High-protein induced renal enlargement is growth hormone independent

Neck, Johan W. van; Cingel, Vesna; Vliet, Arlène K. van; Drop, Stenvert L. S.; Flyvbjerg, Allan

doi:10.1111/j.1523-1755.2002.kid584.x

Cited by 7 publications

(7 citation statements)

References 36 publications

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“…Similar expression pattern of IGF system mRNA, mostly co-localizing with its protein, was observed in kidney of adult Snell dwarf mice [31]. Northern blot analysis revealed abundant expression of IGFBP-1 to -5, while IGFBP-6 could not be detected in the adult mouse kidney [8,19,21]. However, IGFBP-6 was detected by immunohistochemistry in epithelia of the distal tubule, and to some extent in epithelia of proximal tubule in the adult mouse kidney [32].…”

Section: Expression Of Gh/igf System In the Rodent Kidneysupporting

confidence: 51%

“…IGF-I is synthesized by glomerular endothelial, epithelial and mesangial cells suggesting a possible paracrine action of IGF-I in the renal glomerulus [16]. GH receptor (GHR), GH binding protein (GHBP) and all members of IGF system are expressed in the rodent kidney [8,[14][15][16][17][18][19][20][21].…”

Section: Expression Of Gh/igf System In the Rodent Kidneymentioning

confidence: 99%

“…However, GHR mRNA is most abundant in the straight portion of the proximal tubule, where IGF-IR mRNA was not detected, suggesting direct regulation by GH in this part of the nephron. To our knowledge, no localization studies have so far been performed in mice, but Northern blot and reverse transcriptase polymerase chain reaction (RT-PCR) techniques gave evidence that GHR and GHBP mRNAs are abundantly expressed in the mouse kidney, and that their expression is altered in different experimental states accompanied by kidney growth [19,21,[23][24][25][26].…”

Section: Expression Of Gh/igf System In the Rodent Kidneymentioning

confidence: 99%

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The physiological and pathophysiological roles of the GH/IGF-axis in the kidney: Lessons from experimental rodent models

Cingel-Ristić¹,

Flyvbjerg

Drop³

2004

Growth Hormone & IGF Research

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Section: Expression Of Gh/igf System In the Rodent Kidneysupporting

confidence: 51%

Section: Expression Of Gh/igf System In the Rodent Kidneymentioning

confidence: 99%

Section: Expression Of Gh/igf System In the Rodent Kidneymentioning

confidence: 99%

See 1 more Smart Citation

The physiological and pathophysiological roles of the GH/IGF-axis in the kidney: Lessons from experimental rodent models

Cingel-Ristić¹,

Flyvbjerg

Drop³

2004

Growth Hormone & IGF Research

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“…This hypothesis suggests that a primary increase in proximal tubular reabsorption of sodium and/or chloride influences glomerular filtration, not via extracellular volume expansion but through enhanced tubuloglomerular feedback mediated by decreased distal delivery of solute to the macula densa. Habitual high intake of dietary protein or chronic infusion of an AGE-modified protein in rodents also leads to renal hypertrophy, suggesting that dietary AGE could mediate effects of high-protein diets to induce kidney growth (62,64). On the basis of this "tubular hypothesis," increased dietary protein plausibly could predispose to glomerular hyperfiltration because of structural changes in the kidney.…”

Section: Preformed Agementioning

confidence: 99%

Advanced Glycation End Products and Nephrotoxicity of High-Protein Diets

Uribarri

Tuttle

2006

Clinical Journal of the American Society of Nephrology

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The popularity of high-protein diets has surged recently as obesity has become more and more common in the United States and other developed nations. In view of the high prevalence of type 2 diabetes and chronic kidney disease among obese people, it is important to understand potential effects of high-protein diets on the kidney. The hypothesis that high-protein diets are nephrotoxic because of their excessive dietary advanced glycation end product (AGE) content and an increased amino acid load that enhances AGE formation in situ was explored. This review discusses the following evidence: (1) High-protein diets are deleterious to the kidney; (2) AGE are metabolic mediators of kidney damage; (3) dietary protein-derived AGE contribute to proinflammatory and pro-oxidative processes in diabetes and kidney disease; and (4) dietary protein-derived AGE produce functional and structural abnormalities that are involved in kidney damage. Future research should consider dietary AGE as a potential therapeutic target for kidney disease in obesity, diabetes, and perhaps other causes of chronic kidney disease.

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“…It is generally known that kidney hypertrophy is the early step in the process of nephron damage [18]. …”

Section: Discussionmentioning

confidence: 99%

Impaired Bone Formation with a High-Protein Diet in Rats with Adriamycin-Induced Nephrotic Syndrome

Lim

Kim

Lee

et al. 2012

Kidney Blood Press Res

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Background/Aim: The purpose of the study was to investigate the effects of a high-protein (HP) diet on bone metabolism in rats with adriamycin (ADR)-induced nephrotic syndrome. Methods: Nephrotic syndrome was established by weekly injections of ADR (2 mg/kg, i.p.) for 6 weeks. After a final injection, we confirmed that nephrotic syndrome had developed. Then, the rats were divided into two groups for the dietary treatments, namely the HP diet (30% of calories from protein) and the low-protein (LP) diet (7% of calories from protein), and were fed an isocaloric diet for the following 5 weeks. Results: Urinary protein and phosphate excretion were significantly greater in the HP diet group than in the LP diet group (p < 0.05). Serum parathyroid hormone and osteocalcin levels were significantly higher and lower, respectively, in the HP diet group (p < 0.05). Femur weight, femur mass index and femur calcium contents were significantly lower in the HP diet group than in the LP diet group (p < 0.05). Bone mineral density was significantly lower in the HP diet group than in the LP diet group (p < 0.05); however, bone mineral content did not differ between the two groups. Conclusion: We confirmed that an HP diet negatively affects bone mineral metabolism and bone density in ADR-induced nephrotic syndrome rats.

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High-protein induced renal enlargement is growth hormone independent

Abstract: The major new finding is that HP-induced renal growth in adult mice is GH independent.

Cited by 7 publications

References 36 publications

The physiological and pathophysiological roles of the GH/IGF-axis in the kidney: Lessons from experimental rodent models

The physiological and pathophysiological roles of the GH/IGF-axis in the kidney: Lessons from experimental rodent models

Advanced Glycation End Products and Nephrotoxicity of High-Protein Diets

Impaired Bone Formation with a High-Protein Diet in Rats with Adriamycin-Induced Nephrotic Syndrome

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