Liquid fructose supplementation in LDL-R−/− mice fed a western-type diet enhances lipid burden and atherosclerosis despite identical calorie consumption

Hutter, Natalia; Baena, Miguel; Sangüesa, Gemma; Dávalos, Alberto; Latasa, Maria Jesús; Escolà‐Gil, Joan Carles; Sánchez, Rosa María Galán; Roglans, Núria; Alegret, Marta; Laguna, Juan C.

doi:10.1016/j.ijcme.2015.10.002

Cited by 9 publications

(17 citation statements)

References 42 publications

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“…The animal experimental protocols were described in our previous publication [18]. Briefly, male LDL-R −/− mice were randomly assigned to four groups ( n = 10/group): 1.…”

Section: Methodsmentioning

confidence: 99%

“…Western plus fructose group (WF), which received the Western-type diet supplemented with 15% weight/volume fructose in drinking water. The composition of control and Western-type diets was as detailed previously [18]. After 12 weeks, the animals were fasted for 2 h and blood was obtained from the tail vein to determine glucose concentrations.…”

Section: Methodsmentioning

confidence: 99%

“…Our results showed that in this model liquid fructose supplementation increased liver triglyceride and cholesterol levels and diminished whole-body insulin sensitivity only when it was combined with a Western-type diet; however, these effects were not associated with a clear inflammatory reaction in the liver [17]. We also studied the effects of these diets on the development of aortic atherosclerotic lesions in low-density lipoprotein (LDL) receptor-deficient (LDL-R −/− ) mice [18]. As it has been shown that the LDL-R −/− mouse is a good model for studying the progression from steatosis to inflammation in the liver [19], it can be helpful to better understand the relationship between hepatic lipid accumulation, inflammation and IR.…”

Section: Introductionmentioning

confidence: 99%

“…As it has been shown that the LDL-R −/− mouse is a good model for studying the progression from steatosis to inflammation in the liver [19], it can be helpful to better understand the relationship between hepatic lipid accumulation, inflammation and IR. Here, we investigate the effects on insulin signalling and inflammation of liquid fructose supplementation and a Western-type diet, alone and combined, using samples from our previous study conducted on LDL-R −/− mice [18]. …”

Section: Introductionmentioning

confidence: 99%

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The Addition of Liquid Fructose to a Western-Type Diet in LDL-R−/− Mice Induces Liver Inflammation and Fibrogenesis Markers without Disrupting Insulin Receptor Signalling after an Insulin Challenge

et al. 2017

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A high consumption of fat and simple sugars, especially fructose, has been related to the development of insulin resistance, but the mechanisms involved in the effects of these nutrients are not fully understood. This study investigates the effects of a Western-type diet and liquid fructose supplementation, alone and combined, on insulin signalling and inflammation in low-density lipoprotein (LDL) receptor-deficient mice (LDL-R−/−). LDL-R−/− mice were fed chow or Western diet ±15% fructose solution for 12 weeks. Plasma glucose and insulin, and the expression of genes related to inflammation in the liver and visceral white adipose tissue (vWAT), were analysed. V-akt murine thymoma viral oncogene homolog-2 (Akt) activation was measured in the liver of the mice after a single injection of saline or insulin. None of the dietary interventions caused inflammation in vWAT, whereas the Western diet induced hepatic inflammation, which was further enhanced by liquid fructose, leading also to a significant increase in fibrogenesis markers. However, there was no change in plasma glucose or insulin, or insulin-induced Akt phosphorylation. In conclusion, hepatic inflammation and fibrogenesis markers induced by a Western diet supplemented with liquid fructose in LDL-R−/− mice are not associated with a significant impairment of hepatic insulin signalling.

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“…The animal experimental protocols were described in our previous publication [18]. Briefly, male LDL-R −/− mice were randomly assigned to four groups ( n = 10/group): 1.…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The Addition of Liquid Fructose to a Western-Type Diet in LDL-R−/− Mice Induces Liver Inflammation and Fibrogenesis Markers without Disrupting Insulin Receptor Signalling after an Insulin Challenge

et al. 2017

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“…55, 64 Providing liquid fructose supplementation to a western-type diet in mice increases lipid burden and atherosclerosis despite identical calorie consumption. 73 …”

Section: Sugar and Chd Risk Factorsmentioning

confidence: 99%

The Evidence for Saturated Fat and for Sugar Related to Coronary Heart Disease

DiNicolantonio

Lucan

O’Keefe

2016

Progress in Cardiovascular Diseases

284

143

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Dietary guidelines continue to recommend restricting intake of saturated fats. This recommendation follows largely from the observation that saturated fats can raise levels of total serum cholesterol (TC), thereby putatively increasing the risk of atherosclerotic coronary heart disease (CHD). However, TC is only modestly associated with CHD, and more important than the total level of cholesterol in the blood may be the number and size of low-density lipoprotein (LDL) particles that contain it. As for saturated fats, these fats are a diverse class of compounds; different fats may have different effects on LDL and on broader CHD risk based on the specific saturated fatty acids (SFAs) they contain. Importantly, though, people eat foods, not isolated fatty acids. Some food sources of SFAs may pose no risk for CHD or possibly even be protective. Thus, advice to reduce saturated fat in the diet without regard to such nuance could actually increase people’s risk of CHD. When saturated fats are replaced with refined carbohydrates, and specifically with added sugars (like sucrose or high fructose corn syrup), the end result is not favorable for heart health. Such replacement leads to changes in LDL, high-density lipoprotein (HDL), and triglycerides that may increase the risk of CHD. Additionally, diets high in sugar may induce many other abnormalities associated with elevated CHD risk, including elevated levels of glucose, insulin, and uric acid, impaired glucose tolerance, insulin and leptin resistance, non-alcoholic fatty liver disease, and altered platelet function. A diet high in added sugars has been found to cause a 3-fold increased risk of death due to cardiovascular disease. But sugars, like saturated fats, are a diverse class of compounds. The monosaccharide, fructose, and fructose-containing sweeteners (e.g., sucrose) result in greater degrees of metabolic abnormalities than seen with glucose (either isolated as a monomer or in chains as starch) and may present greater risk for CHD. This paper reviews the evidence linking saturated fats and sugars to CHD, and concludes that the latter is more of a problem than the former. Dietary guidelines should shift focus away from reducing saturated fat, and from replacing saturated fat with carbohydrates, specifically when these carbohydrates are refined. To reduce the burden of CHD, guidelines should focus particularly on reducing intake of concentrated sugars, specifically the fructose-containing sugars like sucrose and high-fructose corn syrup in the form of ultra-processed foods and beverages.

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Chronic fructose intake does not induce liver steatosis and inflammation in female Sprague–Dawley rats, but causes hypertriglyceridemia related to decreased VLDL receptor expression

et al. 2018

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Liquid fructose supplementation in LDL-R−/− mice fed a western-type diet enhances lipid burden and atherosclerosis despite identical calorie consumption

Cited by 9 publications

References 42 publications

The Addition of Liquid Fructose to a Western-Type Diet in LDL-R−/− Mice Induces Liver Inflammation and Fibrogenesis Markers without Disrupting Insulin Receptor Signalling after an Insulin Challenge

The Addition of Liquid Fructose to a Western-Type Diet in LDL-R−/− Mice Induces Liver Inflammation and Fibrogenesis Markers without Disrupting Insulin Receptor Signalling after an Insulin Challenge

The Evidence for Saturated Fat and for Sugar Related to Coronary Heart Disease

Chronic fructose intake does not induce liver steatosis and inflammation in female Sprague–Dawley rats, but causes hypertriglyceridemia related to decreased VLDL receptor expression

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