ArticlePloS one2017
Mechanism of insulin resistance in a rat model of kidney disease and the risk of developing type 2 diabetes.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
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- AHA Life's Essential 8 and new-onset CKD: a prospective cohort study from the UK Biobank.Clinical and experimental nephrology · 2024Article
- Human Glucose Transporters in Renal Glucose Homeostasis.International journal of molecular sciences · 2021Review
- Renal mass reduction increases the response to exogenous insulin independent of acid-base status or plasma insulin levels in rats.American journal of physiology. Renal physiology · 2021Article
- Alkali supplementation as a therapeutic in chronic kidney disease: what mediates protection?American journal of physiology. Renal physiology · 2020Review
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- Oxidative Stress in Animal Models of Acute and Chronic Renal Failure.Disease markers · 2019Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
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Abstract
Chronic kidney disease is associated with homeostatic imbalances such as insulin resistance. However, the underlying mechanisms leading to these imbalances and whether they promote the development of type 2 diabetes is unknown. The effect of chronic kidney disease on insulin resistance was studied on two different rat strains. First, in a 5/6th nephrectomised Sprague-Dawley rat model of chronic kidney disease, we observed a correlation between the severity of chronic kidney disease and hyperglycemia as evaluated by serum fructosamine levels (p<0.0001). Further, glucose tolerance tests indicated an increase of 25% in glycemia in chronic kidney disease rats (p<0.0001) as compared to controls whereas insulin levels remained unchanged. We also observed modulation of glucose transporters expression in several tissues such as the liver (decrease of ≈40%, p≤0.01) and muscles (decrease of ≈29%, p≤0.05). Despite a significant reduction of ≈37% in insulin-dependent glucose uptake in the muscles of chronic kidney disease rats (p<0.0001), the development of type 2 diabetes was never observed. Second, in a rat model of metabolic syndrome (Zucker Leprfa/fa), chronic kidney disease caused a 50% increased fasting hyperglycemia (p<0.0001) and an exacerbated glycemic response (p<0.0001) during glucose challenge. Similar modulations of glucose transporters expression and glucose uptake were observed in the two models. However, 30% (p<0.05) of chronic kidney disease Zucker rats developed characteristics of type 2 diabetes. Thus, our results suggest that downregulation of GLUT4 in skeletal muscle may be associated with insulin resistance in chronic kidney disease and could lead to type 2 diabetes in predisposed animals.
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