Anti-inflammatory effects of C-peptide on kidney of type 1 diabetes mellitus animal model

Alves, Michelle Teodoro; Chaves, Amanda Caroline Silva; Almeida, Ana Paula Martins; Silva, Ana Cristina Simões e; Araújo, Stanley de Almeida; Mota, Ana Paula Lucas; Mares-Guia, Thiago Rennó dos; Fernandes, Ana Paula; Gomes, Karina Braga

doi:10.1007/s11033-019-05152-4

Cited by 5 publications

(4 citation statements)

References 15 publications

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“…Replacement of C-peptide in diabetic patients decreased glomerular hyperfiltration and urinary albumin excretion compared with placebo-treated ones. These results support the meaning of C-peptide in diminishing the diabetes-induced kidney damage and were recently confirmed on animal model [ 80 , 96 - 98 ]. Experimental studies performed on diabetic animal models show that C-peptide in replacement doses has the ability to improve peripheral nerve function and prevent or reverse the development of nerve structural changes [ 99 , 100 ].…”

Section: The Clinical and Therapeutic Potential Of C-peptide Replacementsupporting

confidence: 84%

C-peptide and residual β-cell function in pediatric diabetes – state of the art

Jamiołkowska‐Sztabkowska¹,

Głowińska‐Olszewska²,

Bossowski³

2021

pedm

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Section: The Clinical and Therapeutic Potential Of C-peptide Replacementsupporting

confidence: 84%

C-peptide and residual β-cell function in pediatric diabetes – state of the art

Jamiołkowska‐Sztabkowska¹,

Głowińska‐Olszewska²,

Bossowski³

2021

pedm

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“…Therefore, to efficiently induce hyperglycemia in both control and FynKO mice, animals were treated with STZ, a glucosamine–nitrosourea compound that damages pancreatic beta cells and induces diabetes [ 31 ]. Similar hyperglycemia levels were observed in both control (WT) and FynKO mice at 2 weeks of STZ treatment ( Figure 5 A), and mice were maintained on a standard chow diet for an additional 8 weeks, a timeframe long enough to trigger DKD [ 32 ]. Kidneys were collected and slides were prepared to examine signs of autophagy via visualization of p62 puncta using immunohistofluorescence in both WT and FynKO mice treated or not with STZ.…”

Section: Resultsmentioning

confidence: 77%

Fyn Phosphorylates Transglutaminase 2 (Tgm2) and Modulates Autophagy and p53 Expression in the Development of Diabetic Kidney Disease

Uehara

Yamada

Okada

et al. 2023

Cells

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Autophagy is involved in the development of diabetic kidney disease (DKD), the leading cause of end-stage renal disease. The Fyn tyrosine kinase (Fyn) suppresses autophagy in the muscle. However, its role in kidney autophagic processes is unclear. Here, we examined the role of Fyn kinase in autophagy in proximal renal tubules both in vivo and in vitro. Phospho-proteomic analysis revealed that transglutaminase 2 (Tgm2), a protein involved in the degradation of p53 in the autophagosome, is phosphorylated on tyrosine 369 (Y369) by Fyn. Interestingly, we found that Fyn-dependent phosphorylation of Tgm2 regulates autophagy in proximal renal tubules in vitro, and that p53 expression is decreased upon autophagy in Tgm2-knockdown proximal renal tubule cell models. Using streptozocin (STZ)-induced hyperglycemic mice, we confirmed that Fyn regulated autophagy and mediated p53 expression via Tgm2. Taken together, these data provide a molecular basis for the role of the Fyn–Tgm2–p53 axis in the development of DKD.

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“…In studies of type 1 diabetes mellitus (T1DM) mouse models, exogenous supplementation of C-peptide was found to aid in the reduction of pro-inflammatory cytokines such as IL17 and tumor necrosis factor-alpha (TNFα), and anti-inflammatory cytokines, like IL4 and IL10, in the urine (P <0.05). Additionally, an increase in the expression of the IL10 gene and a decrease in the expression of the TNFα gene were observed in the kidneys ( 50 ).…”

Section: C-peptide and Diabetic Kidney Diseasementioning

confidence: 99%

The role of C-peptide in diabetes and its complications: an updated review

Chen,

Huang,

Liu

et al. 2023

Front. Endocrinol.

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Worldwide, diabetes and its complications have seriously affected people’s quality of life and become a serious public health problem. C-peptide is not only an indicator of pancreatic β-cell function, but also a biologically active peptide that can bind to cell membrane surface signaling molecules and activate downstream signaling pathways to play antioxidant, anti-apoptotic and inflammatory roles, or regulate cellular transcription through internalization. It is complex how C-peptide is related to diabetic complications. Both deficiencies and overproduction can lead to complications, but their mechanisms of action may be different. C-peptide replacement therapy has shown beneficial effects on diabetic complications in animal models when C-peptide is deficient, but results from clinical trials have been unsatisfactory. The complex pattern of the relationship between C-peptide and diabetic chronic complications has not yet been fully understood. Future basic and clinical studies of C-peptide replacement therapies will need to focus on baseline levels of C-peptide in addition to more attention also needs to be paid to post-treatment C-peptide levels to explore the optimal range of fasting C-peptide and postprandial C-peptide maintenance.

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Anti-inflammatory effects of C-peptide on kidney of type 1 diabetes mellitus animal model

Cited by 5 publications

References 15 publications

C-peptide and residual β-cell function in pediatric diabetes – state of the art

C-peptide and residual β-cell function in pediatric diabetes – state of the art

Fyn Phosphorylates Transglutaminase 2 (Tgm2) and Modulates Autophagy and p53 Expression in the Development of Diabetic Kidney Disease

The role of C-peptide in diabetes and its complications: an updated review

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