Impact of L-Carnitine and Cinnamon on Insulin-Like Growth Factor-1 and Inducible Nitric Oxide Synthase Gene Expression in Heart and Brain of Insulin Resistant Rats

Mohamed, Mona A.

doi:10.3844/ajbbsp.2010.204.212

Cited by 4 publications

(7 citation statements)

References 53 publications

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“…Insulin resistance induced by a high fructose diet in rats is well documented [3,5,23,28] and has been established in the present study. The degree of insulin resistance was higher in HFD1 and HFD2 groups as indicated by the significant elevation of serum insulin levels and HOMA-IR.…”

Section: Discussionsupporting

confidence: 69%

“…Insulin resistance occurs at multiple levels in cells, from the cell surface to the nucleus, including insulin receptor desensitization and suppression of IRS protein and functionality, all of which can result from inhibition of IRS1 and IRS2 [22]. Previous studies confirmed that the high-fructose diet induces insulin resistance and oxidative stress in rat tissues [3,5,23,24]. Rats fed high-fructose diet showed elevated levels of serum ALT and AST, the specific markers of hepatocellular injury [25,26].…”

Section: Discussionmentioning

confidence: 99%

“…Insulin resistance is defined as an impaired ability of insulin to promote glucose uptake and exert its metabolic effects in the liver, skeletal muscle and adipose tissue [1,2]. Experimental studies in animals documented that the general increase in fructose consumption is correlated with hyperglycemia, dyslipidemia and insulin resistance [3][4][5]. Fructose, a simple sugar found in honey, fruit, and high-fructose corn syrup, has a unique metabolism that results in oxidative stress and lipogenesis [6,7].…”

Section: Introductionmentioning

confidence: 99%

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Rice bran oil ameliorates hepatic insulin resistance by improving insulin signaling in fructose fed-rats

Mohamed

Ahmed

Elbast

et al. 2019

J Diabetes Metab Disord

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Background Insulin resistance is an inadequate metabolic response of the peripheral tissue to circulating insulin. It plays an important pathophysiological role in type 2 diabetes mellitus. The purpose of the study was to investigate the molecular effects of rice bran oil (RBO) on the gene expression of insulin receptor (IR), insulin receptor substrate-1 (IRS-1), glucose transporters-4 and 5 (GLUT-4 and 5) in insulin-resistant rats induced by high fructose diet (HFD). Methods Rats were divided into six groups (10 rats each) as follows: Groups 1 and 2: rats received a standard diet with corn oil or RBO (as the sole source of fat), respectively. Group 3: animals fed on HFD, which was furtherly divided into 2 subgroups: rats fed HFD either for one (HFD1) or for 2 months (HFD2). Group 4, rats fed HFD containing RBO for 1 month (HFD1 + RBO), while rats in group 5 fed HFD for 30 days then RBO was added to the diet for another 30 days (HFD2 + RBO). Serum levels of glucose and insulin, as well as hepatic gene expression of insulin receptors and glucose transporters were determined. Livers were isolated for histopathological study. Results HFD induced insulin resistance with a reduction in the hepatic level of insulin receptor and glucose transporters at both protein and molecular levels. Addition of RBO improved the insulin sensitivity and up-regulated the expression of the tested genes. Conclusion HFD impaired the insulin sensitivity of the hepatocytes by down-regulating the insulin receptor genes. Addition of RBO alleviated all the hazardous effects.

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Section: Discussionsupporting

confidence: 69%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Rice bran oil ameliorates hepatic insulin resistance by improving insulin signaling in fructose fed-rats

Mohamed

Ahmed

Elbast

et al. 2019

J Diabetes Metab Disord

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“…Many studies proved the induction of insulin resistance by feeding rats with HFD (Abd El-Wahab, Mohamed, El Sayed, & Bauomy, 2017;Mahfouz, Ghanem, & Mohamed, 2009;Mohamed, 2010;Shawky, Shehatou, Abdel Rahim, Suddek, & Gameil, 2014) and was established in the current study. Feeding rats with HFD for 1 and 2 months (HFD1 and HFD2, respectively) increased the hepatic insulin insensitivity as indicated by the significant elevation of serum insulin and HOMA-IR.…”

Section: Discussionmentioning

confidence: 52%

Rice Bran Oil Improves Insulin Resistance by Affecting the Expression of Antioxidants and Lipid‐Regulatory Genes

Ahmed

Mohamed

Rashed

et al. 2018

Lipids

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The present study investigated the molecular effects of rice bran oil (RBO) on lipid-regulatory genes (sterol regulatory element binding protein-1 [Srebf1] and peroxisome proliferator-activated receptors-α [Ppara]) and the expression of catalase (CAT) and superoxide dismutase (SOD1) genes in insulin-resistant rats. Rats were divided into five groups: animals that received standard diet (control); rats fed standard diet containing RBO as the sole source of fat (RBO); a high-fructose diet (HFD) group, which was further divided into two subgroups: rats fed HFD either for only 1 month (HFD1) or for 2 months (HFD2) and rats fed HFD containing RBO for 1 month; while rats in the last group fed HFD for 30 days then treated with RBO for another 30 days. The HFD induced a state of insulin resistance (IR) as indicated by the hyperinsulinemia and elevated homeostasis model assessment insulin resistance index. Hepatic lipid levels and radical scavenging enzymes were altered by the HFD. Lipid-regulatory genes, Srebf1 and Ppara, were upregulated while Sod1 and Cat were downregulated in insulin-resistant rats. Addition of RBO to the two diet regimens alleviated the disorders of IR to some extent. RBO reduced the hepatic levels of triacylglycerol, malondialdehyde, SREBP, and PPAR-α mRNA. Hepatic SOD and CAT were elevated at gene and protein levels. The HFD induces de novo lipogenesis by upregulating the lipid-regulatory genes resulting in increased serum and hepatic triacylglycerol. Moreover, IR induced by the HFD caused a state of oxidative stress. Supplementation of RBO to fructose-fed rats not only improves insulin resistance but also downregulates lipogenic genes and improves the unbalanced oxidative status.

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“…Although extensive studies have been performed investigating the effects of fructose-induced IR on various organs (Mohamed 2010;Ghanem 2010), data on lens integrity and composition in this rat model are lacking (Balasaraswathi et al, 2008). Therefore, the present study was undertaken to assess the effects of administration of either L-carnitine or cinnamon extract on soluble lens crystalline, oxidative stress and protein bound sugar in rats fed high fructose diet.…”

Section: Introductionmentioning

confidence: 99%

Effects of L-Carnitine and Cinnamon Extract Treatment on Lens Crystallins of Rats Fed High Fructose Diet

Mahfouz¹,

El-Ghaffar²,

Mohamed³

et al. 2011

American Journal of Biochemistry and Biotechnology

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Problem statement: Rats fed high dietary fructose are documented to form an acquired model of insulin resistance; the present study aims to investigate possible changes in lens crystallins of rats fed high fructose diet and the effects of administration of each exogenous L-Carnitine (CA) and Cinnamon Extract (CE) on protein glycation, oxidative stress and redox homeostasis in this rat model. Approach: A total number of 60 male Wister rats of body weight 120-160 g were divided into 4 groups of 15 rats each. Group 1 received control diet, while groups 2, 3 and 4: rats received high fructose diet (60g/100 g diet). After 2 weeks from fructose feeding, animals of group 3 were treated with L-carnitine (300 mg g −1 body weight/day i.p.), while animals of group 4 were treated with cinnamon extract (0.5 mL/rat/day orally). At the end of experimental period (30 days), serum levels of glucose and insulin were determined. Lenses of each animal were dissected; molecular weights of crystalline, oxidative stress markers, early glycation of lens proteins and carbonyl group were assayed. Results: A significant decline in antioxidants and increase in lipid peroxidation products, protein oxidation and protein glycation were observed in lens samples obtained from fructose-fed rats. Administration of each CA and CE to fructose-fed rats significantly attenuated oxidative damage and protein glycation and returned levels of antioxidants to near those in control group. Chromatographic analysis of lens crystalline of rats fed high fructose diet showed diffused peaks, indicating crystalline aggregation. Conclusion: The results of the present study indicate that dietary fructose disturbs lens integrity and administration of L-carnitine or cinnamon extract may safeguard the lens by minimizing the protein aggregation, preventing glycation and oxidative stress in animals fed high fructose diet. L-carnitine has more potent effects than CE in this animal model.

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Impact of L-Carnitine and Cinnamon on Insulin-Like Growth Factor-1 and Inducible Nitric Oxide Synthase Gene Expression in Heart and Brain of Insulin Resistant Rats

Cited by 4 publications

References 53 publications

Rice bran oil ameliorates hepatic insulin resistance by improving insulin signaling in fructose fed-rats

Rice bran oil ameliorates hepatic insulin resistance by improving insulin signaling in fructose fed-rats

Rice Bran Oil Improves Insulin Resistance by Affecting the Expression of Antioxidants and Lipid‐Regulatory Genes

Effects of L-Carnitine and Cinnamon Extract Treatment on Lens Crystallins of Rats Fed High Fructose Diet

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