Anti-inflammatory potentials of incretin-based therapies used in the management of diabetes

Yaribeygi, Habib; Maleki, Mina; Sathyapalan, Thozhukat; Jamialahmadi, Tannaz; Sahebkar, Amirhossein

doi:10.1016/j.lfs.2019.117152

Cited by 46 publications

(28 citation statements)

References 84 publications

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“…A plausible hypothesis is that GLP-1 receptor agonists protect the heart and kidney via anti-oxidative and anti-inflammatory effects that mitigate key mechanisms of kidney and cardiovascular damage in diabetes. [32][33][34][35] It…”

Section: Putative Mechanisms For Kidney and Cardiovascular Benefits Of Glucagon-like Peptide-1 Receptor Agonistsmentioning

confidence: 99%

Clinical Evidence and Proposed Mechanisms for Cardiovascular and Kidney Benefits from Glucagon-like Peptide-1 Receptor Agonists

Cox¹,

Alicic²,

Neumiller³

et al. 2020

US Endocrinology

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Section: Putative Mechanisms For Kidney and Cardiovascular Benefits Of Glucagon-like Peptide-1 Receptor Agonistsmentioning

confidence: 99%

Clinical Evidence and Proposed Mechanisms for Cardiovascular and Kidney Benefits from Glucagon-like Peptide-1 Receptor Agonists

Cox¹,

Alicic²,

Neumiller³

et al. 2020

US Endocrinology

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“…It is also possible that other mechanisms are involved, such as slowing gastric emptying or changes in dietary patterns in response to the gastrointestinal adverse events that resulted in improved glycaemic control, in the short term. Finally, GLP‐1RAs have been found to have anti‐inflammatory effects which could account for improved metabolic control 22 . However, we did not find changes in immune cells (CD4, CD8) or markers of cell activation (RAGE expression) with exenatide ER treatment (not shown) 23 …”

Section: Discussionmentioning

confidence: 66%

Exenatide extended release in patients with type 1 diabetes with and without residual insulin production

Herold

Reynolds

Dziura

et al. 2020

Diabetes Obesity Metabolism

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Aims: To test whether a long-acting GLP-1 receptor agonist would improve glucose control in patients with type 1 diabetes (T1D) and to determine whether the presence of residual beta cell function would affect the response. In addition, we sought to determine whether the drug would affect beta cell function. Methods: We performed a randomized placebo-controlled trial of exenatide extended release (ER) in participants with T1D with and without detectable levels of C-peptide. Seventy-nine participants were randomized to exenatide ER 2 mcg weekly, or placebo, stratified by the presence or absence of detectable C-peptide levels. The primary outcome was the difference in glycated haemoglobin (HbA1c) levels at 24 weeks. Participants were followed for another 6 months off study drug. Results: At week 24, the time of the primary outcome, the least squares (LS) mean HbA1c level was 7.76% (95% confidence interval [CI] 7.42, 8.10) in the exenatide ER group versus 8.0% (95% CI 7.64, 8.35) in the placebo group (P = 0.08). At week 12 the LS mean HbA1c levels were 7.71% (95% CI 7.37, 8.05) in the exenatide ER group versus 8.05% (95% CI 7.7, 8.4) in the placebo group (P = 0.01). The improvement at week 12 was driven mainly by those with detectable levels of C-peptide. Those treated with exenatide ER lost weight at 12 and 24 weeks compared to those treated with placebo (P <0.001 and P = 0.007). The total insulin dose was lower, but not when corrected for body weight, and was not affected by residual insulin production.

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“…Accordingly, modification of chronic inflammation and fibrosis appears to be importantin the treatment of T2D individuals with CKD. Anti-inflammatory and anti-fibrogenic activity is an intrinsic element ofthe renal protective effect of current antihyperglycemic drugs, such as SGLT-2 inhibitors [85][86][87] and GLP-1 receptor agonists [88][89][90]. In addition, targeting specific mediators of inflammation and fibrosis is considered a promising approach to the treatment of diabetic nephropathy [9,91].…”

Section: Discussionmentioning

confidence: 99%

Multiplex Bead Array Assay of a Panel of Circulating Cytokines and Growth Factors in Patients with Albuminuric and Non-Albuminuric Diabetic Kidney Disease

Климонтов

Korbut

Орлов

et al. 2020

JCM

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A panel of cytokines and growth factors, mediating low-grade inflammation and fibrosis, was assessed in patients with type 2 diabetes (T2D) and different patterns of chronic kidney disease (CKD). Patients with long-term T2D (N = 130) were classified into four groups: no signs of CKD; estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 without albuminuria; albuminuria and eGFR ≥60 mL/min/1.73 m2; albuminuria and eGFR <60 mL/min/1.73 m2. Thirty healthy subjects were acted as control. Twenty-seven cytokines and growth factors were assessed in serum by multiplex bead array assay. Serum hs-CRP, urinary nephrin, podocine, and WFDC2 were measured by ELISA. Patients with T2D showed elevated IL-1Ra, IL-6, IL-17A, G-CSF, IP-10, MIP-1α, and bFGF levels; concentrations of IL-4, IL-12, IL-15, INF-γ, and VEGF were decreased. IL-6, IL-17A, G-CSF, MIP-1α, and bFGF correlated negatively with eGFR; IL-10 and VEGF demonstrated negative associations with WFDC2; no relationships with podocyte markers were found. Adjusted IL-17A and MIP-1α were predictors of non-albuminuric CKD, IL-13 predicted albuminuria with preserved renal function, meanwhile, IL-6 and hsCRP were predictors of albuminuria with eGFR decline. Therefore, albuminuric and non-albuminuric CKD in T2D patients are associated with different pro-inflammatory shifts in the panel of circulating cytokines.

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Anti-inflammatory potentials of incretin-based therapies used in the management of diabetes

Cited by 46 publications

References 84 publications

Clinical Evidence and Proposed Mechanisms for Cardiovascular and Kidney Benefits from Glucagon-like Peptide-1 Receptor Agonists

Clinical Evidence and Proposed Mechanisms for Cardiovascular and Kidney Benefits from Glucagon-like Peptide-1 Receptor Agonists

Exenatide extended release in patients with type 1 diabetes with and without residual insulin production

Multiplex Bead Array Assay of a Panel of Circulating Cytokines and Growth Factors in Patients with Albuminuric and Non-Albuminuric Diabetic Kidney Disease

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