Obesity, immunomodulation and chronic kidney disease

Börgeson, Emma; Sharma, Kumar

doi:10.1016/j.coph.2013.05.011

Cited by 24 publications

(30 citation statements)

References 62 publications

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“…Obesity is an independent risk factor for kidney disease and 25-40% of diabetic individuals develop nephropathy, which is the primary cause of end-stage renal failure [1,2,18]. In this study, we demonstrate that AICAR treatment attenuates cardinal features of HFD-induced kidney disease, namely microalbuminuria, production of reactive oxygen species and renal inflammation.…”

Section: Discussionsupporting

confidence: 50%

AICAR ameliorates high-fat diet-associated pathophysiology in mouse and ex vivo models, independent of adiponectin

et al. 2017

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Aims/hypothesis In this study, we aimed to evaluate the therapeutic potential of 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), an activator of AMP-activated protein kinase, for ameliorating high-fat diet (HFD)-induced pathophysiology in mice. We also aimed to determine whether the beneficial effects of AICAR were dependent on adiponectin. Furthermore, human adipose tissue was used to examine the effect of AICAR ex vivo. Methods Six-week-old male C57BL/6J wild-type and Adipoq −/− mice were fed a standard-fat diet (10% fat) or an HFD (60% fat) for 12 weeks and given vehicle or AICAR (500 μg/g) three times/week from weeks 4-12. Diet-induced pathophysiology was examined in mice after 11 weeks by IPGTT and after 12 weeks by flow cytometry and western blotting. Human adipose tissue biopsies from obese (BMI 35-50 kg/m 2 ) individuals were incubated with vehicle or AICAR (1 mmol/l) for 6 h at 37°C, after which inflammation was characterised by ELISA (TNF-α) and flow cytometry. Results AICAR attenuated adipose inflammation in mice fed an HFD, promoting an M1-to-M2 macrophage phenotype switch, while reducing infiltration of CD8 + T cells. AICAR treatment of mice fed an HFD partially restored glucose tolerance and attenuated hepatic steatosis and kidney disease, as evidenced by reduced albuminuria (p < 0.05), urinary H 2 O 2 (p < 0.05) and renal superoxide levels (p < 0.01) in both wild-type and Adipoq −/− mice. AICAR-mediated protection occurred independently of adiponectin, as similar protection was observed in wild-type and Adipoq −/− mice. In addition, AICAR promoted an M1-to-M2 macrophage phenotype switch and reduced TNF-α production in tissue explants from obese human patients. Conclusions/interpretation AICAR may promote metabolic health and protect against obesity-induced systemic diseases Catherine Godson and Kumar Sharma are joint senior authors.Electronic supplementary material The online version of this article

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Section: Discussionsupporting

confidence: 50%

AICAR ameliorates high-fat diet-associated pathophysiology in mouse and ex vivo models, independent of adiponectin

et al. 2017

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“…Obesity-related co-morbid disease states, including the development of chronic renal disease, type 2 diabetes mellitus, atherosclerosis, and malignancy, are strongly associated with an accompanying systemic low-grade inflammatory state. However, even when excluding co-existing morbidities such as hypertension and diabetes, obesity remains an independent risk factor for the development of chronic renal disease [28][29][30]. In a recent multivariate analysis, the relative risk for the development of chronic renal disease strongly correlated with the severity of obesity [31].…”

Section: Discussionmentioning

confidence: 99%

Obesity is a Risk Factor for Renal Toxicity and Wound Complications among a Cohort of Pediatric Cancer Patients at a Single Tertiary Care Institution

Aldrink

Paris²,

Wang³

et al. 2014

J Obes Weight Loss Ther

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“…13 Stone prevention may be of particular importance in obese patients, who are already at risk for several chronic conditions, including coronary artery disease and CKD. 14,15 In addition, the morbidity associated with surgical management of stone disease in the morbidly obese can be significant.…”

Section: Discussionmentioning

confidence: 99%