ArticleAmerican journal of physiology. Renal physiology2009
Proinsulin C-peptide reduces diabetes-induced glomerular hyperfiltration via efferent arteriole dilation and inhibition of tubular sodium reabsorption.
Article in American journal of physiology. Renal physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.
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Who cites it
23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.
- Pooled it
- The role of C-peptide in the attenuation of outcomes of diabetic kidney disease: a systematic review and meta-analysis.Jornal brasileiro de nefrologiaPooled it
- Renoprotective effects of empagliflozin are linked to activation of the tubuloglomerular feedback mechanism and blunting of the complement system.American journal of physiology. Cell physiology · 2023Article
- The role of C-peptide in diabetes and its complications: an updated review.Frontiers in endocrinology · 2023Review
- Metabolite aberrations in early diabetes detected in rat kidney using mass spectrometry imaging.Analytical and bioanalytical chemistry · 2019Article
- Acute renal metabolic effect of metformin assessed with hyperpolarised MRI in rats.Diabetologia · 2018Article
- Current approaches in regenerative medicine for the treatment of diabetes: introducing CRISPR/CAS9 technology and the case for non-embryonic stem cell therapy.American journal of stem cells · 2018Review
- Endothelin type A receptor inhibition normalises intrarenal hypoxia in rats used as a model of type 1 diabetes by improving oxygen delivery.Diabetologia · 2015Article
- Modeling oxygen consumption in the proximal tubule: effects of NHE and SGLT2 inhibition.American journal of physiology. Renal physiology · 2015Article
- Physiological effects and therapeutic potential of proinsulin C-peptide.American journal of physiology. Endocrinology and metabolism · 2014Review
- Diastolic dysfunction is associated with an increased risk of contrast-induced nephropathy: a retrospective cohort study.BMC nephrology · 2013Article
- Angiotensin II contributes to glomerular hyperfiltration in diabetic rats independently of adenosine type I receptors.American journal of physiology. Renal physiology · 2013Article
- Renoprotective effects of C-peptide in the Dahl salt-sensitive rat.American journal of physiology. Renal physiology · 2012Article
- Review
- Renal function in diabetic disease models: the tubular system in the pathophysiology of the diabetic kidney.Annual review of physiology · 2012Review
- The role of insulin C-peptide in the coevolution analyses of the insulin signaling pathway: a hint for its functions.PloS one · 2012Article
- C-Peptide reduces mitochondrial superoxide generation by restoring complex I activity in high glucose-exposed renal microvascular endothelial cells.ISRN endocrinology · 2012Article
- The clinical significance of hyperfiltration in diabetes.Diabetologia · 2010 · on this mapReview
- Tubular reabsorption and diabetes-induced glomerular hyperfiltration.Acta physiologica (Oxford, England) · 2010Review
- Role of triglyceride-rich lipoproteins in diabetic nephropathy.Nature reviews. Nephrology · 2010Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
C-peptide reduces diabetes-induced glomerular hyperfiltration in diabetic patients and experimental animal models. However, the mechanisms mediating the beneficial effect of C-peptide remain unclear. We investigated whether altered renal afferent-efferent arteriole tonus or alterations in tubular Na+ transport (T(Na)) in response to C-peptide administration mediate the reduction of diabetes-induced glomerular hyperfiltration. Glomerular filtration rate, filtration fraction, total and cortical renal blood flow, total kidney O2 consumption (QO2), T(Na), fractional Na+ and Li+ excretions, and tubular free-flow and stop-flow pressures were measured in anesthetized adult male normoglycemic and streptozotocin-diabetic Sprague-Dawley rats. The specific effect of C-peptide on transport-dependent QO2 was investigated in vitro in freshly isolated proximal tubular cells. C-peptide reduced glomerular filtration rate (-24%), stop-flow pressure (-8%), and filtration fraction (-17%) exclusively in diabetic rats without altering renal blood flow. Diabetic rats had higher baseline T(Na) (+40%), which was reduced by C-peptide. Similarly, C-peptide increased fractional Na+ (+80%) and Li+ (+47%) excretions only in the diabetic rats. None of these parameters was affected by vehicle treatments in either group. Baseline QO2 was 37% higher in proximal tubular cells from diabetic rats than controls and was normalized by C-peptide. C-peptide had no effect on ouabain-pretreated diabetic cells from diabetic rats. C-peptide reduced diabetes-induced hyperfiltration via a net dilation of the efferent arteriole and inhibition of tubular Na+ reabsorption, both potent regulators of the glomerular net filtration pressure. These findings provide new mechanistic insight into the beneficial effects of C-peptide on diabetic kidney function.
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Registered trials
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