Effect of GLP-1 receptor agonist, liraglutide, on muscle in spontaneously diabetic torii fatty rats

Yamada, Shohei; Ogura, Yuji; Inoue, Kenji; Tanabe, Jun; Sugaya, Takeshi; Ohata, Keiichi; Nagai, Yoshio; Natsuki, Yasunori; Hoshino, Seiko; Watanabe, Sumi; Ichikawa, Daisuke; Kimura, Kenjiro; Shibagaki, Yugo; Kamijo‐Ikemori, Atsuko

doi:10.1016/j.mce.2021.111472

Cited by 12 publications

(14 citation statements)

References 28 publications

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“…Entire images of western blotting are shown in online supplementary resource Figure S1 (c and d). All data were expressed as mean ± SEM Because we previously found that GLP-1R was expressed in the vascular walls of both kidney and muscle [16,24], we presumed the expression of GLP-1R in the vascular walls of the retina. However, contrary to our expectations, the localization of GLP-1R was not found in the retinas of either SD or SDT fatty rats, and we did not observe a more effective response of liraglutide on the retina beyond blood glucose-and blood pressure-lowing effects induced by insulin-hydralazine treatment.…”

Section: Discussionmentioning

confidence: 99%

“…Male SDT fatty rats derived from a Sprague-Dawley (SD) colony were used as a type 2 diabetes model [14]. We previously reported that injection of GLP-1RA decreased the levels of both blood glucose and blood pressure and brought beneficial effects on both kidney and muscle in male SDT fatty rats, independent on blood glucose and blood pressure levels [15,16]. Rats were subcutaneously injected with GLP-1RA from the age of 8 weeks to 16 weeks [16].…”

Section: Animalsmentioning

confidence: 99%

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Glucagon-like peptide-1 receptor agonist, liraglutide, attenuated retinal thickening in spontaneously diabetic Torii fatty rats

et al. 2022

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Background This study aims to investigate the effect of the glucagon-like peptide-1 (GLP-1) receptor agonist (GLP-1RA) liraglutide on retinal pathological findings as compared with insulin and hydralazine using an animal model of type 2 diabetes with obesity, hypertension, and hyperlipidemia. Methods Male spontaneously diabetic Torii (SDT) fatty rats at 8 weeks of age were randomly assigned to three groups: the liraglutide group (SDT-lira, n = 6) received a subcutaneous injection of liraglutide from the age of 8 to 16 weeks, the SDT-ins-hyd group (n = 6) was provided both insulin against hyperglycemia and hydralazine against hypertension to match levels of both blood glucose and blood pressure to those of the liraglutide group, and the control group of SDT fatty rats (SDT-vehicle, n = 7) and a nondiabetic control group of Sprague–Dawley rats (SD, n = 7) were injected with vehicle only. Both eyeballs of all groups were collected at the age of 16 weeks. Results Retinal thickness, which was found in the SDT-vehicle group, was significantly prevented to similar levels in both the SDT-lira and SDT-ins-hyd groups. Immunohistological analysis revealed that GLP-1 receptor was not expressed in the retina of all rats. The ocular protein expression of monocyte chemoattractant protein-1, which causes a proinflammatory situation, was significantly upregulated in all SDT fatty rats as compared to SD rats, but the expression levels were similar between all SDT fatty rats. With regard to neovascularization in the eyes, there were no significant differences in protein expressions of vascular endothelial growth factor, CD31, or endothelial nitric oxide synthase in all rats. Conclusions The present study indicates that liraglutide prevents retinal thickening, dependent on blood glucose and blood pressure levels in SDT fatty rats without ocular neovascularization. However, the effects did not improve the ocular proinflammatory state.

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Section: Discussionmentioning

confidence: 99%

Section: Animalsmentioning

confidence: 99%

Glucagon-like peptide-1 receptor agonist, liraglutide, attenuated retinal thickening in spontaneously diabetic Torii fatty rats

et al. 2022

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“…Hyperglycaemia stimulates the production of metabolites such as ROS and AGEs, which promote oxidative stress, inflammation and impair autophagy, while drugs can slow the progression of DKD by inducing or restoring autophagy (Zheng et al, 2020;Winiarska et al, 2021). In recent years relevant reports have discussed drugs that target autophagy in the treatment of DKD, such as the herbal extracts, the emerging GLP-1 activators and SGLT2 inhibitors and so on, all of which have been shown to modulate the autophagic process and improve renal function (Huang et al, 2017;Wang et al, 2018b;Winiarska et al, 2021;Yamada et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

“…The use of GLP-1 in Zucker diabetic fatty rats and AGEs induced Ins 1 cells model showed that GLP-1 showed renoprotective effects independent of hypoglycaemia (Yang S. et al, 2020). Using liraglutide in an animal model of spontaneously diabetic tori fatty rats, it was concluded that liraglutide protected the kidney and activated autophagy in early DKD via the AMPK/eNOS pathway independent of reductions in blood glucose and blood pressure (Yamada et al, 2021). Caffeic acid, ethyl acetate or Huang-Gui Solid Dispersion (HGSD) was used in a model of Wistar rats with established DM, and it was ultimately concluded that all three drugs could activate autophagy through AMPK-mediated pathways, switching on of key downstream genes (Matboli et al, 2017;Zhang et al, 2020;Ezzat et al, 2021).…”

Section: Other Studies On Autophagosome Formation In Dkdmentioning

confidence: 99%

The critical role of dysregulated autophagy in the progression of diabetic kidney disease

et al. 2022

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Diabetic kidney disease (DKD) is one of the major public health problems in society today. It is a renal complication caused by diabetes mellitus with predominantly microangiopathy and is a major cause of end-stage renal disease (ESRD). Autophagy is a metabolic pathway for the intracellular degradation of cytoplasmic products and damaged organelles and plays a vital role in maintaining homeostasis and function of the renal cells. The dysregulation of autophagy in the hyperglycaemic state of diabetes mellitus can lead to the progression of DKD, and the activation or restoration of autophagy through drugs is beneficial to the recovery of renal function. This review summarizes the physiological process of autophagy, illustrates the close link between DKD and autophagy, and discusses the effects of drugs on autophagy and the signaling pathways involved from the perspective of podocytes, renal tubular epithelial cells, and mesangial cells, in the hope that this will be useful for clinical treatment.

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“…Another important group of drugs developed in recent years are glucagon-like peptide 1 receptor agonists (GLP1-RAs), such as exenatide, dulaglutide, semaglutide, liraglutide and lixisenatide. To date, liraglutide has been shown to exert a strong effect on mitochondrial function, improving mitochondrial content and function in the muscle of spontaneous diabetic Torii (SDT) rats (Yamada et al, 2022). These mechanisms imply the blocking of mitochondrial dysfunction and triggering of apoptosis, as seen in a study on human renal mesangial cells subjected to hyperglycaemia.…”

Section: ) Introductionmentioning

confidence: 99%

Targeting mitochondria: a great boon to fight type 2 diabetes

Rovira‐Llopis

Rocha

Víctor

2022

Redox Experimental Medicine

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Type 2 diabetes is a chronic metabolic disease characterised by the development of low-grade systemic inflammation, hyperglycaemia, and hyperlipidaemia. These pathogenic traits have a profound impact on mitochondrial function as the intermediary organelles between nutrients and energy production. Moreover, the mitochondrial quality control system is also altered and rendered defective by type 2 diabetes. These alterations entail the accumulation of defective mitochondria, which causes the diabetic background to deteriorate further. In this context, it is of paramount importance to improve mitochondrial function and ameliorate the consequences of mitochondrial dysfunction. This review assesses different treatments that target mitochondrial dysfunction as a way of treating type 2 diabetes. Lifestyle interventions and pharmacological treatments such as biguanides, thiazolidinediones, a-glucosidase inhibitors or SGLT2 inhibitors protect mitochondrial function; while novel mitochondria-targeted molecules including natural compounds, mitochondria-targeted antioxidants, inhibitors of mPTP opening, NO and H2S donors, and inhibitors of mitochondrial fission positively impact on mitochondrial function and its quality control mechanisms. Most of these therapeutic tools require more research, but they already show promising therapeutic mechanisms that improve type 2 diabetes and its cellular consequences.

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Effect of GLP-1 receptor agonist, liraglutide, on muscle in spontaneously diabetic torii fatty rats

Cited by 12 publications

References 28 publications

Glucagon-like peptide-1 receptor agonist, liraglutide, attenuated retinal thickening in spontaneously diabetic Torii fatty rats

Glucagon-like peptide-1 receptor agonist, liraglutide, attenuated retinal thickening in spontaneously diabetic Torii fatty rats

The critical role of dysregulated autophagy in the progression of diabetic kidney disease

Targeting mitochondria: a great boon to fight type 2 diabetes

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