The present study was aimed to evaluate the influence of flaxseed oil on renal toxicity induced by thioacetamide in male rats. The animals were distributed into four groups. Rats of the first group were served as control. Rats of the second group were exposed to thioacetamide. Rats of the third group were treated with flaxseed oil and thioacetamide. Rats of the fourth group were treated with flaxseed oil. Significant increases of blood creatinine and uric acid were observed in TAA-treated rats after three weeks. In thioacetamide group, the levels of serum creatinine, blood urea nitrogen and uric acid were significantly elevated after six weeks. Histopathologically, the renal sections from thioacetamide-treated rats showed severe alterations in the structure of renal corpuscles including a degeneration of glomeruli and Bowman’s capsules. Administration of flaxseed oil protects the observed biochemical and histopathological alterations induced by thioacetamide exposure. Hence, the results of this study suggest that flaxseed oil protects against thioacetamide-induced renal injury and the protective influence of flaxseed oil may be attributed to its antioxidant role.

Introduction: Angiotensin-converting enzyme ( ACE), which contributes to adipocyte growth, differentiation and function, has recently been linked with both salt metabolism and obesity development. Therefore, this study has aimed to investigate the putative relationship between ACE genetic polymorphism, serum ACE levels and salt consumption on the risk of developing obesity in the Saudi population. Materials and methods: ACE genotype status of 267 adult Saudi volunteers (124 obese and 143 non-obese) was correlated with their serum ACE activity and dietary salt intake amounts. Results: Obesity was more prevalent in deletion-deletion genotype individuals ( p<0.03), under dominant, co-dominant and monoallelic conditions ( p<0.04). Deletion allele corresponds to serum ACE activity in obese patients ( p<0.05). The amount of salt intake (<6 g/d) was significantly associated with obesity and particularly high in deletion-deletion and insertion-deletion genotype carriers ( p<0.001). STITCH analysis underlined interactions of the ACE protein with sodium molecule, REN, ACE2, KNG1 and AGTR1 in a biological network. Conclusions: Our findings suggest the positive association between ACE deletion genotype, serum ACE activity and sodium intake with risk of obesity development in the Saudi population.

Obesity is a multifactorial metabolic disorder characterized by low grade chronic inflammation. Rare and novel mutations in genes which are vital in several key pathways have been reported to alter the energy expenditure which regulates body weight. The TP53 or p53 gene plays a prominent role in regulating various metabolic activities such as glycolysis, lipolysis, and glycogen synthesis. Recent genome-wide association studies reported that tumor suppressor gene p53 variants play a critical role in the predisposition of type 2 diabetes and obesity. Till date, no reports are available from the Arabian population; hence the present study was intended to assess the association between p53 variants with risk of obesity development in the Saudi population. We have selected three p53 polymorphisms, rs1642785 (C > G), and rs9894946 (A > G), and rs1042522 (Pro72Arg; C > G) and assessed their association with obesity risk in the Saudi population. Phenotypic and biochemical parameters were also evaluated to check their association with p53 genotypes and obesity. Genotyping was carried out on 136 obese and 122 normal samples. We observed that there is significantly increased prevalence p52 Pro72Arg (rs1042522) polymorphism in obese persons when compared to controls at GG genotype in overall comparison (OR: 2.169, 95% CI: 1.086-4.334, p = 0.02716). Male obese subjects showed three-fold higher risk at GG genotype (OR: 3.275, 95% CI: 1.230-8.716, p = 0.01560) and two-fold risk at G allele (OR: 1.827, 95% CI: 1.128-2.958, p = 0.01388) of p53 variant Pro72Arg respectively. This variant has also shown significant influence on cholesterol, LDL level, and random insulin levels in obese subjects (p ≤ 0.05). In conclusion, p53 Pro72Arg variant is highly prevalent among obese individuals and may act as a genetic modifier for obesity development among Saudis.

Obesity is a multifactorial disease caused by complex interactions between genes and dietary factors. Salt-rich diet is related to the development and progression of several chronic diseases including obesity. However, the molecular basis of how salt sensitivity genes (SSG) contribute to adiposity in obesity patients remains unexplored. In this study, we used the microarray expression data of visceral adipose tissue samples and constructed a complex protein-interaction network of salt sensitivity genes and their co-expressed genes to trace the molecular pathways connected to obesity. The Salt Sensitivity Protein Interaction Network (SS PIN) of 2691 differentially expressed genes and their 15474 interactions has shown that adipose tissues are enriched with the expression of 23 SSGs, 16 hubs and 84 bottlenecks (p = 2.52 x 10-16) involved in diverse molecular pathways connected to adiposity. Fifteen of these 23 SSGs along with 8 other SSGs showed a co-expression with enriched obesity-related genes (r � 0.8). These SSGs and their co-expression partners are involved in diverse metabolic pathways including adipogenesis, adipocytokine signaling pathway, renin-angiotensin system, etc. This study concludes that SSGs could act as molecular signatures for tracing the basis of adipogenesis among obese patients. Integrated network centered methods may accelerate the identification of new molecular targets from the complex obesity genomics data.

The journal retracts the article, “Safety of Commercially Available Beef Burger in Saudi Arabia [...]