Mechanism of insulin resistance in fructose-fed rats

Tobey, Ted A.; Mondon, Carl E.; Zavaroni, Ivana; Reaven, Gerald M.

doi:10.1016/0026-0495(82)90100-7

Cited by 176 publications

(86 citation statements)

References 19 publications

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“…From this point, excessive fruit intake seem to be undesirable. Although high-fructose diets induce insulin resistance in animal models, including mice and rats, 26,27) most studies of chronic fructose ingestion have been shown some benefits of the substitution of -᭺-, normal-diet group; -᭝-, 1% fruit extract-; -ᮀ-, 3% fruit extract-; --, 10% fruit extract-containing diet groups. Ordinate shows relaxation of aortic strips as a percentage of the contraction induced by an equieffective concentration of norepinephrine (5ϫ10 Ϫ8 -3ϫ10 Ϫ7 M).…”

Section: Discussionmentioning

confidence: 99%

Effects of Chronic Administration of Fruit Extract (Citrus unshiu MARC) on Endothelial Dysfunction in Streptozotocin-Induced Diabetic Rats

Kamata

Kobayashi

Matsumoto

et al. 2005

Biological & Pharmaceutical Bulletin

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Section: Discussionmentioning

confidence: 99%

Effects of Chronic Administration of Fruit Extract (Citrus unshiu MARC) on Endothelial Dysfunction in Streptozotocin-Induced Diabetic Rats

Kamata

Kobayashi

Matsumoto

et al. 2005

Biological & Pharmaceutical Bulletin

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“…In experimental animal studies, giving a high fructose diet causes the development of features of metabolic syndrome, including insulin resistance (Tobey et al, 1982;Hwang et al, 1987), elevation of triglycerides (Sleder et al, 1980;Bocarsly et al, 2010;Hwang et al, 1987), abdominal obesity (Bocarsly et al, 2010), elevation of blood pressure (Hwang et al, 1987) and hyperuricemia (Sanchez-Lozada et al, 2007;Nakagawa et al, 2006) in normal rats and enhances diabetic complications in diabetes model rats (Bell et al, 2000). Some studies focusing on the effect of fructose on the kidneys showed that excessive fructose intake causes renal injury, including glomerular hypertension, renal microvascular damage and tubulointerstitial injury in normal rats (Sanchez-Lozada et al, 2007;Nakayama et al, 2010) and increases oxidative stress in the kidneys of diabetes model rats (Bell et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

High fructose diet feeding accelerates diabetic nephropathy in Spontaneously Diabetic Torii (SDT) rats

et al. 2018

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-Diabetic nephropathy (DN) is one of the complications of diabetes and is now the most common cause of end-stage renal disease. Fructose is a simple carbohydrate that is present in fruits and honey and is used as a sweetener because of its sweet taste. Fructose has been reported to have the potential to progress diabetes and DN in humans even though fructose itself does not increase postprandial plasma glucose levels. In this study, we investigated the effects of high fructose intake on the kidney of the Spontaneously Diabetic Torii (SDT) rats which have renal lesions similar to those in DN patients and compared these with the effects in normal SD rats. This study revealed that a 4-week feeding of the high fructose diet increased urinary excretion of kidney injury makers for tubular injury and accelerated mainly renal tubular and interstitial lesions in the SDT rats but not in normal rats. The progression of the nephropathy in the SDT rats was considered to be related to increased internal uric acid and blood glucose levels due to the high fructose intake. In conclusion, high fructose intake exaggerated the renal lesions in the SDT rats probably due to effects on the tubules and interstitium through metabolic implications for uric acid and glucose.

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“…Compared to glucose, little is known about the impact of the other monosaccharides and disaccharides on macrophage oxidative status, lipid accumulation, and foam cell formation. Previous studies in serum showed that chronic feeding with fructose or sucrose leads to hyperinsulinemia, high triglyceride levels, as well as a significant loss of insulin sensitivity in rodent models [54][55][56][57]. Another study showed that high fructose diet in rats, was associated with an increase in ROS production and other oxidative stress markers in the aorta and the heart; and also.…”

Section: Discussionmentioning

confidence: 97%

Atherogenicity of Monosaccharides, Disaccharides and Artificial Sweeteners in the Lipid-Laden Macrophage Model System: Cell Culture and Mice Studies

Na¹,

Hamoud²,

Aviram³

et al. 2017

J Hortic

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IntroductionAtherosclerosis is the underlying cause of cardiovascular diseases (CVD), the major cause of death worldwide [1,2]. Atherosclerosis is an inflammatory disease of the arteries in which activated macrophages are abundant in the atherosclerotic lesions [3]. Macrophages and their oxidative status play key roles during early atherogenesis [3,4]. After differentiating from peripheral monocytes, the formed intimal macrophages incorporate oxidized lipoproteins and are transformed into lipid-rich foam cells, the hallmark feature of early atherosclerosis [3]. In addition to lipoprotein uptake, lipid accumulation in macrophages can also result from alterations in cellular lipid metabolism, e.g. attenuated reverse cholesterol transport or enhanced rates of lipid biosynthesis; all are considerably affected by the oxidative status of the cells [4].High intake of added sugars increases the risk of CVD and type 2 diabetes mellitus (T2DM) [5]. T2DM and hyperglycemia are associated with accelerated atherosclerosis mediated by enhanced macrophage foam cell formation [6]. Numerous studies have demonstrated the detrimental role of high glucose on macrophage oxidative status or lipid metabolism leading to foam cell formation. Accelerated atherosclerosis in diabetic mice was associated with macrophage lipid peroxidation and increased generation of reactive oxygen species (ROS) via induction of NADPH oxidase [7,8]. In addition, macrophages from diabetic mice or under high glucose conditions exhibit lipid accumulation mediated by various mechanisms that regulate intracellular lipid metabolism [7][8][9][10][11][12][13][14][15]. These include enhanced uptake of oxidized (ox)-LDL via up-regulation of the scavenger receptors CD36 and SR-A [7-9,11], enhanced cholesterol or triglyceride biosynthesis rates via induction of lipid biosynthesis regulators e.g. the sterol regulator elements binding proteins (SREBPs), 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) or diacylglycerol acyltransferase1 (DGAT1) [12,14], and attenuation of HDL-mediated cholesterol efflux from macrophages via suppression of ATP-binding cassette (ABC) transporters ABCA1 and ABCG1 [10,13,15].Although the pro-oxidative and pro-atherogenic role of glucose in macrophage foam cell formation has been established, little is Abstract Background: Glucose is known to enhance macrophage foam cell formation and atherosclerosis development. However, the role of other monosaccharides, disaccharides or artificial sweeteners in macrophage atherogenicity remains unclear.

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Mechanism of insulin resistance in fructose-fed rats

Cited by 176 publications

References 19 publications

Effects of Chronic Administration of Fruit Extract (Citrus unshiu MARC) on Endothelial Dysfunction in Streptozotocin-Induced Diabetic Rats

Effects of Chronic Administration of Fruit Extract (Citrus unshiu MARC) on Endothelial Dysfunction in Streptozotocin-Induced Diabetic Rats

High fructose diet feeding accelerates diabetic nephropathy in Spontaneously Diabetic Torii (SDT) rats

Atherogenicity of Monosaccharides, Disaccharides and Artificial Sweeteners in the Lipid-Laden Macrophage Model System: Cell Culture and Mice Studies

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