Pancreatic islet β-cell deficit and glucose intolerance in rats with uninephrectomy

Sui, Yi; Zhao, Hai-Lu; Ma, Rong; Ho, Chung-Shun; Kong, Alice Pik Shan; Lai, Fernand M.M.; Ng, Ho Keung; Rowlands, Dewi K.; Chan, Juliana C.N.; Tong, Peter C.Y.

doi:10.1007/s00018-007-7395-1

Cited by 25 publications

(26 citation statements)

References 45 publications

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“…These findings demonstrate that reduced kidney function in rats fed ad libitum leads to severe disturbances in lipid homeostasis. Most of the observed changes, including the chronic renal failure, could be prevented by the angiotensin-converting enzyme (ACE) inhibitor lisinopril, indicating involvement of the renin-angiotensinaldosterone system (RAAS) (136,157). The association between experimental glomerulosclerosis and hyperlipidemia and the deposition of lipid in glomeruli emphasizes that an intact glomerular function is essential for maintaining lipid homeostasis (157,158).…”

Section: Association Of the Western-style Diet And Metabolic Disease mentioning

confidence: 99%

The Western-style diet: a major risk factor for impaired kidney function and chronic kidney disease

Odermatt

2011

American Journal of Physiology-Renal Physiology

218

128

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The Western-style diet is characterized by its highly processed and refined foods and high contents of sugars, salt, and fat and protein from red meat. It has been recognized as the major contributor to metabolic disturbances and the development of obesity-related diseases including type 2 diabetes, hypertension, and cardiovascular disease. Also, the Western-style diet has been associated with an increased incidence of chronic kidney disease (CKD). A combination of dietary factors contributes to the impairment of renal vascularization, steatosis and inflammation, hypertension, and impaired renal hormonal regulation. This review addresses recent progress in the understanding of the association of the Western-style diet with the induction of dyslipidemia, oxidative stress, inflammation, and disturbances of corticosteroid regulation in the development of CKD. Future research needs to distinguish between acute and chronic effects of diets with high contents of sugars, salt, and fat and protein from red meat, and to uncover the contribution of each component. Improved therapeutic interventions should consider potentially altered drug metabolism and pharmacokinetics and be combined with lifestyle changes. A clinical assessment of the long-term risks of whole-body disturbances is strongly recommended to reduce metabolic complications and cardiovascular risk in kidney donors and patients with CKD.

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Section: Association Of the Western-style Diet And Metabolic Disease mentioning

confidence: 99%

The Western-style diet: a major risk factor for impaired kidney function and chronic kidney disease

Odermatt

2011

American Journal of Physiology-Renal Physiology

218

128

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“…Sprague-Dawley rats develop glucose intolerance and islet b-cell loss 8 months after uninephrectomy. 49,50 To date, there is no evidence to confirm an increased risk of developing T2DM in humans following kidney donation. No effect on insulin resistance was detected in an uncontrolled observational cohort study of 58 living donors at 6 months after donation.…”

Section: Risk Of Diabetes Mellitus After Kidney Donationmentioning

confidence: 99%

Understanding the effects of chronic kidney disease on cardiovascular risk: are there lessons to be learnt from healthy kidney donors?

et al. 2011

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Chronic kidney disease (CKD) is now a recognized global public health problem. It is highly prevalent and strongly associated with hypertension and cardiovascular disease (CVD); far more patients with a glomerular filtration rate below 60 ml min À1 per 1.73 m 2 will die from cardiovascular causes than progress to end-stage renal disease. A better understanding of the complex mechanisms underlying the development of CVD among CKD patients is required if we are to begin devising therapy to prevent or reverse this process. Observational studies of CVD in CKD are difficult to interpret because renal impairment is almost always accompanied by confounding factors. These include the underlying disease process itself (for example, diabetes mellitus and systemic vasculitis) and the complications of CKD, such as hypertension, anaemia and inflammation. Kidney donors provide an ideal opportunity to study healthy subjects without manifest vascular disease who experience an acute change from having normal to modestly impaired renal function at the time of uninephrectomy. Prospectively examining the cardiovascular consequences of uninephrectomy using donors as a model of CKD may provide useful insight into the pathophysiology of CVD in CKD and, therefore, into how the CVD risk associated with renal impairment might eventually be reduced.

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“…In addition, live kidney donation may increase the risk of developing insulin resistance and metabolic syndrome (3,4). Such clinical observation is supported by recent experimental studies in rats showing the development of glucose intolerance, dyslipidemia, and ectopic fat accumulation in parallel with the development of uremia in uninephrectomized animals (5,6). Mechanistically, overnutrition may activate the renin-angiotensin system (RAS) and thus may contribute to the pathogenesis of the metabolic syndrome in the presence of reduced renal function.…”

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confidence: 96%

Opposing Effects of Reduced Kidney Mass on Liver and Skeletal Muscle Insulin Sensitivity in Obese Mice

et al. 2014

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Reduced kidney mass and/or function may result in multiple metabolic derangements, including insulin resistance. However, underlying mechanisms are poorly understood. Herein, we aimed to determine the impact of reduced kidney mass on glucose metabolism in lean and obese mice. To that end, 7-week-old C57BL/6J mice underwent uninephrectomy (UniNx) or sham operation. After surgery, animals were fed either a chow (standard) diet or a high-fat diet (HFD), and glucose homeostasis was assessed 20 weeks after surgery. Intraperitoneal glucose tolerance was similar in sham-operated and UniNx mice. However, insulin-stimulated glucose disposal in vivo was significantly diminished in UniNx mice, whereas insulin-stimulated glucose uptake into isolated skeletal muscle was similar in sham-operated and UniNx mice. Of note, capillary density was significantly reduced in skeletal muscle of HFD-fed UniNx mice. In contrast, hepatic insulin sensitivity was improved in UniNx mice. Furthermore, adipose tissue hypoxia-inducible factor 1α expression and inflammation were reduced in HFD-fed UniNx mice. Treatment with the angiotensin II receptor blocker telmisartan improved glucose tolerance and hepatic insulin sensitivity in HFD-fed sham-operated but not UniNx mice. In conclusion, UniNx protects from obesity-induced adipose tissue inflammation and hepatic insulin resistance, but it reduces muscle capillary density and, thus, deteriorates HFD-induced skeletal muscle glucose disposal.

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Pancreatic islet β-cell deficit and glucose intolerance in rats with uninephrectomy

Cited by 25 publications

References 45 publications

The Western-style diet: a major risk factor for impaired kidney function and chronic kidney disease

The Western-style diet: a major risk factor for impaired kidney function and chronic kidney disease

Understanding the effects of chronic kidney disease on cardiovascular risk: are there lessons to be learnt from healthy kidney donors?

Opposing Effects of Reduced Kidney Mass on Liver and Skeletal Muscle Insulin Sensitivity in Obese Mice

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