Crosstalk of Hyperglycemia and Dyslipidemia in Diabetic Kidney Disease

Su, Wen; Cao, Rong; He, Yong; Guan, You Fei; Ruan, Xiong Z.

doi:10.1159/000479874

Cited by 42 publications

(29 citation statements)

References 91 publications

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“…Herein, we also confirmed that rutin treatment can reduce blood sugar in DMR rats ( Figure 2 ). Insulin resistance caused by hyperglycemia promotes the pathogenesis of hyperlipidemia, but the underlying mechanism is still unclear [ 27 ]. Figure 1 shows that STZ induces AST, ALT, ALP, CHO and TG and that rutin has beneficial effects on AST, ALP, and CHO.…”

Section: Discussionmentioning

confidence: 99%

Effects of Rutin on Wound Healing in Hyperglycemic Rats

et al. 2020

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Long-term poor glycemic control negatively affects macrovascular and microvascular diseases, as well as wound restoration. Buckwheat is a good source of rutin (quercetin-3-O-rutoside) and has benefits in regulating blood sugar. This study was to evaluate the antioxidant and anti-inflammatory effects of rutin on wound healing in streptozotocin-induced hyperglycemic rats. Eighteen male Wistar rats were randomly divided into three groups: normal (NDM), hyperglycemic (DM), and hyperglycemic with rutin (DMR). After induction of hyperglycemia for 2 days, a 15 × 15 mm wound was induced on the back of each rat. Intraperitoneal injection of rutin significantly ameliorated diabetes-induced body weight loss and improved metabolic dysfunctions of hyperglycemic rats. Based on appearance and histopathological staining, rutin promotes wound healing and inhibits production of inflammatory cells. The immunoblotting data indicated that rutin promotes production of antioxidant enzymes induced by nuclear factor erythroid 2-related factor 2 (NRF2), inhibits the expression of matrix metalloproteinases (MMPs) regulated by NF-κB, and decreases the expression of vascular endothelial growth factor (VEGF). It also promotes the expression of neurogenic-related protein (UCH-L1). The aforementioned results indicated that rutin reduces oxidative stress and inflammatory response in hyperglycemic rats, promoting wound healing and subsequently reducing the risk of wound ulcers.

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Section: Discussionmentioning

confidence: 99%

Effects of Rutin on Wound Healing in Hyperglycemic Rats

et al. 2020

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“…Conversely, weight regained and improvement in metabolic indicators will further help control the development of DKD. Because high blood glucose fluctuations may damage glomerular mesangial cells and promote cell apoptosis, and lipid metabolism disorder and abnormal lipid deposition in the glomerulus may lead to proliferation of glomerular cell membrane, causing gradual accumulation of ECM, which explains the pathological basis of DKD [26].…”

Section: Discussionmentioning

confidence: 99%

20(S)-Ginsenoside Rg3 Protects Kidney from Diabetic Kidney Disease via Renal Inflammation Depression in Diabetic Rats

Zhou

Sun

Yang

et al. 2020

Journal of Diabetes Research

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Rg3) has been shown to induce apoptosis by interfering with several signaling pathways. Furthermore, it has been reported to have anticancer and antidiabetic effects. In order to detect the protective effect of 20(S)-Rg3 on diabetic kidney disease (DKD), diabetic rat models which were established by administering high-sugar, high-fat diet combined with intraperitoneal injection of streptozotocin (STZ), and age-matched wild-type (WT) rat were given 20(S)-Rg3 for 12 weeks, with three groups: control group (normal adult rats with saline), diabetic group (diabetic rats with saline), and 20(S)-Rg3 treatment group (diabetic rats with 20(S)-Rg3 (10 mg/kg body weight/day)). The biochemical indicators and the changes in glomerular basement membrane and mesangial matrix were detected. TUNEL staining was used to detect glomerular and renal tubular cell apoptosis. Immunohistochemical staining was used to detect the expression of fibrosis factors and inflammation factors in rat kidney tissues. Through periodic acid-Schiff staining, we observed that the change in renal histology was improved and renal tubular epithelial cell apoptosis decreased significantly by treatment with 20(S)-Rg3. Plus, the urine protein decreased in the rats with the 20(S)-Rg3 treatment. Fasting blood glucose, creatinine, total cholesterol, and triglyceride levels in the 20(S)-Rg3 treatment group were all lower than those in the diabetic group. Mechanistically, 20(S)-Rg3 dramatically downregulated the expression of TGF-β1, NF-κB65, and TNF-α in the kidney. These resulted in a significant prevention of renal damage from the inflammation. The results of the current study suggest that 20(S)-Rg3 could potentially be used as a novel treatment against DKD.

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“…Regarding lipid metabolism, phosphorylated AMPK can also improve high-fat-diet-induced NASH through the suppression of several key lipogenic factors in the liver related to cholesterol and fatty acid synthesis, such as sterol regulatory element-binding protein (SREBP-1), which results in reduced triglyceride synthesis, HMG-CoAR levels, cholesterol synthesis, and ACC enzyme activation, which in turn decreases malonyl-CoA levels and reduces free fatty acids and VLDL synthesis (Musso et al, 2016;Su et al, 2017).…”

Section: Ampkmentioning

confidence: 99%

“…PPAR-α is also a transcriptional regulator of genes involved in fatty acid transport and in peroxisomal and mitochondrial βoxidation. PPAR-α phosphorylation reduces triglyceride levels by increasing lipolysis, inducing LPL to catalyze the hydrolysis of triglycerides into free fatty acids and monoacylglycerol; PPAR-α inhibits VLDL production and stimulates the production of ApoA-I and ApoA-II, which are associated with HDL (Musso et al, 2016;Pawlak et al, 2015;Su et al, 2017).…”

Section: Ppar-αmentioning

confidence: 99%

Central cellular signaling pathways involved with the regulation of lipid metabolism in the liver: a review

Lopes

Santana

Cruz

et al. 2020

Acta Sci. Biol. Sci.

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The liver is primarily responsible for energy homeostasis and the regulation of lipid, carbohydrate and protein metabolism. Lipid metabolism consists of distributing lipids to peripheral tissues or ensuring their return to the liver to be reprocessed. Additionally, cellular metabolism is regulated by several molecules in different signaling pathways. Lipid homeostasis in the liver is mainly regulated by AKT, AMPK, SREBP, PPAR, and JNK. The PI3K/AKT/mTOR signaling pathway results in the biosynthesis of macromolecules and regulates lipogenesis and the expression of lipogenic genes. AMPK is an energy sensor that regulates metabolism and is activated when stored ATP is depleted, and it is responsible for the suppression of several key lipogenic factors in the liver related to cholesterol and fatty acid synthesis. SREBPs control lipogenic gene expression and cholesterol metabolism and act in the nutritional regulation of fatty acids and triglycerides. The continued activation of SREBPs is associated with cellular stress, inflammation and ultimately steatosis. PPARs are intrinsically important regulators of lipid metabolism. These genes are essential to various metabolic processes, especially lipid and glucose homeostasis, and can play a role in cell differentiation. JNK signaling is related to insulin resistance and its activation results in decreased mitochondrial activity and fat accumulation. Therefore, the study of cell signaling pathways related to lipid metabolism and liver function may help to identify abnormalities and develop strategies to manage and regulate metabolic disorders and resulting complications.

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Crosstalk of Hyperglycemia and Dyslipidemia in Diabetic Kidney Disease

Cited by 42 publications

References 91 publications

Effects of Rutin on Wound Healing in Hyperglycemic Rats

Effects of Rutin on Wound Healing in Hyperglycemic Rats

20(S)-Ginsenoside Rg3 Protects Kidney from Diabetic Kidney Disease via Renal Inflammation Depression in Diabetic Rats

Central cellular signaling pathways involved with the regulation of lipid metabolism in the liver: a review

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