Development of therapeutic options on type 2 diabetes in years: Glucagon-like peptide-1 receptor agonist’s role intreatment; from the past to future

Doğruel, Hakan; Balcı, Mustafa Kemal

doi:10.4239/wjd.v10.i8.446

Cited by 18 publications

(18 citation statements)

References 84 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…GLP-1 showed its neuroprotective effects in several previous studies. Lower GLP-1 levels were detected not only in the serum of T2DM patients but also in obesity individuals without diabetes [ 43 , 44 ]. Additionally, decreased GLP-1R levels in obese or diabetic mice with cognitive impairment in multiple tissue, including brain were observed [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

Liraglutide improved the cognitive function of diabetic mice via the receptor of advanced glycation end products down-regulation

Zhang

Chu

Zheng

et al. 2020

Aging

View full text Add to dashboard Cite

Background and aims Advanced glycation end products (AGEs) and receptor of advanced glycation end products (RAGE), are associated with cognition decline. We aim to investigate the effect of liraglutide on cognitive function in diabetic mice. Results Diabetic mice showed decreased cognitive function. Moreover, lower glucagon like peptide-1 (GLP-1) levels in plasma were detected in db/db mice. Additionally, up-regulated RAGE and down-regulated glucagon like peptide-1 (GLP-1R) levels were observed in db/db mice. However, decreased GLP-1R and increased RAGE were reversed by liraglutide. We also found decreased cellular activity in cells with AGEs. Moreover, AGEs up-regulated RAGE in PC12 and HT22 cells. However, liraglutide improved the cell activity damaged by AGEs. Although we did not discover the direct-interaction between RAGE and GLP-1R, elevated RAGE levels induced by AGEs were restored by liraglutide. Conclusion We demonstrated that the cognitive function of diabetic mice was improved by liraglutide via the down-regulation of RAGE. Methods db/db mice and db/m mice were used in this study. Liraglutide was used to remedy diabetic mice. Neurons and RAGE in hippocampus were shown by immunofluorescence. And then, PC12 cells or HT22 cells with AGEs were treated with liraglutide. GLP-1R and RAGE were measured by western blotting.

show abstract

Section: Discussionmentioning

confidence: 99%

Liraglutide improved the cognitive function of diabetic mice via the receptor of advanced glycation end products down-regulation

Zhang

Chu

Zheng

et al. 2020

Aging

View full text Add to dashboard Cite

show abstract

“…Diabetes is a chronic disease characterized by hyperglycemia. The increasing prevalence of diabetes becomes a serious global health problem [ 1 , 2 , 3 ]. There are various chronic complications of diabetes, which are the main cause of morbidity and mortality of diabetes, including: diabetic nephropathy, neuropathy, retinopathy, lower extremity vascular lesions, and gastroenteropathy [ 4 , 5 , 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

Dihydromyricetin Improves Endothelial Dysfunction in Diabetic Mice via Oxidative Stress Inhibition in a SIRT3-Dependent Manner

Hua

Zhang

Gong

et al. 2020

IJMS

View full text Add to dashboard Cite

Dihydromyricetin (DHY), a flavonoid component isolated from Ampelopsis grossedentata, exerts versatile pharmacological activities. However, the possible effects of DHY on diabetic vascular endothelial dysfunction have not yet been fully elucidated. In the present study, male C57BL/6 mice, wild type (WT) 129S1/SvImJ mice and sirtuin 3 (SIRT3) knockout (SIRT3-/-) mice were injected with streptozotocin (STZ, 60 mg/kg/day) for 5 consecutive days. Two weeks later, DHY were given at the doses of 250 mg/kg by gavage once daily for 12 weeks. Fasting blood glucose (FBG) and glycosylated hemoglobin (HbA1c) level, endothelium-dependent relaxation of thoracic aorta, reactive oxygen species (ROS) production, SIRT3, and superoxide dismutase 2 (SOD2) protein expressions, as well as mitochondrial Deoxyribonucleic Acid (mtDNA) copy number, in thoracic aorta were detected. Our study found that DHY treatment decreased FBG and HbA1c level, improved endothelium-dependent relaxation of thoracic aorta, inhibited oxidative stress and ROS production, and enhanced SIRT3 and SOD2 protein expression, as well as mtDNA copy number, in thoracic aorta of diabetic mice. However, above protective effects of DHY were unavailable in SIRT3-/- mice. The study suggested DHY improved endothelial dysfunction in diabetic mice via oxidative stress inhibition in a SIRT3-dependent manner.

show abstract

“…GLP-1 Ras, or incretin mimetics used for T2D and obesity treatment, are analogues of GLP-1 and primarily act in the pancreas and liver. Side effects of such treatment include reduced hunger and lower stroke risk [89]. Since mitochondrial mutations are known to cause higher ROS production, they are especially dangerous for the cardiovascular system, where they can cause cardiomyopathy, atherosclerosis and hypertension.…”

Section: Pharmacotherapymentioning

confidence: 99%

The Role of Mitochondrial Mutations and Chronic Inflammation in Diabetes

Dabravolski

Orekhova

Baig

et al. 2021

IJMS

View full text Add to dashboard Cite

Diabetes mellitus and related disorders significantly contribute to morbidity and mortality worldwide. Despite the advances in the current therapeutic methods, further development of anti-diabetic therapies is necessary. Mitochondrial dysfunction is known to be implicated in diabetes development. Moreover, specific types of mitochondrial diabetes have been discovered, such as MIDD (maternally inherited diabetes and deafness) and DAD (diabetes and Deafness). Hereditary mitochondrial disorders are caused by certain mutations in the mitochondrial DNA (mtDNA), which encodes for a substantial part of mitochondrial proteins and mitochondrial tRNA necessary for mitochondrial protein synthesis. Study of mtDNA mutations is challenging because the pathogenic phenotype associated with such mutations depends on the level of its heteroplasmy (proportion of mtDNA copies carrying the mutation) and can be tissue-specific. Nevertheless, modern sequencing methods have allowed describing and characterizing a number of mtDNA mutations associated with human disorders, and the list is constantly growing. In this review, we provide a list of mtDNA mutations associated with diabetes and related disorders and discuss the mechanisms of their involvement in the pathology development.

show abstract

Development of therapeutic options on type 2 diabetes in years: Glucagon-like peptide-1 receptor agonist’s role intreatment; from the past to future

Cited by 18 publications

References 84 publications

Liraglutide improved the cognitive function of diabetic mice via the receptor of advanced glycation end products down-regulation

Liraglutide improved the cognitive function of diabetic mice via the receptor of advanced glycation end products down-regulation

Dihydromyricetin Improves Endothelial Dysfunction in Diabetic Mice via Oxidative Stress Inhibition in a SIRT3-Dependent Manner

The Role of Mitochondrial Mutations and Chronic Inflammation in Diabetes

Contact Info

Product

Resources

About