A low-protein diet concomitant with high calorie intake preserves renal function and structure in diabetic OLETF rats

Matsuda, Shinji; Iwata, Koichi; Takahashi, Katsumi; Homma, Hitoshi; Tamura, Yoshifuru; Kanda, Yuko; Inokami, Taketoshi; Nosaka, Hitonari; Nagase, Mitsumasa; Uchida, Shunya

doi:10.1007/s10157-004-0312-0

Cited by 6 publications

(5 citation statements)

References 25 publications

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“…Renal lesions in OLETF rats were characterized by thickening of the glomerular basement membrane, mesangial expansion, sclerotic lesions, interstitial fibrosis (29) and interstitial lymphocyte infiltration (30). In this study, histological appearances revealed findings comparable to these observations.…”

Section: Thiamine Mitigated Albuminuria Renal Interstitial Fibrosissupporting

confidence: 81%

Thiamine Prevents Obesity and Obesity-Associated Metabolic Disorders in OLETF Rats

Tanaka

Kono

Terasaki

et al. 2010

J Nutr Sci Vitaminol

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SummaryWe previously found that thiamine mitigates metabolic disorders in spontaneously hypertensive rats, harboring defects in glucose and fatty acid metabolism. Mutation of thiamine transporter gene SLC19A2 is linked to type 2 diabetes mellitus. The current study extends our hypothesis that thiamine intervention may impact metabolic abnormalities in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, exhibiting obesity and metabolic disorders similar to human metabolic syndrome. Male OLETF rats (4 wk old) were given free access to water containing either 0.2% or 0% of thiamine for 21 and 51 wk. At the end of treatment, blood parameters and cardiac functions were analyzed. After sacrifice, organs weights, histological findings, and hepatic pyruvate dehydrogenase (PDH) activity in the liver were evaluated. Thiamine intervention averted obesity and prevented metabolic disorders in OLETF rats which accompanied mitigation of reduced lipid oxidation and increased hepatic PDH activity. Histological evaluation revealed that thiamine alleviated adipocyte hypertrophy, steatosis in the liver, heart, and skeletal muscle, sinusoidal fibrosis with formation of basement membranes (called pseudocapillarization) which accompanied significantly reduced expression of laminin ␤ 1 and nidogen-1 mRNA, interstitial fibrosis in the heart and kidney, fatty degeneration in the pancreas, thickening of the basement membrane of the vasculature, and glomerulopathy and mononuclear cell infiltration in the kidney. Cardiac and renal functions were preserved in thiamine treatment. Thiamine has a potential to prevent obesity and metabolic disorders in OLETF rats.

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Section: Thiamine Mitigated Albuminuria Renal Interstitial Fibrosissupporting

confidence: 81%

Thiamine Prevents Obesity and Obesity-Associated Metabolic Disorders in OLETF Rats

Tanaka

Kono

Terasaki

et al. 2010

J Nutr Sci Vitaminol

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“…Thus, the treatment strategies for renal failure, including the use of protein-restricted diets [1], have gained increased interest for the treatment of patients with diabetic nephropathy. Despite the few studies that suggest that protein intake restriction fails to improve renal prognosis in type 1 or type 2 diabetic patients with incipient or overt nephropathy[2] and confers renoprotection[3], several findings have demonstrated that a low-protein diet preserves renal function and structure in animal models [4] and in type 2 diabetic patients with macroalbuminuria[5] and improves disease prognosis[6], low-grade inflammation and proteinuria[7] and depressive symptoms[8]. However, there has been increasing concern regarding the risk of the subsequent development of malnutrition due to these diets.…”

Section: Introductionmentioning

confidence: 99%

Effect of a Low-Protein Diet Supplemented with Ketoacids on Skeletal Muscle Atrophy and Autophagy in Rats with Type 2 Diabetic Nephropathy

Huang

Wang

et al. 2013

PLoS ONE

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A low-protein diet supplemented with ketoacids maintains nutritional status in patients with diabetic nephropathy. The activation of autophagy has been shown in the skeletal muscle of diabetic and uremic rats. This study aimed to determine whether a low-protein diet supplemented with ketoacids improves muscle atrophy and decreases the increased autophagy observed in rats with type 2 diabetic nephropathy. In this study, 24-week-old Goto-Kakizaki male rats were randomly divided into groups that received either a normal protein diet (NPD group), a low-protein diet (LPD group) or a low-protein diet supplemented with ketoacids (LPD+KA group) for 24 weeks. Age- and weight-matched Wistar rats served as control animals and received a normal protein diet (control group). We found that protein restriction attenuated proteinuria and decreased blood urea nitrogen and serum creatinine levels. Compared with the NPD and LPD groups, the LPD+KA group showed a delay in body weight loss, an attenuation in soleus muscle mass loss and a decrease of the mean cross-sectional area of soleus muscle fibers. The mRNA and protein expression of autophagy-related genes, such as Beclin-1, LC3B, Bnip3, p62 and Cathepsin L, were increased in the soleus muscle of GK rats fed with NPD compared to Wistar rats. Importantly, LPD resulted in a slight reduction in the expression of autophagy-related genes; however, these differences were not statistically significant. In addition, LPD+KA abolished the upregulation of autophagy-related gene expression. Furthermore, the activation of autophagy in the NPD and LPD groups was confirmed by the appearance of autophagosomes or autolysosomes using electron microscopy, when compared with the Control and LPD+KA groups. Our results showed that LPD+KA abolished the activation of autophagy in skeletal muscle and decreased muscle loss in rats with type 2 diabetic nephropathy.

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“…In nonobese and normoglycemic control LETO rats (group NA), protein restriction also improved the increasing rates of UAE induced by higher energy intake. Matsuda et al, 21 using OLETF rats, reported that the lowprotein diet suppressed urinary protein excretion by more than half after 60 weeks of age, even though the rats fed on a low protein diet showed hyperglycemia and higher hemoglobin Aic levels by hyperphagia. In this study, the amount of food consumed was the same among the three subgroups at 28 weeks of age, although a slight increase was observed between rats at 22 weeks and 28 weeks of age in subgroup AP-10.…”

Section: Discussionmentioning

confidence: 96%

The suppressive effects of dietary protein restriction on the progression of renal impairment in OLETF rats

Sakamoto

Akehi

Mimura³

et al. 2006

Clin Exp Nephrol

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Dietary protein restriction starting very early in the life of OLETF rats, in combination with energy restriction, clearly suppressed UAE and the typical morphological changes that otherwise occurred at around 16 weeks of age. This method also seemed to be more effective than energy restriction alone in slowing down any increase in UAE. The influence of BG levels on UAE was lower at an early age, while it became an increasingly important factor at later ages in the experimental rat model.

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A low-protein diet concomitant with high calorie intake preserves renal function and structure in diabetic OLETF rats

Abstract: A low-protein diet, despite the worsening hyperglycemia caused by hyperphagia, not only reduced proteinuria but also ameliorated hyperlipidemia in OLETF rats, thereby preserving renal function and structure in diabetic nephropathy, probably via a macrophage-mediated mechanism.

Cited by 6 publications

References 25 publications

Thiamine Prevents Obesity and Obesity-Associated Metabolic Disorders in OLETF Rats

Thiamine Prevents Obesity and Obesity-Associated Metabolic Disorders in OLETF Rats

Effect of a Low-Protein Diet Supplemented with Ketoacids on Skeletal Muscle Atrophy and Autophagy in Rats with Type 2 Diabetic Nephropathy

The suppressive effects of dietary protein restriction on the progression of renal impairment in OLETF rats

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