BackgroundPsammomys obesus gerbils are particularly prone to develop diabetes and obesity after brief period of abundant food intake. A hypercaloric high fat diet has been shown to affect cardiac function. Here, we sought to determine whether a short period of high fat feeding might alter myocardial structure and expression of calcium handling proteins in this particular strain of gerbils.MethodsTwenty Psammomys obesus gerbils were randomly assigned to receive a normal plant diet (controls) or a high fat diet. At baseline and 16-week later, body weight, plasma biochemical parameters (including lipid and carbohydrate levels) were evaluated. Myocardial samples were collected for pathobiological evaluation.ResultsSixteen-week high fat dieting resulted in body weight gain and hyperlipidemia, while levels of carbohydrates remained unchanged. At myocardial level, high fat diet induced structural disorganization, including cardiomyocyte hypertrophy, lipid accumulation, interstitial and perivascular fibrosis and increased number of infiltrating neutrophils. Myocardial expressions of pro-apoptotic Bax-to-Bcl-2 ratio, pro-inflammatory cytokines [interleukin (IL)-1β and tumor necrosis factor (TNF)-α], intercellular (ICAM1) and vascular adhesion molecules (VCAM1) increased, while gene encoding cardiac muscle protein, the alpha myosin heavy polypeptide (MYH6), was downregulated. Myocardial expressions of sarco(endo)plasmic calcium-ATPase (SERCA2) and voltage-dependent calcium channel (Cacna1c) decreased, while protein kinase A (PKA) and calcium-calmodulin-dependent protein kinase (CaMK2D) expressions increased. Myocardial expressions of ryanodine receptor, phospholamban and sodium/calcium exchanger (Slc8a1) did not change.ConclusionsWe conclude that a relative short period of high fat diet in Psammomys obesus results in severe alterations of cardiac structure, activation of inflammatory and apoptotic processes, and altered expression of calcium-cycling determinants.

Context. Nigella sativa seeds are usually used as traditional medicine for a wide range of therapeutic purposes. Objective. To investigate the subacute toxicity of NS aqueous extract and select its lowest dose to study its antidiabetic effect. Methods. 5 AqE.NS doses (2, 6.4, 21, 33, and 60 g/Kg) were daily administered to mice by gavage. Biochemical parameters measurements and histological study of the liver and the kidney were performed after 6 weeks of supplementation. Thereafter, and after inducing diabetes by alloxan, rats were treated by 2 g/Kg of AqE.NS during 8 weeks. Metabolic parameters were measured on sera. A horizontal electrophoresis of plasmatic lipoprotein was conducted. Glycogen, total lipids, and triglycerides were measured in the liver. TBARS were evaluated on adipose tissue, liver, and pancreas. Results. AqE.NS showed no variation in urea and albumin at the 5 doses, but hepatotoxicity from 21 g/Kg was confirmed by histopathological observations of the liver. In diabetic rats, AqE.NS significantly decreased glycemia, TG, T-cholesterol, LDL-c, and TBARS and showed a restored insulinemia and a significant increase in HDL-c. Results on the liver indicated a decrease in lipids and a possible glycogenogenesis. Conclusion. AqE.NS showed its safety at low doses and its evident antihyperglycemic, antihyperlipidemic, and antioxidant effect.

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Context. Brassica rapa is considered as natural source of antioxidants and is used to treat diabetes. Objective. Our study carried the impact of glucotoxicity induced in vivo and in vitro in vascular smooth muscle cells (VSMCs) in Psammomys and the therapeutic effect of Brassica rapa (AEBr). Materials and Methods. We administered a hyperglucidic diet (30% sucrose) for 9 months and a treatment for 20 days with AEBr at 100 mg/kg. VSMCs were submitted to D-Glucose (0.6%) for 48 hours and treated with AEBr (2100 μg/mL) for 24 hours. We measured, in blood metabolic parameters, the redox statues and inflammatory markers in adipose tissue. Histological study was effectuated in liver. In VSMCs, we measured markers of glucotoxicity (IRS1p Serine, AKT) inflammation (NO, MCP1, TNFα, and NF-κB) and oxidative stress (oxidants and antioxydants markers). Cell viability and apoptosis were estimated by the morphological study. Results. AEBr corrects the metabolic parameters and inflammatory and oxidative markers in blood and homogenate tissue and reduces lipid droplets in liver. It induces, in VSMCs, a significant decrease of IRS1p serine, cyt c, NO, MCP1, TNFα, NF-κB, protein, and lipid oxidation and increases cell viability, AKT, ERK1/2, catalase, and SOD activity. Conclusion. Brassica enhanced the antidiabetic, anti-inflammatory, and antioxidant defense leading to the protection of cardiovascular diseases.