Effect of chromium on carbohydrate and lipid metabolism in a rat model of type 2 diabetes mellitus: the fat-fed, streptozotocin-treated rat

Şahin, Kazım; Onderci, Muhittin; Tuzcu, Mehmet; Üstündağ, Bilal; Çıkım, Gürkan; Özercan, İbrahim Hanifı; Sriramoju, Vidyasagar; Juturu, Vijaya; Komorowski, James

doi:10.1016/j.metabol.2007.04.021

Cited by 147 publications

(122 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The hepatocytes' nuclei were generally enlarged and sometimes showed irregular contours and intranuclear inclusions. 20,21,25 In this study, we observed similar morphological changes in STZ-NA treated diabetic rat liver. In untreated diabetic rats and L-NNA treated diabetic rats, the nuclei of hepatocytes were enlarged.…”

Section: Histopatologysupporting

confidence: 76%

Antioxidant and Free Radical-Scavenging Properties of Stevia rebaudiana (Bertoni) Extracts and L-NNA in Streptozotocine-Nicotinamide Induced Diabetic Rat Liver

Özbayer¹,

Değirmenci²,

Kurt³

et al. 2011

Turkiye Klinikleri J Med Sci

View full text Add to dashboard Cite

A AB BS S T TR RA AC CT T O Ob b j je ec c t ti i v ve e: : Fre e ra di cal pro duc ti on is imp li ca ted in the pat ho ge ne sis of di a be tes mel li tus, in which seve ral path ways and dif fe rent mec ha nisms are shown to in vol ve in the pat hoph ysi o logy of the comp li ca ti ons. Thro ugh the ad mi nis tra ti on of ni co ti na mi de(NA) and strep to zo to cin(STZ), a mo del of hu man type II di a be tes can be in du ced in rats. The aim of this study was to de ter mi ne the ef fects of Ste vi a re ba u di a na (SrB) and L-NNA (N-nit ro-L-ar gi ni ne) in the for ma ti on of fre e ra di cals in STZ-NA in du ced type II di a be tic rats. M Ma a t te e r ri i a al l a an nd d M Me et t --h ho od ds s: : In this study, rats we re tre a ted with SrB and L-NNA 5-8 we eks af ter the in duc ti on of di a be tes. The le vels of glu tat hi o ne pe ro xi da se (GPx), su pe ro xi de dis mu ta se (SOD), ca ta la se (CAT) and ma lon di al dehy de (MDA) were de ter mi ned in the li ver ho mo ge na te and eryt hrocy te he moly sa te. The nit ric oxi de syntha se (NOS) le vels were al so me a su red in the li ver ho mo ge na te and se rum. To study the his to lo gi cal chan ges in di a be tes, the li ver tis su e samp les sta i ned with he ma toxy lein-eo sin and we re in ves ti ga ted under light mic ros co pe. R Re e s su ul lt ts s: : Alt ho ugh fas ting and post pran di al blo od su gar le vels we re high in di a be tic gro ups, blo od su gar le vels we re sig ni fi cantly re duced in di a be tic tre a ted gro ups. Whi le the erythrocyte MDA le vels of ste vi a-tre a ted di a be tic gro up dec re a sed, li pid pe ro xi da ti on in cre a sed with L-NNA tre at ment in both con trol and di a be tic gro ups. The re was no sig ni fi cant diffe ren ce for the tis su e CAT, NOS, and eryt hrocy te SOD and CAT ac ti vi ti es between. Li ver samp les in con trol group had a nor mal struc tu re. Nor mal his to lo gi cal ar ran ge ment was no ti ced in the li vers of con trol gro up. In he pa tocy tes of the di a be tic con trol gro up, nec ro tic cells with pycno tic nuc le us and eo si noph ylic cytop lasm as well as si nu so i dal di la ta ti on were se en. The he pa tocy te struc tu re was mo re pro tec ted in di a be tic LNNA gro up than in di a be tic gro up. The ma xi mum pro tec ti on was se en in he pa tocy tes of di a be tic ste vi a L-NNA gro up. C Co on nc c l lu u s si i --o on n: : SrB and L-NNA re du ced blo od glu co se le vels in di a be tic rats and had so me be ne fi ci al ef fects on oxi da ti ve and his to lo gi cal chan ges. Ho we ver, a NOS in hi bi tor, L-NNA was less ef fec ti ve than SrB tre at ment in type II di a betes.K Ke ey y W Wo or rd ds s: : Di a be tes mel li tus, type 2; ste vi a; nit ro ar gi ni ne; nit ric oxi de syntha se; fre e ra di cals Ö ÖZ ZE ET T A Am ma aç ç: : Ser best ra di kal üre ti mi di ya bet pa to ge ne zin de rol oy nar, bu ne den le ser best ra di kal ler di ya bet kompli kas yon la rı nın çe şit li yol la rı ve fark lı me ka niz ma la rın pa to fiz yo lo ji sin de et ki l...

show abstract

Section: Histopatologysupporting

confidence: 76%

Antioxidant and Free Radical-Scavenging Properties of Stevia rebaudiana (Bertoni) Extracts and L-NNA in Streptozotocine-Nicotinamide Induced Diabetic Rat Liver

Özbayer¹,

Değirmenci²,

Kurt³

et al. 2011

Turkiye Klinikleri J Med Sci

View full text Add to dashboard Cite

show abstract

“…Subsequently, administration of low-dose STZ resulted in apparent hyperglycemia by slightly reducing the number of β cells [15]. This well-established model was characterized by impaired insulin sensitivity associated with insulin resistance [13, 16, 17], which replicated the natural history and metabolic characteristics of human type 2 diabetes [18]. …”

Section: Discussionmentioning

confidence: 99%

Impaired Elastic Properties of the Aorta in Fat-Fed, Streptozotocin-Treated Rats

et al. 2009

View full text Add to dashboard Cite

Background: Vascular complications associated with diabetes are the major cause for the increased morbidity and mortality in diabetic patients. However, the progression of vascular complications in diabetes is not well understood. We aimed to investigate the biomechanical and biochemical changes associated with vascular dysfunction in diabetic rats. Methods:Male Wistar rats were randomly divided into two groups: normal control (n = 8) and fat-fed, streptozotocin-treated diabetic rats (n = 11). After 16 weeks, Peterson’s modulus of elasticity (Ep) and cross-sectional distensibility (CD) were calculated and compared between the two groups. Aortas were harvested from rats for histopathological and electron-microscopic analysis. Results: Collagenous fibers were scattered in the extracellular matrix and invaded the elastic lamina in the aortas of diabetic rats, suggesting a significant accumulation of collagen in diabetic vessels. Compared with normal rats, diabetic rats showed significantly reduced aortic distensibility (CD: 0.10 ± 0.04 vs. 0.17 ± 0.08 kPa^–1, p = 0.033) and an increased aortic stiffness index (Ep: 0.25 ± 0.13 vs. 0.15 ± 0.05 × 10⁶ dyn/cm², p = 0.045). Ep was positively and CD negatively correlated with glucose and collagen in diabetic rats. Conclusions: In diabetic rats, elastic properties of the aorta are impaired, being closely related to hyperglycemia-induced vascular wall remodeling.

show abstract

“…Effect of rutaecarpine on pathological changes and function of the liver Steatosis is a major pathological change in the livers of Fatfed/STZ rats [39] . As shown in Figure 8B, livers of Fat-fed/ STZ rats showed hepatocellular degeneration, sinusoid dilation, and inflammatory cell infiltration, reflecting the signs of steatosis.…”

Section: Effect Of Rutaecarpine On the Irs-1/pi3k/akt Pathway In Rat mentioning

confidence: 99%

Rutaecarpine ameliorates hyperlipidemia and hyperglycemia in fat-fed, streptozotocin-treated rats via regulating the IRS-1/PI3K/Akt and AMPK/ACC2 signaling pathways

et al. 2016

View full text Add to dashboard Cite

Aim:We have shown that rutaecarpine extracted from the dried fruit of Chinese herb Evodia rutaecarpa (Juss) Benth (Wu Zhu Yu) promotes glucose consumption and anti-inflammatory cytokine expression in insulin-resistant primary skeletal muscle cells. In this study we investigated whether rutaecarpine ameliorated the obesity profiles, lipid abnormality, glucose metabolism and insulin resistance in rat model of hyperlipidemia and hyperglycemia. Methods: Rats fed on a high-fat diet for 8 weeks, followed by injection of streptozotocin (30 mg/kg, ip) to induce hyperlipidemia and hyperglycemia. One week after streptozotocin injection, the fat-fed, streptozotocin-treated rats were orally treated with rutaecarpine (25 mg·kg -1 ·d -1 ) or a positive control drug metformin (250 mg·kg -1 ·d -1 ) for 7 weeks. The body weight, visceral fat, blood lipid profiles and glucose levels, insulin sensitivity were measured. Serum levels of inflammatory cytokines were analyzed. IRS-1 and Akt/PKB phosphorylation, PI3K and NF-κB protein levels in liver tissues were assessed; pathological changes of livers and pancreases were examined. Glucose uptake and AMPK/ACC2 phosphorylation were studied in cultured rat skeletal muscle cells in vitro. Results: Administration of rutaecarpine or metformin significantly decreased obesity, visceral fat accumulation, water consumption, and serum TC, TG and LDL-cholesterol levels in fat-fed, streptozotocin-treated rats. The two drugs also attenuated hyperglycemia and enhanced insulin sensitivity. Moreover, the two drugs significantly decreased NF-κB protein levels in liver tissues and plasma TNF-α, IL-6, CRP and MCP-1 levels, and ameliorated the pathological changes in livers and pancreases. In addition, the two drugs increased PI3K p85 subunit levels and Akt/PKB phosphorylation, but decreased IRS-1 phosphorylation in liver tissues. Treatment of cultured skeletal muscle cells with rutaecarpine (20-180 μmol/L) or metformin (20 μmol/L) promoted the phosphorylation of AMPK and ACC2, and increased glucose uptake. Conclusion: Rutaecarpine ameliorates hyperlipidemia and hyperglycemia in fat-fed, streptozotocin-treated rats via regulating IRS-1/ PI3K/Akt signaling pathway in liver and AMPK/ACC2 signaling pathway in skeletal muscles.

show abstract

Effect of chromium on carbohydrate and lipid metabolism in a rat model of type 2 diabetes mellitus: the fat-fed, streptozotocin-treated rat

Cited by 147 publications

References 49 publications

Antioxidant and Free Radical-Scavenging Properties of Stevia rebaudiana (Bertoni) Extracts and L-NNA in Streptozotocine-Nicotinamide Induced Diabetic Rat Liver

Antioxidant and Free Radical-Scavenging Properties of Stevia rebaudiana (Bertoni) Extracts and L-NNA in Streptozotocine-Nicotinamide Induced Diabetic Rat Liver

Impaired Elastic Properties of the Aorta in Fat-Fed, Streptozotocin-Treated Rats

Rutaecarpine ameliorates hyperlipidemia and hyperglycemia in fat-fed, streptozotocin-treated rats via regulating the IRS-1/PI3K/Akt and AMPK/ACC2 signaling pathways

Contact Info

Product

Resources

About