scholarly journals Effect of Caffeic Acid Phenethyl Ester on Vascular Damage Caused by Consumption of High Fructose Corn Syrup in Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-8
Author(s):  
Aburrahman Gun ◽  
Mehmet Kaya Ozer ◽  
Sedat Bilgic ◽  
Nevin Kocaman ◽  
Gonca Ozan
Keyword(s):  
Metabolic Syndrome ◽  
Caffeic Acid ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Caffeic Acid Phenethyl Ester ◽  
High Fructose Corn Syrup ◽  
Corn Syrup ◽  
Beneficial Effects ◽  
Fructose Intake ◽  
High Fructose

Fructose corn syrup is cheap sweetener and prolongs the shelf life of products, but fructose intake causes hyperinsulinemia, hypertriglyceridemia, and hypertension. All of them are referred to as metabolic syndrome and they are risk factors for cardiovascular diseases. Hence, the harmful effects of increased fructose intake on health and their prevention should take greater consideration. Caffeic Acid Phenethyl Ester (CAPE) has beneficial effects on metabolic syndrome and vascular function which is important in the prevention of cardiovascular disease. However, there are no known studies about the effect of CAPE on fructose-induced vascular dysfunction. In this study, we examined the effect of CAPE on vascular dysfunction due to high fructose corn syrup (HFCS). HFCS (6 weeks, 30% fed with drinking water) caused vascular dysfunction, but treatment with CAPE (50 micromol/kg i.p. for the last two weeks) effectively restored this problem. Additionally, hypertension in HFCS-fed rats was also decreased in CAPE supplemented rats. CAPE supplements lowered HFCS consumption-induced raise in blood glucose, homocysteine, and cholesterol levels. The aorta tissue endothelial nitric oxide synthase (eNOS) production was decreased in rats given HFCS and in contrast CAPE supplementation efficiently increased its production. The presented results showed that HFCS-induced cardiovascular abnormalities could be prevented by CAPE treatment.

High-fructose corn syrup causes vascular dysfunction associated with metabolic disturbance in rats: Protective effect of resveratrol

2012 ◽  
Vol 50 (6) ◽  
pp. 2135-2141 ◽  
Author(s):  
Fatma Akar ◽  
Orhan Uludağ ◽  
Ali Aydın ◽  
Yasin Atacan Aytekin ◽  
Sehri Elbeg ◽  
...  
Keyword(s):  
Protective Effect ◽  
Vascular Dysfunction ◽  
Metabolic Disturbance ◽  
High Fructose Corn Syrup ◽  
Corn Syrup ◽  
High Fructose

The Role of High-Fructose Corn Syrup in Metabolic Syndrome and Hypertension

2010 ◽  
Vol 12 (2) ◽  
pp. 105-112 ◽  
Author(s):  
Leon Ferder ◽  
Marcelo Damián Ferder ◽  
Felipe Inserra
Keyword(s):  
Metabolic Syndrome ◽  
High Fructose Corn Syrup ◽  
Corn Syrup ◽  
High Fructose

scholarly journals High Fructose Corn Syrup-Moderate Fat Diet Potentiates Anxio-Depressive Behavior and Alters Ventral Striatal Neuronal Signaling

2021 ◽  
Vol 15 ◽  
Author(s):  
Ayanabha Chakraborti ◽  
Christopher Graham ◽  
Sophie Chehade ◽  
Bijal Vashi ◽  
Alan Umfress ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Gut Microbiota ◽  
Glycogen Synthase ◽  
Serum Levels ◽  
High Fructose Corn Syrup ◽  
Corn Syrup ◽  
Neuronal Signaling ◽  
High Fructose ◽  
Glur1 Subunit ◽  
The Impact

The neurobiological mechanisms that mediate psychiatric comorbidities associated with metabolic disorders such as obesity, metabolic syndrome and diabetes remain obscure. High fructose corn syrup (HFCS) is widely used in beverages and is often included in food products with moderate or high fat content that have been linked to many serious health issues including diabetes and obesity. However, the impact of such foods on the brain has not been fully characterized. Here, we evaluated the effects of long-term consumption of a HFCS-Moderate Fat diet (HFCS-MFD) on behavior, neuronal signal transduction, gut microbiota, and serum metabolomic profile in mice to better understand how its consumption and resulting obesity and metabolic alterations relate to behavioral dysfunction. Mice fed HFCS-MFD for 16 weeks displayed enhanced anxiogenesis, increased behavioral despair, and impaired social interactions. Furthermore, the HFCS-MFD induced gut microbiota dysbiosis and lowered serum levels of serotonin and its tryptophan-based precursors. Importantly, the HFCS-MFD altered neuronal signaling in the ventral striatum including reduced inhibitory phosphorylation of glycogen synthase kinase 3β (GSK3β), increased expression of ΔFosB, increased Cdk5-dependent phosphorylation of DARPP-32, and reduced PKA-dependent phosphorylation of the GluR1 subunit of the AMPA receptor. These findings suggest that HFCS-MFD-induced changes in the gut microbiota and neuroactive metabolites may contribute to maladaptive alterations in ventral striatal function that underlie neurobehavioral impairment. While future studies are essential to further evaluate the interplay between these factors in obesity and metabolic syndrome-associated behavioral comorbidities, these data underscore the important role of peripheral-CNS interactions in diet-induced behavioral and brain function. This study also highlights the clinical need to address neurobehavioral comorbidities associated with obesity and metabolic syndrome.

Metabolic Effects of Fructose and the Worldwide Increase in Obesity

2010 ◽  
Vol 90 (1) ◽  
pp. 23-46 ◽  
Author(s):  
Luc Tappy ◽  
Kim-Anne Lê
Keyword(s):  
De Novo ◽  
Epidemiological Studies ◽  
High Energy ◽  
De Novo Lipogenesis ◽  
Metabolic Effects ◽  
Major Constituent ◽  
High Fructose Corn Syrup ◽  
Corn Syrup ◽  
Fructose Intake ◽  
High Fructose

While virtually absent in our diet a few hundred years ago, fructose has now become a major constituent of our modern diet. Our main sources of fructose are sucrose from beet or cane, high fructose corn syrup, fruits, and honey. Fructose has the same chemical formula as glucose (C6H12O6), but its metabolism differs markedly from that of glucose due to its almost complete hepatic extraction and rapid hepatic conversion into glucose, glycogen, lactate, and fat. Fructose was initially thought to be advisable for patients with diabetes due to its low glycemic index. However, chronically high consumption of fructose in rodents leads to hepatic and extrahepatic insulin resistance, obesity, type 2 diabetes mellitus, and high blood pressure. The evidence is less compelling in humans, but high fructose intake has indeed been shown to cause dyslipidemia and to impair hepatic insulin sensitivity. Hepatic de novo lipogenesis and lipotoxicity, oxidative stress, and hyperuricemia have all been proposed as mechanisms responsible for these adverse metabolic effects of fructose. Although there is compelling evidence that very high fructose intake can have deleterious metabolic effects in humans as in rodents, the role of fructose in the development of the current epidemic of metabolic disorders remains controversial. Epidemiological studies show growing evidence that consumption of sweetened beverages (containing either sucrose or a mixture of glucose and fructose) is associated with a high energy intake, increased body weight, and the occurrence of metabolic and cardiovascular disorders. There is, however, no unequivocal evidence that fructose intake at moderate doses is directly related with adverse metabolic effects. There has also been much concern that consumption of free fructose, as provided in high fructose corn syrup, may cause more adverse effects than consumption of fructose consumed with sucrose. There is, however, no direct evidence for more serious metabolic consequences of high fructose corn syrup versus sucrose consumption.

Fructose and high fructose corn syrup: are they a two-edged sword?

2021 ◽  
pp. 1-23
Author(s):  
Nasim Khorshidian ◽  
Mahdi Shadnoush ◽  
Maryam Zabihzadeh Khajavi ◽  
Sara Sohrabvandi ◽  
Mojtaba Yousefi ◽  
...  
Keyword(s):  
High Fructose Corn Syrup ◽  
Corn Syrup ◽  
High Fructose
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