Mechanisms of high glucose-induced apoptosis and its relationship to diabetic complications

Allen, David A.; Yaqoob, Muhammad; Harwood, Steven

doi:10.1016/j.jnutbio.2005.06.007

Cited by 216 publications

(173 citation statements)

References 95 publications

(84 reference statements)

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“…High blood glucose level causes deterioration of pancreatic β-cells due to oxidative stress that the generation of reactive oxygen species rapidly induces apoptotic cell death via both mitochondria-dependent andindependent pathways. 35 With regard to the reduction of pancreatic apoptosis through decreasing p53 expression levels, effect of crocin may be related to the antioxidant properties and its effects in reducing blood glucose and HbA1c levels. In addition, Xu et al (2006)demonstrated that crocin has preventive effects on the cell apoptosis induced by hydrogen peroxide through antagonising apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Effect of Crocin and Voluntary Exercise on P53 Protein in Pancreas of Type2 Diabetic Rats

Ghorbanzadeh¹,

Mohammadi²,

Mohaddes³

et al. 2017

Pharm Sci

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Section: Discussionmentioning

confidence: 99%

Effect of Crocin and Voluntary Exercise on P53 Protein in Pancreas of Type2 Diabetic Rats

Ghorbanzadeh¹,

Mohammadi²,

Mohaddes³

et al. 2017

Pharm Sci

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“…Cell loss by apoptosis is preceded by cell cycle arrest, which may lead to either hypertrophy or death, depending on several factors, including the tumour protein p53/p21 (also known as cyclin-dependent kinase inhibitor 1A, CIP1 and WAF1) pathway [13]. The p53 protein, activated through post-translational modifications [14], induces apoptosis via transcription-dependent and transcriptionindependent mechanisms [15], whereas its downstream target p21 causes growth arrest by inhibiting the activity of the cyclin/cyclin-dependent kinase complexes [16].…”

Section: Introductionmentioning

confidence: 99%

Increased glomerular cell (podocyte) apoptosis in rats with streptozotocin-induced diabetes mellitus: role in the development of diabetic glomerular disease

et al. 2007

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Aims/hypothesis Podocyte loss by apoptosis, in addition to favouring progression of established diabetic nephropathy, has been recently indicated as an early phenomenon triggering the initiation of glomerular lesions. This study aimed to assess the rate of glomerular cell death and its relationship with renal functional, structural and molecular changes in rats with experimental diabetes. Methods Male Sprague-Dawley rats with streptozotocininduced diabetes and coeval non-diabetic control animals were killed at 7 days and at 2, 4 and 6 months for the assessment of apoptosis, renal function, renal structure and the expression of podocyte markers and apoptosis-and cell cycle-related proteins. Results Glomerular cell apoptosis was significantly increased in diabetic vs non-diabetic rats at 4 months and to an even greater extent at 6 months, with podocytes accounting for 70% of apoptosing cells. The increase in apoptosis was preceded by increases in proteinuria, albuminuria and mean glomerular and mesangial areas, and by reductions in glomerular cell density and content of synaptopodin and Wilms' tumour protein-1. It coincided with the development of mesangial expansion and glomerular sclerosis, and with the upregulation/activation both of tumour protein p53, which increased progressively throughout the study, and of p21 (also known as cyclin-dependent kinase inhibitor 1A, CIP1 and WAF1), which peaked at 4 months and decreased thereafter. Conclusions/interpretation Glomerular cell (podocyte) apoptosis is not an early feature in the course of experimental diabetic glomerulopathy, since it is preceded by glomerular hypertrophy, which may decrease glomerular cell density to the point of inducing compensatory podocyte hypertrophy. This is associated with reduced podocyte protein expression (podocytopathy) and proteinuria, and ultimately results in apoptotic cell loss (podocytopenia), driving progression to mesangial expansion and glomerular sclerosis.

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“…Indeed, other possible mechanism in cause of program cell deaths in diabetes mellitus (Allen et al, 2005;Arroba et al, 2003Arroba et al, , 2005Arroba et al, , 2007Klein et al, 2004;Lechuga-Sancho et al, 2006a, 2006b) can be due to insulin decrease or insulin-like growth factor signaling (Ishii, 1995) or an increase in cytokines such as TNFa (Chen & Goeddel, 2002).…”

Section: Discussionmentioning

confidence: 99%

Hippocampal Neuronal Apoptosis in Rat Offspring Due to Gestational Diabetes

et al. 2016

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GHAFARI, S.; ASADI, E.; SHABANI, R. & GOLALIPOUR, M. J.Hippocampal neuronal apoptosis in rat offspring due to gestational diabetes. Int. J. Morphol., 34(1):205-211, 2016. SUMMARY:Gestational diabetes mellitus (GDM) defined as impaired glucose tolerance affects approximately 6 % of all pregnant women who have never before had diabetes, but who do have high blood glucose levels during pregnancy. This study was done to evaluate the apoptosis in the neuronal cells in the CA1, CA2 and CA3 subfields of hippocampus and dentate gyrus in offspring of gestational diabetes at the 7, 21 and 28 d in postnatal rats. Thirty Wistar rat dams were randomly allocated in control and diabetic group. Dams in diabetic group were received 40 mg/kg/BW of streptozotocin at the first day of gestation and control groups received an equivalent volume normal saline injection intraperitoneally (IP). Six offspring of GDM and control dams, at the 7, 21, 28 postnatal day were randomly were sacrificed quickly with anesthesia. The coronal sections of brain serially collected. The apoptosis neurons were evaluated with TUNEL Assay. In the CA1, the number of apoptotic cells in 7, 21 and 28 d of postnatal life were significantly increased in GDM compared to controls (P<0.001). In the CA2, CA3 the number of apoptotic cells in 7, 21 and 28 d age-old offspring were significantly increased in GDM compared to controls (P<0.001). In the dentate gyrus, the number of apoptotic cells in 7, 21 and 28 d of postnatal life were significantly increased in GDM compared to controls (P<0.01). This study showed that the uncontrolled gestational diabetes significantly increases neuronal apoptosis in hippocampal and dentate gyrus in rat offspring.

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Mechanisms of high glucose-induced apoptosis and its relationship to diabetic complications

Cited by 216 publications

References 95 publications

Effect of Crocin and Voluntary Exercise on P53 Protein in Pancreas of Type2 Diabetic Rats

Effect of Crocin and Voluntary Exercise on P53 Protein in Pancreas of Type2 Diabetic Rats

Increased glomerular cell (podocyte) apoptosis in rats with streptozotocin-induced diabetes mellitus: role in the development of diabetic glomerular disease

Hippocampal Neuronal Apoptosis in Rat Offspring Due to Gestational Diabetes

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