to beta cells. Control, long life, and diagnosis of these metabolic disorders have become vital sources for many scientists and researchers. After 2000, the latest approaches to molecular medicine were introduced as one of the possible therapeutic options for diabetes type 1 diagnosis. Many genes have been reported as a clinical trial so that damaged genes can be treated and three main approaches shown about 50 years ago are islet transplantation, β cell regeneration, and insulin gene therapy to cure and prevent diabetes type. Treating diabetes through gene therapy can promise children and adolescents, but more clinical applications are needed to recognize it as a permanent route.


2016 ◽  
Vol 174 (4) ◽  
pp. R127-R138 ◽  
Author(s):  
F S Hough ◽  
D D Pierroz ◽  
C Cooper ◽  
S L Ferrari ◽  
_ _

Subjects with type 1 diabetes mellitus (T1DM) have decreased bone mineral density and an up to sixfold increase in fracture risk. Yet bone fragility is not commonly regarded as another unique complication of diabetes. Both animals with experimentally induced insulin deficiency syndromes and patients with T1DM have impaired osteoblastic bone formation, with or without increased bone resorption. Insulin/IGF1 deficiency appears to be a major pathogenetic mechanism involved, along with glucose toxicity, marrow adiposity, inflammation, adipokine and other metabolic alterations that may all play a role on altering bone turnover. In turn, increasing physical activity in children with diabetes as well as good glycaemic control appears to provide some improvement of bone parameters, although robust clinical studies are still lacking. In this context, the role of osteoporosis drugs remains unknown.


2018 ◽  
Vol 56 (2) ◽  
pp. 151-161 ◽  
Author(s):  
Rosario Caruso ◽  
Paola Rebora ◽  
Federica Dellafiore ◽  
Diletta Fabrizi ◽  
Barbara Riegel ◽  
...  

2000 ◽  
Vol 50 ◽  
pp. 417
Author(s):  
Kisho Kobayashi ◽  
Shin Amemiya ◽  
Koji Kobayashi ◽  
Mie Mochizuki ◽  
Tomoaki Sano ◽  
...  

2013 ◽  
Vol 57 (9) ◽  
pp. 667-676 ◽  
Author(s):  
Ana Paula Bouças ◽  
Fernanda dos Santos de Oliveira ◽  
Luis Henrique Canani ◽  
Daisy Crispim

Type 1 diabetes mellitus (T1DM) is a chronic, progressive, autoimmune disease characterized by metabolic decompensation frequently leading to dehydration and ketoacidosis. Viral pathogens seem to play a major role in triggering the autoimmune destruction that leads to the development of T1DM. Among several viral strains investigated so far, enteroviruses have been consistently associated with T1DM in humans. One of the mediators of viral damage is the double-stranded RNA (dsRNA) generated during replication and transcription of viral RNA and DNA. The IFIH1 gene encodes a cytoplasmic receptor of the pattern-recognition receptors (PRRs) family that recognizes dsRNA, playing a role in the innate immune response triggered by viral infection. Binding of dsRNA to this PRR triggers the release of proinflammatory cytokines, such as interferons (IFNs), which exhibit potent antiviral activity, protecting uninfected cells and inducing apoptosis of infected cells. The IFIH1 gene appears to play a major role in the development of some autoimmune diseases, and it is, therefore, a candidate gene for T1DM. Within this context, the objective of the present review was to address the role of IFIH1 in the development of T1DM.


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