High-Fructose Diet Initially Promotes Increased Aortic Wall Thickness, Liver Steatosis, and Cardiac Histopathology Deterioration, but Does Not Increase Body Fat Index

Abstract

Background: Dietary fats and fructose have been responsible for inducing obesity and body tissues damage due to the consequence of metabolic syndrome through several mechanisms. The body fat index (BFI) is one of the anthropometric measures used to detect obesity in rats. This study aims to examine the correlation between high-fat high-fructose diet and liver steatosis cell count, early atherosclerosis characteristics, and BFI in Sprague Dawley Rats.Design and methods: This was an experimental design using 2 groups of 12-weeks-old Sprague Dawley (SD) rats. The control group received a standard diet and tap water beverages for 17 weeks. The intervention group was fed with high-fat diet from modified AIN 93-M and additional 30% fructose drink. We analyzed the foam cell count, aortic wall thickness, cardiac histopathology, and liver steatosis cell count after the sacrifice process.Results: The rats in the intervention group had a higher aortic wall thickness, liver steatosis, and foam cell count (+125%, p<0.01; +317%, p<0.01 and +165%, p<0.01 respectively) compared to the control group. The intervention group also showed higher mononuclear inflammatory and hypertrophic cell count. A significant positive correlation was found between dietary fructose with premature atherosclerosis by increasing foam cell count (r=0.66) and aortic wall thickness (r=0.68). In addition, 30% dietary fructose increased liver steatosis (r =0.69) and mononuclear inflammatory cardiac cell count (r=0.61). Interestingly, the intervention had no effect on BFI (p>0.5; r=0.13).Conclusions: Dietary fat and fructose consumption for 17 weeks promote atherosclerosis, liver steatosis, and cardiac histopathology alteration without increasing BFI.

The role of carboxymethyl chitosan/Hyaluronic acid embedded gold nanoparticles as hyperlipidemic and leptin resistance agent

“…The HFD group (G2) had the highest RW with a significantly difference values compared by the control group (see Figure 8, h). Additionally, hydropic degeneration in cardiac muscle found in Microphotograph of rat heart in Figure (8, b) that might be a result of excess consuming of fructose which represented a hazard agent for the consequence of metabolic syndrome through several mechanisms with dysfunctions in various organs and tissues as heart, these results found to be in agreement with Handayani et al [58] as they reported that dietary fat and fructose consumption promote atherosclerosis and cardiac histopathology alteration. Photomicrographs of treated groups with CMCTS+HA and AuNPs fig.…”

Ethanol Extract of Pinus koraiensis Leaves Mitigates High Fructose-Induced Hepatic Triglyceride Accumulation and Hypertriglyceridemia

“…Regular fructose intake contributes to the development of lipid disorders, oxidative stress, and mild chronic inflammation, which are directly associated with obesity, NAFLD, and cardiovascular diseases [24]. This concern is supported by observations in human and rodent epidemiological studies that HFrD induces hepatic intrahepatocellular lipids, hepatic DNL, and abdominal aortic thickness, and increases hepatic insulin resistance [25][26][27]. Furthermore, consistent with our data, several studies have reported that HFrD-fed rats have increased hepatic levels of upstream regulators of DNL, such as SREBP-1, ChREBP, key lipogenic enzymes, and pro-inflammatory cytokines [28][29][30][31][32].…”

The interplay between nonalcoholic fatty liver disease and atherosclerotic cardiovascular disease

“…Since fructose largely replaced sucrose as a source of sweeteners in soft drinks in the 1970's, an association between high-fructose corn syrup consumption and obesity became increasingly observed ( 98 ). In addition, beyond increasing hepatic steatosis, fructose enhances aortic wall thickness and foam cell count in Sprague-Dawley rats fed a high-fat diet ( 99 ). Van den Hoek and colleagues fed Ldlr −/− .Leiden mice an obesogenic diet for 28 weeks containing 41% calories from fat, 0.05% cholesterol, and 44% calories from fructose ( 100 ), which recapitulated multiple aspects of NASH like inflammation ( 100 ), fibrosis ( 101 ), and circulating AST and ALT ( 102 ), as well as established atherosclerotic lesions ( 100 ).…”

“…Since fructose largely replaced sucrose as a source of sweeteners in soft drinks in the 1970's, an association between high-fructose corn syrup consumption and obesity became increasingly observed (98). In addition, beyond increasing hepatic steatosis, fructose enhances aortic wall thickness and foam cell count in ).…”