Fat redistribution and adipocyte transformation in uninephrectomized rats
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Updated: Jul 5, 2026
Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
Hai-Lu Zhao1, Yi Sui, Jing Guan
1Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China. zhaohailu@yahoo.com
Abstract:
Dyslipidemia complicates renal function leading to disturbances of major homeostatic organs in the body. Here we examined the effect of chronic renal dysfunction induced by uninephrectomy on fat redistribution and lipid peroxidation in rats treated with an angiotensin-converting enzyme (ACE) inhibitor (lisinopril) for up to 10 months. Uninephrectomized rats developed fat redistribution and hypercholesterolemia typical of chronic renal failure when compared with sham-operated rats or lisinopril-treated uninephrectomized rats. The weight of the peri-renal fat was significantly less in the untreated compared to the lisinopril-treated uninephrectomized rats or those rats with a sham operation. We also found that there was a shift of heat-protecting unilocular adipocytes to heat-producing multilocular fat cells in the untreated uninephrectomized rats. Similarly in these rats we found a shift of subcutaneous and visceral fat to ectopic fat with excessive lipid accumulation and lipofuscin pigmentation. Lisinopril treatment prevented fat redistribution or transformation and lipid peroxidation. This study shows that ACE inhibition may prevent the fat anomalies associated with chronic renal dysfunction.
Insights
Chronic kidney dysfunction causes fat redistribution and lipid damage in rats. Angiotensin-converting enzyme (ACE) inhibitor lisinopril treatment prevented these harmful effects, suggesting ACE inhibition may protect against kidney disease-related fat anomalies.
Area of Science:
- Nephrology
- Endocrinology
- Biochemistry
Background:
- Dyslipidemia significantly impacts renal function and homeostasis.
- Chronic renal dysfunction can lead to detrimental alterations in fat metabolism and distribution.
- Lipid peroxidation is a key pathological process in chronic diseases.
Purpose of the Study:
- To investigate the effects of chronic renal dysfunction on fat redistribution and lipid peroxidation.
- To evaluate the protective role of angiotensin-converting enzyme (ACE) inhibitor lisinopril in uninephrectomized rats.
- To understand the impact of ACE inhibition on lipid metabolism in the context of chronic kidney disease.
Main Methods:
- Induction of chronic renal dysfunction via uninephrectomy in rats.
- Treatment with lisinopril, an ACE inhibitor, for up to 10 months.
- Assessment of fat redistribution, adipocyte morphology, and lipid peroxidation markers.
Main Results:
- Uninephrectomized rats exhibited significant fat redistribution and hypercholesterolemia.
- A shift from unilocular to multilocular adipocytes and increased ectopic fat accumulation was observed in untreated rats.
- Lisinopril treatment effectively prevented fat redistribution, adipocyte transformation, and lipid peroxidation.
Conclusions:
- Chronic renal dysfunction induces significant fat anomalies, including redistribution and lipid peroxidation.
- ACE inhibition with lisinopril demonstrates a protective effect against these fat-related complications.
- ACE inhibition may serve as a therapeutic strategy to mitigate metabolic disturbances in chronic kidney disease.
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