Liver proteomics analysis reveals abnormal metabolism of bile acid and arachidonic acid in Chinese hamsters with type 2 diabetes mellitus

2021 ◽  
Vol 239 ◽  
pp. 104186
Author(s):  
Wentao Wang ◽  
Zeya Shi ◽  
Ruihu Zhang ◽  
Jingjing Yu ◽  
Chenyang Wang ◽  
...  
2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 747-747
Author(s):  
Undurti Das

Abstract Objectives To evaluate the effect of arachidonic acid (AA) in the pathobiology of chemical-induced type 1 and type 2 diabetes mellitus in experimental animals. Methods In vitro studies were performed using RIN 5F cells and animal studies in 3–4 week old Wistar rats. Alloxan and streptozotocin (STZ) were used to induce type 1 diabetes and STZ employed to induce type 2 diabetes mellitus. RIN5F cell proliferation was measured using MTT assay. Establishment of alloxan and STZ-induced diabetes in animals was confirmed by measuring plasma glucose levels. Plasma insulin, IL-6, TNF levels were measured by ELISA. Expression of cyclo-oxygenase-2, lipoxiygenase, NF-kB and IkB genes was performed in pancreatic and adipose tissues. Results Alloxan and STZ-induced cytotoxicity to RIN5F cells was inhibited by arachidonic acid that was not blocked by both COX and LOX enzymes. Alloxan and STZ-induced type 1 diabetes mellitus and STZ-induced type 2 diabetes was prevented by arachidonic acid treatment. Plasma levels of glucose, insulin, IL-6 and TNF and expressions of NF-kB, IkB, COX-2, LOX in pancrreatic and adipose tissues and lipocalin-2 in adipose tissue were restored to normal by arachidonic acid treatment. AA treatment enhanced plasma lipoxin A4 (LXA4) levels. LXA4 also prevented both type 1 and type 2 diabetes induction by STZ. Conclusions AA prevented the development of both type 1 and type 2 diabetes mellitus in Wistar rats and protected pancreatic beta cells form the cytotoxicity of alloxan and STZ. AA showed strong anti-inflammatory actions. AA seems to bring about its anti-inflammatory and anti-diabetic actions by enhancing LXA4 formation. Funding Sources None.


2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Marina A. Berkovskaya ◽  
Yulia P. Sych ◽  
Olesya Yu. Gurova ◽  
Valentin V. Fadeev

Bariatric surgery is among successful methods of obesity treatment, with effects going beyond weight reduction alone, but rather involving improved glucose tolerance, along with control or remission of the type 2 diabetes mellitus. The precise mechanisms causing metabolic effects of bariatric surgery are not fully elucidated, even though substantial evidence suggest that they include changes in the gut microbiota, bile acid homeostasis, and the close interactions of these factors. Intestinal microflora is directly involved in the energy metabolism of a host human. Obesity and type 2 diabetes mellitus are associated with certain changes in the species composition and diversity of intestinal microflora, which are considered important factors in the development and progression of these ailments. Bariatric surgery leads to significant and persistent changes in the composition of the intestinal microbiota, often bringing it closer to the characteristics of the microbiota of an average person with a normal weight. An important role in implementing the metabolic effects of bariatric surgery, primarily in the improvement of glucose metabolism, belongs to postoperative changes in homeostasis of bile acids. These changes imply close metabolism. Moreover, changes in the bile acid metabolism after bariatric surgery affect the microbiota of the host. Further study of these relationships would clarify the mechanisms underlying metabolic surgery, make it more predictable, targeted and controlled, as well as open new therapeutic targets in the treatment of obesity and associated conditions.


Sign in / Sign up

Export Citation Format

Share Document