Treatment with Ginger Ameliorates Fructose-Induced Fatty Liver and Hypertriglyceridemia in Rats: Modulation of the Hepatic Carbohydrate Response Element-Binding Protein-Mediated Pathway

Gao, Huanqing; Guan, Tao; Li, Chunli; Zuo, Guo‐Wei; Yamahara, Johji; Wang, Jianwei; Li, Yuhao

doi:10.1155/2012/570948

Cited by 66 publications

(70 citation statements)

References 50 publications

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“…Fructose consumption may induce excessive lipid accumulation in liver [27]. We have recently demonstrated that treatment with the ethanolic extract of ginger attenuates fructose-induced fatty liver in rats [24]. In the present study, however, five-week fructose feeding did not alter renal accumulation of triglyceride and total cholesterol in rats.…”

Section: Discussioncontrasting

confidence: 75%

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Ginger extract diminishes chronic fructose consumption-induced kidney injury through suppression of renal overexpression of proinflammatory cytokines in rats

Yang

Liu

Jiang³

et al. 2014

BMC Complement Altern Med

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BackgroundThe metabolic syndrome is associated with an increased risk of development and progression of chronic kidney disease. Renal inflammation is well known to play an important role in the initiation and progression of tubulointerstitial injury of the kidneys. Ginger, one of the most commonly used spices and medicinal plants, has been demonstrated to improve diet-induced metabolic abnormalities. However, the efficacy of ginger on the metabolic syndrome-associated kidney injury remains unknown. This study aimed to investigate the impact of ginger on fructose consumption-induced adverse effects in the kidneys.MethodsThe fructose control rats were treated with 10% fructose in drinking water over 5 weeks. The fructose consumption in ginger-treated rats was adjusted to match that of fructose control group. The ethanolic extract of ginger was co-administered (once daily by oral gavage). The indexes of lipid and glucose homeostasis were determined enzymatically, by ELISA and/or histologically. Gene expression was analyzed by Real-Time PCR.ResultsIn addition to improve hyperinsulinemia and hypertriglyceridemia, supplement with ginger extract (50 mg/kg) attenuated liquid fructose-induced kidney injury as characterized by focal cast formation, slough and dilation of tubular epithelial cells in the cortex of the kidneys in rats. Furthermore, ginger also diminished excessive renal interstitial collagen deposit. By Real-Time PCR, renal gene expression profiles revealed that ginger suppressed fructose-stimulated monocyte chemoattractant protein-1 and its receptor chemokine (C-C motif) receptor-2. In accord, overexpression of two important macrophage accumulation markers CD68 and F4/80 was downregulated. Moreover, overexpressed tumor necrosis factor-alpha, interleukin-6, transforming growth factor-beta1 and plasminogen activator inhibitor (PAI)-1 were downregulated. Ginger treatment also restored the downregulated ratio of urokinase-type plasminogen activator to PAI-1.ConclusionsThe present results suggest that ginger supplement diminishes fructose-induced kidney injury through suppression of renal overexpression of macrophage-associated proinflammatory cytokines in rats. Our findings provide evidence supporting the protective effect of ginger on the metabolic syndrome-associated kidney injury.

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Section: Discussioncontrasting

confidence: 75%

“…Therefore, fructose in drinking water was used in the present study, in accordance to this rationale and the previous research protocol [24,25,28,29]. …”

Section: Methodsmentioning

confidence: 99%

Ginger extract diminishes chronic fructose consumption-induced kidney injury through suppression of renal overexpression of proinflammatory cytokines in rats

Yang

Liu

Jiang³

et al. 2014

BMC Complement Altern Med

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“…Similar effect was observed by Al-Hoory et al, [36] who reported a reduction in serum triglyceride in alloxan-induced diabetic rats after 4 weeks of raw ginger extract administration at a dosage of 500mg/kg body weight. On the other hand the significant increase in serum triglyceride by cooked ginger extract corroborates the report of Gao et al, [38] who observed an increase in plasma triglyceride in fructose-induced hypertriglyceridemic rats by 5 weeks oral administration of alcoholic ginger extract at 50mg/kg body weight.…”

Section: Serum Triglyceridessupporting

confidence: 90%

Effect of Raw and Cooked Ginger (<i>Zingiber officinale</i> Roscoe) Extracts on Serum Cholesterol and Triglyceride in Normal and Diabetic Rats

Paulina¹,

Rasaki²,

Veronica³

2018

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Dyslipidemia is a risk factor of concern in public health even in a state of anomaly in blood glucose level. The effect of different ginger extracts on body lipids has been reported, few scientific studies have documented the effect of raw ginger extracts while the effect of cooked ginger extract (the form in which the spice is commonly consumed) is yet to be explored. This experimental study was therefore designed to determine the effect of raw and cooked ginger extracts on serum triglycerides and total cholesterol in diabetic rats and compare this with that of non-diabetic rats. Fresh ginger rhizomes were washed peeled, washed, wet-milled (without addition of water) and sieved to give the raw extract. A portion of of the extract was boiled for one hour and cooled to give cooked ginger extract. Seventy male albino rats of weight range 155g-195g were divided into 7 groups (n=10) with 3 groups kept as normal or non-diabetic while the remaining 4 groups were rendered diabetic by intraperitoneal administration of 60mg/kg body weight of streptozocin (STZ) to mimic Type 1 diabetes mellitus. These were repeated with another set of seventy rats but diabetes was induced in the 4 diabetic groups here with a 12 week consumption of high-fat diet (HFD) to mimic Type 2 diabetes mellitus. Serum total cholesterol and triglyceride were determined before and after diabetes induction as well as at the 2 nd and 4 th weeks of extracts and diabetic drugs administration using standard methods. Mean data were compared using Least Significant Difference at p≤0.05.Raw and cooked ginger extracts significantly reduced serum total cholesterol and triglyceride in both medium (2 weeks) and long (4 weeks) terms administration in non diabetic rats. In STZ-induced diabetic rats only raw ginger extract lowered these parameters significantly while the cooked extracts and glybenclamide increased these significantly. However, in HFD-induced diabetic rats, raw, cooked ginger extracts and Metformin reduced both serum total cholesterol and triglyceride significantly. Ginger in both raw and cooked forms may therefore be useful in ameliorating hyperlipidemia which commonly associates diabetic state. Human trial is hereby recommended.

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“…Real-time PCR was performed as described previously [21, 22]. Total RNA was isolated from livers of individual rats using TRIzol (Takara, Dalian, China).…”

Section: Methodsmentioning

confidence: 99%

Oleanolic Acid Diminishes Liquid Fructose-Induced Fatty Liver in Rats: Role of Modulation of Hepatic Sterol Regulatory Element-Binding Protein-1c-Mediated Expression of Genes Responsible for De Novo Fatty Acid Synthesis

Liu

Zuo

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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Oleanolic acid (OA), contained in more than 1620 plants and as an aglycone precursor for naturally occurred and synthesized triterpenoid saponins, is used in China for liver disorders in humans. However, the underlying liver-protecting mechanisms remain largely unknown. Here, we found that treatment of rats with OA (25 mg/kg/day, gavage, once daily) over 10 weeks diminished liquid fructose-induced excess hepatic triglyceride accumulation without effect on total energy intake. Attenuation of the increased vacuolization and Oil Red O staining area was evident on histological examination of liver in OA-treated rats. Hepatic gene expression profile demonstrated that OA suppressed fructose-stimulated overexpression of sterol regulatory element-binding protein-(SREBP-) 1/1c mRNA and nuclear protein. In accord, overexpression of SREBP-1c-responsive genes responsible for fatty acid synthesis was also downregulated. In contrast, overexpressed nuclear protein of carbohydrate response element-binding protein and its target genes liver pyruvate kinase and microsomal triglyceride transfer protein were not altered. Additionally, OA did not affect expression of peroxisome proliferator-activated receptor-gamma- and -alpha and their target genes. It is concluded that modulation of hepatic SREBP-1c-mediated expression of the genes responsible for de novo fatty acid synthesis plays a pivotal role in OA-elicited diminishment of fructose-induced fatty liver in rats.

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Treatment with Ginger Ameliorates Fructose-Induced Fatty Liver and Hypertriglyceridemia in Rats: Modulation of the Hepatic Carbohydrate Response Element-Binding Protein-Mediated Pathway

Cited by 66 publications

References 50 publications

Ginger extract diminishes chronic fructose consumption-induced kidney injury through suppression of renal overexpression of proinflammatory cytokines in rats

Ginger extract diminishes chronic fructose consumption-induced kidney injury through suppression of renal overexpression of proinflammatory cytokines in rats

Effect of Raw and Cooked Ginger (<i>Zingiber officinale</i> Roscoe) Extracts on Serum Cholesterol and Triglyceride in Normal and Diabetic Rats

Oleanolic Acid Diminishes Liquid Fructose-Induced Fatty Liver in Rats: Role of Modulation of Hepatic Sterol Regulatory Element-Binding Protein-1c-Mediated Expression of Genes Responsible for De Novo Fatty Acid Synthesis

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