Inhibition of Islet Immunoreactivity by Adiponectin Is Attenuated in Human Type 1 Diabetes

Pang, Terence; Chimen, Myriam; Goble, Edward; Dixon, Natalie; Benbow, Aled; Eldershaw, Suzy; Thompson, Dylan; Gough, Stephen; Narendran, Parth

doi:10.1210/jc.2012-3516

Cited by 22 publications

(18 citation statements)

References 40 publications

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“…These findings suggest that the mechanisms for wound-healing abnormalities associated with TID could be related to loss of insulin actions in fibroblasts. Metabolic changes such as hyperglycemia can inhibit insulin actions in several tissues in T1D and T2D patients (40). This supportive evidence in fibroblasts from other studies demonstrated selective inhibition of insulin action in the IRS/PI3K/AKT cascade, without loss of activation of MAPK (41).…”

Section: Discussionsupporting

confidence: 77%

PKCδ inhibition normalizes the wound-healing capacity of diabetic human fibroblasts

Khamaisi¹,

Katagiri²,

Keenan³

et al. 2016

Journal of Clinical Investigation

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Section: Discussionsupporting

confidence: 77%

PKCδ inhibition normalizes the wound-healing capacity of diabetic human fibroblasts

Khamaisi¹,

Katagiri²,

Keenan³

et al. 2016

Journal of Clinical Investigation

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“…Switching the cytokine environment to an anti-inflammatory profile could potentially modulate the immune response that leads to beta cell destruction in type 1 diabetes. Work in our laboratory has also demonstrated that the expression of adiponectin receptors by peripheral blood immune cells is reduced in patients with type 1 diabetes [20]. This reduction in receptor expression releases effector T cells from the anti-inflammatory effects of adiponectin, resulting in a proinflammatory response to beta cell antigen.…”

Section: Search Strategymentioning

confidence: 86%

The time has come to test the beta cell preserving effects of exercise in patients with new onset type 1 diabetes

et al. 2014

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Type 1 diabetes is characterised by immunemediated destruction of insulin-producing beta cells. Significant beta cell function is usually present at the time of diagnosis with type 1 diabetes, and preservation of this function has important clinical benefits. The last 30 years have seen a number of largely unsuccessful trials for beta cell preservation, some of which have been of therapies that have potential for significant harm. There is a need to explore new, more tolerable approaches to preserving beta cell function that can be implemented on a large clinical scale. Here we review the evidence for physical exercise as a therapy for the preservation of beta cell function in patients with newly diagnosed type 1 diabetes. We highlight possible mechanisms by which exercise could preserve beta cell function and then present evidence from other models of diabetes that demonstrate that exercise preserves beta cell function. We conclude by proposing that there is now a need for studies to explore whether exercise can preserve beta cell in patients newly diagnosed with type 1 diabetes.

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“…ADIPOR1 and ADIPOR2 are also abundantly expressed in the hypothalamus and cerebral vascular endothelial cells (Carson et al, 2013). Studies showed that adiponectin receptors are closely associated with diabetes (Pang et al, 2013), metabolic syndrome (Peters et al, 2013), and cardiovascular disease (Ding et al, 2012). They can affect cell metabolism and function and are one of the important mechanisms in the promotion and development of disease (Richards et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Association between adiponectin receptor 2 gene polymorphisms and cerebral infarction

Yuan¹,

Teng²

2014

Genet. Mol. Res.

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ABSTRACT. We examined the association between the adiponectin receptor 2 gene and the risk of ischemic stroke. Polymerase chain reaction-restriction fragment length polymorphism was used to detect rs12342 genotypes of the adiponectin receptor 2 gene in 300 ischemic stroke patients and 320 age-and gender-matched healthy controls. In the patient group, the AA, GA, and GG genotype frequencies were 39.3, 42.7, and 18.0%, respectively. The A and G allele frequencies were 0.607 and 0.393, respectively. In the control group, the AA, GA, and GG genotype frequencies were 29.0, 51.7, and 19.3%, respectively. The A and G allele frequencies were 0.548 and 0.452, respectively. The AA genotype and A allele frequencies in the patient group were significantly higher than those in the control group (both P < 0.01). The risk of ischemic stroke in AA genotype carriers was 1.786-fold greater than that in GG genotype carriers (odds ratio = 1.786, 95% confidence interval: 1.432-2.775; P = 0.013). After adjusting for various confounding factors, the difference remained significant (odds ratio = 1.874, 95% confidence interval: 1.221-2.765; P = 0.012). The AA genotype and A allele of rs12342 in the adiponectin receptor 2 7809 ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 13 (3): 7808-7814 (2014) Adiponectin and cerebral infarction gene may increase the risk of ischemic stroke, particularly the risk of atherosclerosis cerebral infarction.

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Inhibition of Islet Immunoreactivity by Adiponectin Is Attenuated in Human Type 1 Diabetes

Cited by 22 publications

References 40 publications

PKCδ inhibition normalizes the wound-healing capacity of diabetic human fibroblasts

PKCδ inhibition normalizes the wound-healing capacity of diabetic human fibroblasts

The time has come to test the beta cell preserving effects of exercise in patients with new onset type 1 diabetes

Association between adiponectin receptor 2 gene polymorphisms and cerebral infarction

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