High fat and fructose diet induced journal

Ultra-thin sections 70 nm were cut with an ultramicrotome UC6, Leica, CA and mounted onto copper grids. Hepatic tissues were examined using Fourier-transform infrared spectroscopy for assessment of any molecular changes.

The reaction parameters were as follows: Fossati P, Prencipe L. Finally, weight, leptinemia, and NEFA levels are comparable in both groups. The liver, spleen, kidney, epididymal and perirenal fat pads were dissected and weighed immediately. Apigenin significantly decreased adipose fat and leptin levels and increased adiponectin levels.

Rats were also equipped for ECG recording, centered in the scanner for heart imaging before receiving a first caudal injection of 20 MBq [11C]-acetate. Results 3. In previous studies, the effects of these compounds on metabolic dysregulations were mostly evaluated under high fat feeding regimen.

Cytokine production is altered in the NASH stage which is further characterized by lobular inflammation, hepatocyte ballooning, and fibrosis [ 5 ].

Competing interests: We demonstrated the role of oxidative stress in pathogenesis as well as in complications hepatic and vascularreinforcing interest in the use of antioxidants in the prevention and treatment of metabolic diseases, including T2D.

Compounds labelled by the acetylcholinesterase of Electrophorus Electricus. Conclusion The continuous consumption of a high-fat, high-fructose diet caused oxidative stress in mice: Oxidative stress can be detected by measuring the activity of antioxidative enzymes, for example, superoxide dismutase SODcatalase CATand glutathione peroxidase GPxas well as the level of malondialdehyde MDAparticularly in the liver.

Determination of Lipid Peroxidation The thiobarbituric acid TBA assay was used to determine lipid peroxidation according to the method of Chatuphonprasert et al.

Hype or reality: Early striatal dendrite deficits followed by neuron loss with advanced age in the absence of anterograde cortical brain-derived neurotrophic factor. The specific fatty foods used in the diets vary across studies, ranging from Crisco to lard to palm oil.

All the flavonoids exerted significant functions on improving insulin resistance and fasting glucose. Involvement of inducible nitric oxide synthase in hydroxyl radical-mediated lipid peroxidation in streptozotocin-induced diabetes.

Effect of TNF-alpha-converting enzyme inhibitor on insulin resistance in fructose-fed rats. Biochemistry Therefore, there is a heightened interest in identifying highly effective compounds that lessen the health-threatening effects of fructose and fats while maintaining food palatability.

Vessel count was performed and normalized by the periphery of the retina mm. Renal and cardiac effects of DPP4 inhibitors—from preclinical development to clinical research. Other illnesses[ edit ] Multiple mental and physical illnesses, along with some of the medications that treat such illnesses can increase someone's risk of obesity.

Furthermore, dietary components would provide a spectrum of results since both type of diets one with mixture of ingredients-"cafeteria diet" and one with predefined ingredients would alter different impact on the metabolism of the body.

In addition to being a secondary consequence of metabolic syndrome, NAFLD is also in itself a major risk factor for diabetes [ 15 ], and also contributes to cardiovascular morbidity and mortality, with a two-fold increase in the risk of death [ 16 ].

Reitman S, Frankel S. Indeed, fructose which is a highly lipogenic monosaccharide promotes insulin resistance, impaired glucose metabolism, dyslipidemia, hepatic fibrosis and steatosis, as well as both cardiac and renal dysfunctions 1011 However, recent epidemiological studies of sugar consumption and diabetes prevalence [ 11 ] suggest that a diet rich in fat as well as sugar is a greater risk factor for these disorders than a diet that is rich in either fats or sugars.

Diet-induced obesity model

This is an open access article distributed under the Creative Commons Attribution Licensewhich permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Lieber et al. Common such measures include stress both physiological and psychologicalchanges in hormonesand insulin.The intake of a high-fat/high-fructose (HF/HFr) diet is described to be deleterious to cognitive performances, possibly via the induction of inflammatory elbfrollein.com by: 9.

The present study aimed to evaluate the effect of trigonelline (TRG) on the hepatic complications associated with high-fat high-fructose (HFHF) diet-induced insulin resistance (IR) in elbfrollein.com by: 2. · For instance, a high fructose diet is often conjugated with a high fat diet (HF/HF) to induce T2DM in rodents 17,18, However, this model refers only to the early stage of T2DM pathology or Cited by: 5.


Here, we focus on the structural effects of flavonoids by comparing the effect of five purified subclasses of flavonoids on high-fat and high-fructose diet (HFFD) induced metabolic syndrome in vivo. Sprague–Dawley (SD) rats were fed with (i) basal diet ( kcal/g) (ii) HFFD (25% lard and 25% fructose, kcal/g), and (iii) HFFD with flavonoids representing different subclasses ( mmol/kg Cited by: 2.

Given the adverse effects of fructose on metabolic balance, such as hepatic damage, dyslipidemia and IR (Alwahsh et al.,Sloboda et al., ), as well as the prevalence of both high fat and fructose in the typical western diet, it is important to examine the effects of C3G on combined dietary fat- and fructose-induced elbfrollein.com by: 7.

N. Jearapong, W. Chatuphonprasert, and K. Jarukamjorn, “Effect of tetrahydrocurcumin on the profiles of drug-metabolizing enzymes induced by a high fat and high fructose diet in mice,” Chemico-Biological Interactions, vol.pp.

Canadian Journal of Physiology and Pharmacology

67–75, Cited by: 9.

High fat and fructose diet induced journal
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