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. 2010:2010:136502.
doi: 10.1155/2010/136502. Epub 2010 Feb 17.

Body weight control by a high-carbohydrate/low-fat diet slows the progression of diabetic kidney damage in an obese, hypertensive, type 2 diabetic rat model

Shuichi Ohtomo  1 , Yuko Izuhara, Masaomi Nangaku, Takashi Dan, Sadayoshi Ito, Charles van Ypersele de Strihou, Toshio Miyata
Affiliations

Body weight control by a high-carbohydrate/low-fat diet slows the progression of diabetic kidney damage in an obese, hypertensive, type 2 diabetic rat model

Shuichi Ohtomo et al. J Obes. 2010.

Abstract

Obesity is one of several factors implicated in the genesis of diabetic nephropathy (DN). Obese, hypertensive, type 2 diabetic rats SHR/NDmcr-cp were given, for 12 weeks, either a normal, middle-carbohydrate/middle-fat diet (MC/MF group) or a high-carbohydrate/low-fat diet (HC/LF group). Daily caloric intake was the same in both groups. Nevertheless, the HC/LF group gained less weight. Despite equivalent degrees of hypertension, hyperglycemia, hyperlipidemia, hyperinsulinemia, and even a poorer glycemic control, the HC/LF group had less severe renal histological abnormalities and a reduced intrarenal advanced glycation and oxidative stress. Mediators of the renoprotection, specifically linked to obesity and body weight control, include a reduced renal inflammation and TGF-beta expression, together with an enhanced level of adiponectin. Altogether, these data identify a specific role of body weight control by a high-carbohydrate/low-fat diet in the progression of DN. Body weight control thus impacts on local intrarenal advanced glycation and oxidative stress through inflammation and adiponectin levels.

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Figures

Figure 1
Figure 1
Daily diet intake. (a) Daily calorie intake, (b) carbohydrate intake, (c) fat intake, (d) protein intake, and (e) sodium intake in MC/MF (closed square) and HC/LF (open square). **P < .01, ***P < .001 versus MC/MF.
Figure 2
Figure 2
Metabolic abnormalities. (a) Body weight, (b) HbA1c, (c) triglycerides, (d) insulin, and (d) systolic blood pressure. WKY (closed triangle), MC/MF (closed square), and HC/LF (open square). *P < .05, **P < .01, ***P < .001 versus WKY; ††P < .01, †††P < .001 versus MC/MF.
Figure 3
Figure 3
Changes of proteinuria. WKY (closed triangle), MC/MF (closed square), and HC/LF (open square). **P < .01, ***P < .001 versus WKY; †††P < .001 versus MC/MF.
Figure 4
Figure 4
Glomerular sclerosis, tubulointerstitial fibrosis, and macrophage infiltration. PAS-stained (a)–(c), Masson trichrome-stained (d)–(f), or ED-1-immunostained (g) and (h) renal tissues. WKY rats (a), (d), MC/MF (c), (f), (h), and HC/LF (b), (e), (g) at the end of study. Arrows indicate ED-1 positive cells. Original magnification 400× ((a)–(c), (g), (h)) and 200× (d)–(f).
Figure 5
Figure 5
Inflammation in renal tissues. (a) ED-1 positive cells in tubulointerstitial area, (b) gene expressions of TNF-alpha, ICAM-1, and VCAM-1, and (c) plasma adiponectin level in MC/MF (white bar) and HC/LF (black bar). *P < .05, **P < .01.
Figure 6
Figure 6
TGF-beta in renal tissues and its induction in vitro by TNF-alpha. (a) Gene expressions of TGF-beta, CTGF, and PAI-1 in MC/MF (white bar) and HC/LF (black bar).*P < .05, **P < .01. (b) Effects of TNF-alpha on TGF-beta mRNA expressions in vitro in cultured rat proximal tubular cells (IRPTC). *P < .05, **P < .01.
Figure 7
Figure 7
Advanced glycation and oxidative stress in renal tissues. (a) Renal pentosidine content, and (b) gene expressions of Nox2 and p47phox in MC/MF (white bar) and HC/LF (black bar).*P < .05, **P < .01.
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References

    1. Sarafidis PA, Ruilope LM. Insulin resistance, hyperinsulinemia, and renal injury: mechanisms and implications. American Journal of Nephrology. 2006;26(3):232–244. - PubMed
    1. Trovati M, Cavalot F. Optimization of hypolipidemic and antiplatelet treatment in the diabetic patient with renal diseas. Journal of the American Society of Nephrology. 2004;15(supplement 1):S12–S20. - PubMed
    1. Sarafidis PA, Bakris GL. Protection of the kidney by thiazolidinediones: an assessment from bench to bedside. Kidney International. 2006;70(7):1223–1233. - PubMed
    1. Remuzzi G, Macia M, Ruggenenti P. Prevention and treatment of diabetic renal disease in type 2 diabetes: the BENEDICT study. Journal of the American Society of Nephrology. 2006;17(supplement 2):S90–S97. - PubMed
    1. Fioretto P, Bruseghin M, Berto I, Gallina P, Manzato E, Mussap M. Renal protection in diabetes: role of glycemic control. Journal of the American Society of Nephrology. 2006;17(supplement 2):S86–S89. - PubMed

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