Nutritional Intervention for a Patient with Diabetic Nephropathy

Kim, Hee Young

doi:10.7762/cnr.2014.3.1.64

Cited by 20 publications

(13 citation statements)

References 8 publications

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“…DN occurs in 20% to 40% of patients with diabetes and is the most likely cause of end-stage renal disease reported worldwide [ 6 ]. Although numerous factors contributing to the development of diabetic complications including DN have been proposed, AGEs are thought to be of major importance [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

Diphlorethohydroxycarmalol Attenuates Methylglyoxal‐Induced Oxidative Stress and Advanced Glycation End Product Formation in Human Kidney Cells

Cha

Hwang

Heo

et al. 2018

Oxidative Medicine and Cellular Longevity

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Diabetic nephropathy is the leading cause of end-stage renal disease in patients with diabetes mellitus. Oxidative stress has been shown to play an important role in pathogeneses of renal damage in diabetic patients. Here, we investigated the protective effect of diphlorethohydroxycarmalol (DPHC), which is a polyphenol isolated from an edible seaweed, Ishige okamurae, on methylglyoxal-induced oxidative stress in HEK cells, a human embryonic kidney cell line. DPHC treatment inhibited methylglyoxal- (MGO-) induced cytotoxicity and ROS production. DPHC activated the Nrf2 transcription factor and increased the mRNA expression of antioxidant and detoxification enzymes, consequently reducing MGO-induced advanced glycation end product formation. In addition, DPHC increased glyoxalase-1 mRNA expression and attenuated MGO-induced advanced glycation end product formation in HEK cells. These results suggest that DPHC possesses a protective activity against MGO-induced cytotoxicity in human kidney cells by preventing oxidative stress and advanced glycation end product formation. Therefore, it could be used as a potential therapeutic agent for the prevention of diabetic nephropathy.

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Section: Introductionmentioning

confidence: 99%

Diphlorethohydroxycarmalol Attenuates Methylglyoxal‐Induced Oxidative Stress and Advanced Glycation End Product Formation in Human Kidney Cells

Cha

Hwang

Heo

et al. 2018

Oxidative Medicine and Cellular Longevity

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“…Sarcopenia is the progressive generalized loss of skeletal muscle mass, strength, and function. Although sarcopenia is essentially a disorder of advanced age, it can also occur at younger ages secondary to chronic nutritional problems, chronic diseases, malignancies, low level of physical activity, some drugs side effects ( 1 , 2 ). Chronic kidney disease (CKD) can lead to sarcopenia.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Sarcopenia in Renal Transplant Recipients

et al. 2014

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Background:Chronic kidney disease can lead to sarcopenia; however, no study has described sarcopenia in the patients undergoing renal transplantation.Objectives:The aim of the present study was to assess the prevalence of sarcopenia in renal transplant recipients (RTR) and to evaluate the demographic and metabolic risk factors associated with sarcopenia in these patients.Patients and Methods:Sarcopenia was diagnosed by measuring handgrip strength in 166 RTR (68 females and 98 males; mean age, 37.9 ± 11.9 years). Basal metabolic rate, fat mass, free-fat mass, total body water, body mass index, and calf circumference were determined, along with blood biochemistry, vitamin D levels, and glomerular filtration rate.Results:Among 166 patients, sarcopenia was present in 34 (20.5%). Handgrip, basal metabolic rate, free fat mass, and total body water were significantly lower in patients with sarcopenia in comparison with those without sarcopenia. There were no differences between patients with and without sarcopenia in terms of mean time since transplantation, the presence of diabetes mellitus, hypertension, coronary artery disease, hyperlipidemia, glomerular filtration rate, and body mass index. Univariate analysis revealed significant differences between patients with and without sarcopenia with respect to age (mean of 43.70 ± 13.97 and 36.37 ± 10.82 years, respectively; P = 0.007) and 25-OH vitamin D levels (median (IQR) of 12 (2-39) and 17.70 (3-68) μg/L, respectively; P = 0.024). There was a statistically significant positive correlation between vitamin D levels and handgrip strength (r = 0.334; P < 0.001). Multivariate regression analysis determined that age was an independent predictive variable of sarcopenia in RTR (β = 1.060; 95% CI, 1.017-1.105; and P = 0.006).Conclusions:Chronic renal disease contributes to sarcopenia, which may develop at an earlier age in RTR.

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“…The induction of insulin resistance by high fructose diet was considered to enhance impaired glucose tolerance in the high fructose-fed SDT rats. In humans, high blood glucose level is one of the risk factors for DN of diabetes patients (Delahanty and Halford, 1993;Kim, 2014). Therefore, elevation of plasma glucose levels in the SDT rats fed a high fructose diet was considered to contribute to progression of the kidney injury.…”

Section: D a B E Fmentioning

confidence: 99%

“…Some recent trials report that strict blood glucose management using a carbohydrate-limited diet ameliorates hyperglycemia and such carbohydrate management is effective for delaying of the progression to DN (Delahanty and Halford, 1993;Kim, 2014). While the intake of glucose is one of the most important factors influencing the development of diabetes and DN, some studies revealed that other nutrients also contribute to the progression of diabetes and DN.…”

Section: Introductionmentioning

confidence: 99%

High fructose diet feeding accelerates diabetic nephropathy in Spontaneously Diabetic Torii (SDT) rats

et al. 2018

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-Diabetic nephropathy (DN) is one of the complications of diabetes and is now the most common cause of end-stage renal disease. Fructose is a simple carbohydrate that is present in fruits and honey and is used as a sweetener because of its sweet taste. Fructose has been reported to have the potential to progress diabetes and DN in humans even though fructose itself does not increase postprandial plasma glucose levels. In this study, we investigated the effects of high fructose intake on the kidney of the Spontaneously Diabetic Torii (SDT) rats which have renal lesions similar to those in DN patients and compared these with the effects in normal SD rats. This study revealed that a 4-week feeding of the high fructose diet increased urinary excretion of kidney injury makers for tubular injury and accelerated mainly renal tubular and interstitial lesions in the SDT rats but not in normal rats. The progression of the nephropathy in the SDT rats was considered to be related to increased internal uric acid and blood glucose levels due to the high fructose intake. In conclusion, high fructose intake exaggerated the renal lesions in the SDT rats probably due to effects on the tubules and interstitium through metabolic implications for uric acid and glucose.

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Nutritional Intervention for a Patient with Diabetic Nephropathy

Cited by 20 publications

References 8 publications

Diphlorethohydroxycarmalol Attenuates Methylglyoxal‐Induced Oxidative Stress and Advanced Glycation End Product Formation in Human Kidney Cells

Diphlorethohydroxycarmalol Attenuates Methylglyoxal‐Induced Oxidative Stress and Advanced Glycation End Product Formation in Human Kidney Cells

Evaluation of Sarcopenia in Renal Transplant Recipients

High fructose diet feeding accelerates diabetic nephropathy in Spontaneously Diabetic Torii (SDT) rats

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