Tissue oxidative stress The oxidative fluorescent dye dihydroethidine DHE was used to evaluate in situ formation of ROS according to a method described by Dal-Ros et al. Accordingly, cross-sections of the retina revealed the presence of morphological lesions, including thickening of the retinal parenchyma and pathological neovascularization with presence of endothelial cell marker CD31 within the parenchyma, which are both characteristic of diabetic retinopathy Black arrows in Fig.
Biotherapy 3: There are many animal models of obesity and T2D [ 25 ], some of which show a genetic predisposition to the disease [ 26 ], while others may develop the disease spontaneously [ 27 ] or in a diet-induced manner [ 28 ]. The specific fatty foods used in the diets vary across studies, ranging from Crisco to lard to palm oil.
Degree of steatosis was scored as the percentage of hepatocytes per lipid droplet: Because of the commonalities between the two, rats may prove to be helpful in the search for the cause of human obesity. Finelli C, Tarantino G.
Effects of chronic dietary fructose with and without copper supplementation on glycaemic control, adiposity, insulin binding to adipocytes and glomerular basement membrane thickness in normal rats.
Aluminium induced structural, metabolic alterations and protective effects of desferrioxamine in the brain tissue of mice: Our results showed that structurally different flavonoid subclasses prevented the HFFD-induced metabolic syndrome.
The ages of all of the mice at the end of treatment were between 10 and 16 weeks, consistent with adult-aged mice 2—4 months. The control mice were fed with commercial regular diet RD and water ad libitum for 4 weeks. Early striatal dendrite deficits followed by neuron loss with advanced age in the absence of anterograde cortical brain-derived neurotrophic factor.
The most commonly used non-genetic rodent models of diabetes are those induced by streptozotocine or alloxan, in addition to diet [ 29 ], or models obtained by partial pancreatectomy [ 25 ] which leads to insulin deficiency, hyperglycaemia, and ketosis.
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 Fossati P, Prencipe L. After a 1 h habituation period, the plantar surface of the hind paw was exposed three times cut-off time 20 s to a controlled infrared noxious radiant heat stimulus allowing the measurement of the precise withdrawal latency s.
Weight put on during the high-fat diet also tends to persist. Liver homogenates were used for assessment of hepatic lipids, oxidative stress biomarkers, and inflammatory cytokines.
Hepatic steatosis in obese patients: BMB Rep. Non-specific staining was determined by excluding the primary antibody whereas the auto-fluorescence was chemically bleached using cupric sulfate 10 mM in ammonium acetate buffer 50 mM, pH 5. Rodents are nocturnal and are mostly feeding at night, in their natural habitat.
One such characteristic is insulin resistancewhich comes with diet-induced obesity in both rats and humans.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 vsfmorocco.com by: 9.
The increase consumption of fructose in diet is associated with liver inflammation. As a specific fructan substrate, fructose may modify the gut microbiota which is involved in obesity-induced liver disease. Here, we aimed to assess whether fructose-induced liver damage was associated with a specific dysbiosis, especially in mice fed a high fat diet (HFD).
To this end, four groups of mice were fed with Cited by: 7. The diet-induced obesity model (DIO model) is an animal model used to study obesity using animals that have obesity caused by being fed high-fat or high-density diets.
It is intended to mimic the most common cause of obesity in humans. Typically mice, rats, dogs, or non-human primates are used in these models. 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.
Nash, Robert Azantsa, Boris Kuate, Dieudonne Singh, Harrinder and Oben, Julius The Use of a Stem and Leaf Aqueous Extract of Cissus Quadrangularis (CQR) to Reduce Body Fat and Other Components of Metabolic Syndrome in Overweight vsfmorocco.com by: · 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.