ArticleJCI insight2021
Proximal tubular epithelial insulin receptor mediates high-fat diet-induced kidney injury.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Insulin resistance and hyperinsulinaemia in kidney disease: mechanisms and metabolic effects.Nature reviews. Nephrology · 2026Review
- AMPK is dispensable for physiological podocyte and glomerular functions but prevents glomerular fibrosis in experimental diabetes.Cell death discovery · 2026Article
- The CLCA1/TMEM16A/Cl- current axis associates with H2S deficiency in diabetic kidney injury.JCI insight · 2025Article
- Profiling of insulin-resistant kidney models and human biopsies reveals common and cell-type-specific mechanisms underpinning Diabetic Kidney Disease.Nature communications · 2024Article
- Sex-specific molecular signature of mouse podocytes in homeostasis and in response to pharmacological challenge with rapamycin.Biology of sex differences · 2024Article
- Female Protection Against Diabetic Kidney Disease Is Regulated by Kidney-Specific AMPK Activity.Diabetes · 2024Article
- Role of miR-379 in high-fat diet-induced kidney injury and dysfunction.American journal of physiology. Renal physiology · 2022Article
- Renal Function Following Bariatric Surgery: a Literature Review of Potential Mechanisms.Obesity surgery · 2022Review
- A Mendelian randomization study to assess the genetic liability of type 1 diabetes mellitus for IgA nephropathy.Frontiers in endocrinology · 2022Article
- Protective effect of hydrogen sulfide on the kidney (Review).Molecular medicine reports · 2021Review
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 3 countries.
Funding
Abstract
The role of insulin receptor (IR) activated by hyperinsulinemia in obesity-induced kidney injury is not well understood. We hypothesized that activation of kidney proximal tubule epithelial IR contributes to obesity-induced kidney injury. We administered normal-fat diet (NFD) or high-fat diet (HFD) to control and kidney proximal tubule IR-knockout (KPTIRKO) mice for 4 months. Renal cortical IR expression was decreased by 60% in male and female KPTIRKO mice. Baseline serum glucose, serum creatinine, and the ratio of urinary albumin to creatinine (ACR) were similar in KPTIRKO mice compared to those of controls. On HFD, weight gain and increase in serum cholesterol were similar in control and KPTIRKO mice; blood glucose did not change. HFD increased the following parameters in the male control mice: renal cortical contents of phosphorylated IR and Akt, matrix proteins, urinary ACR, urinary kidney injury molecule-1-to-creatinine ratio, and systolic blood pressure. Renal cortical generation of hydrogen sulfide was reduced in HFD-fed male control mice. All of these parameters were ameliorated in male KPTIRKO mice. Interestingly, female mice were resistant to HFD-induced kidney injury in both genotypes. We conclude that HFD-induced kidney injury requires renal proximal tubule IR activation in male mice.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.