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Basic Research
The Role of CD36 in Type 2 Diabetes Mellitus: β-Cell Dysfunction and Beyond
Jun Sung Moon, Udayakumar Karunakaran, Elumalai Suma, Seung Min Chung, Kyu Chang Won
Diabetes Metab J. 2020;44(2):222-233.   Published online April 23, 2020
DOI: https://doi.org/10.4093/dmj.2020.0053
  • 8,942 View
  • 188 Download
  • 19 Web of Science
  • 19 Crossref
AbstractAbstract PDFPubReader   

Impaired β-cell function is the key pathophysiology of type 2 diabetes mellitus, and chronic exposure of nutrient excess could lead to this tragedy. For preserving β-cell function, it is essential to understand the cause and mechanisms about the progression of β-cells failure. Glucotoxicity, lipotoxicity, and glucolipotoxicity have been suggested to be a major cause of β-cell dysfunction for decades, but not yet fully understood. Fatty acid translocase cluster determinant 36 (CD36), which is part of the free fatty acid (FFA) transporter system, has been identified in several tissues such as muscle, liver, and insulin-producing cells. Several studies have reported that induction of CD36 increases uptake of FFA in several cells, suggesting the functional interplay between glucose and FFA in terms of insulin secretion and oxidative metabolism. However, we do not currently know the regulating mechanism and physiological role of CD36 on glucolipotoxicity in pancreatic β-cells. Also, the downstream and upstream targets of CD36 related signaling have not been defined. In the present review, we will focus on the expression and function of CD36 related signaling in the pancreatic β-cells in response to hyperglycemia and hyperlipidemia (ceramide) along with the clinical studies on the association between CD36 and metabolic disorders.

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Original Articles
Basic Research
Article image
Inhibition of Ceramide Accumulation in Podocytes by Myriocin Prevents Diabetic Nephropathy
Chang-Yun Woo, Ji Yeon Baek, Ah-Ram Kim, Chung Hwan Hong, Ji Eun Yoon, Hyoun Sik Kim, Hyun Ju Yoo, Tae-Sik Park, Ranjan Kc, Ki-Up Lee, Eun Hee Koh
Diabetes Metab J. 2020;44(4):581-591.   Published online November 4, 2019
DOI: https://doi.org/10.4093/dmj.2019.0063
  • 7,343 View
  • 178 Download
  • 33 Web of Science
  • 35 Crossref
AbstractAbstract PDFPubReader   ePub   
Background

Ceramides are associated with metabolic complications including diabetic nephropathy in patients with diabetes. Recent studies have reported that podocytes play a pivotal role in the progression of diabetic nephropathy. Also, mitochondrial dysfunction is known to be an early event in podocyte injury. Thus, we tested the hypothesis that ceramide accumulation in podocytes induces mitochondrial damage through reactive oxygen species (ROS) production in patients with diabetic nephropathy.

Methods

We used Otsuka Long Evans Tokushima Fatty (OLETF) rats and high-fat diet (HFD)-fed mice. We fed the animals either a control- or a myriocin-containing diet to evaluate the effects of the ceramide. Also, we assessed the effects of ceramide on intracellular ROS generation and on podocyte autophagy in cultured podocytes.

Results

OLETF rats and HFD-fed mice showed albuminuria, histologic features of diabetic nephropathy, and podocyte injury, whereas myriocin treatment effectively treated these abnormalities. Cultured podocytes exposed to agents predicted to be risk factors (high glucose, high free fatty acid, and angiotensin II in combination [GFA]) showed an increase in ceramide accumulation and ROS generation in podocyte mitochondria. Pretreatment with myriocin reversed GFA-induced mitochondrial ROS generation and prevented cell death. Myriocin-pretreated cells were protected from GFA-induced disruption of mitochondrial integrity.

Conclusion

We showed that mitochondrial ceramide accumulation may result in podocyte damage through ROS production. Therefore, this signaling pathway could become a pharmacological target to abate the development of diabetic kidney disease.

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Effects of Endurance Exercise and High-Fat Diet on Insulin Resistance and Ceramide Contents of Skeletal Muscle in Sprague-Dawley Rats
Hyun Lyung Jung, Ho Youl Kang
Korean Diabetes J. 2010;34(4):244-252.   Published online August 31, 2010
DOI: https://doi.org/10.4093/kdj.2010.34.4.244
  • 3,864 View
  • 31 Download
  • 9 Crossref
AbstractAbstract PDFPubReader   
Background

We evaluated the effects of endurance exercise and a high-fat diet on insulin resistance and ceramide contents of skeletal muscle in Sprague-Dawley rats.

Methods

We randomly divided 32 rats into four groups: control (CON, n = 8), high fat diet (HF, n = 8), exercise (Ex, 24 m/min for 2 hours, 5 days/wk, n = 8), HF/Ex (n = 8). After 4-week treatments, plasma lipid profiles, glucose and insulin concentrations were measured. The triglycerides (TG), ceramide, and glucose transporter 4 (GLUT-4) contents were measured in the skeletal muscle. The rate of glucose transport was determined under submaximal insulin concentration during the muscle incubation.

Results

Free fatty acid levels were significantly higher in CON and HF than Ex (P = 0.032). Plasma glucose levels in HF were significantly higher than the two Ex groups (P = 0.002), and insulin levels were significantly higher in HF than in other three groups (P = 0.021). Muscular TG concentrations were significantly higher in HF than CON and Ex and also in HF/Ex than Ex, respectively (P = 0.005). Hepatic TG concentrations were significantly higher in HF than other three groups but Ex was significantly lower than HF/Ex (P = 0.000). Muscular ceramide content in HF was significantly greater than that in either Ex or HF/Ex (P = 0.031). GLUT-4 levels in CON and HF were significantly lower than those in Ex and HF/Ex (P = 0.009, P = 0.003). The glucose transport rate in submaximal insulin concentration was lower in CON than in either Ex or HF/Ex (P = 0.043), but not different from HF.

Conclusion

This study suggests that high fat diet for 4 weeks selectively impairs insulin resistance, but not glucose transport rate, GLUT-4 and ceramide content in skeletal muscle per se. However, endurance exercise markedly affects the content of ceramide and insulin resistance in muscle.

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