C-C chemokine receptor type 5 (CCR5) is known for its role as a co-receptor for HIV-1 infection. Some individuals possess a 32 bp deletion, known as Delta-32 allele which has been reported to confer resistance to HIV-1 infection. In order to estimate the distribution of Delta-32 allele of CCR5 gene, 1034 mestizo individuals from the Northwest of Mexico, including 385 HIV-1-infected individuals, 472 healthy controls and 177 uninfected female sex workers; were examined by allele-specific PCR. There was no statistically significant difference in the frequency of Delta-32 allele between HIV-1 positive and healthy individuals (OR= 1.1, p= 0.6). However, we found a significantly reduced prevalence of CCR5 Delta-32 heterozygous genotype in female patients (OR= 0.084, 95% CI= 0.011 - 0.630, p= 0.002), as well as in allele frequency, compared to male patients. Furthermore, we observed an inverse relationship between allele frequency and the risk of HIV-1 transmission and AIDS progression among female healthy controls, sex workers and HIV-1 infected groups. Our findings support previous data showing Delta-32 as a genetic protective factor against HIV-1 infection in Mexican women, as well as in women from other populations.
The high intake of sweetened drinks is associated with obesity and insulin resistance. These pathologies are directly related to the development of nonalcoholic fatty liver disease (NAFLD), considered a condition of metabolic syndrome (MS). Due to their increasing worldwide prevalence, experimental animal models have been developed to gain a better understanding of its physiopathology; notwithstanding, few studies have evaluated its progression in association with MS and ingestion of sweetened drinks. Therefore, the aim of this study was to understand the pathophysiologic characteristics of NAFLD related to sucrose concentration and time of ingestion in rats. Wistar rats were divided into 2 groups with free access to either tap water or 30% sucrose, and euthanized at 12, 16, or 20 weeks; and 2 additional groups were given free access to either 40% or 50% sucrose and were euthanized at 20 weeks. Biochemical parameters and levels of serum cytokines were measured, and histology was performed. Ingestion of 30% sucrose induced liver steatosis until 16 weeks (grade 2) and 20 weeks (grade 3). Meanwhile, during 20 weeks, 40% sucrose induced grade 5 of nonalcoholic steatohepatitis (NASH) and 50% sucrose induced grade 6 of NASH and fibrosis. This study demonstrated that increasing time of induction and concentration of sucrose ingestion resulted in a higher grade of NAFLD.
Introduction
Overconsumption of sucrose has been associated with negative metabolic effects related to non‐communicable diseases. However, this relationship continues to be a controversial topic and further studies are needed to generate scientific evidence to help clarify existing questions and which can be used in the future for the implementation of prevention and control strategies of this important health problem.
Objective
The aim of this study was to evaluate the sucrose‐enriched diet consumption in the development of risk factors associated to type 2 diabetes, atherosclerosis and non‐alcoholic fatty liver disease in a murine model.
Methodology
Twelve healthy male Wistar rats were randomly divided into two experimental groups (n=6 each) which received one of two different diets for twenty five weeks. Control group (CG) was fed with a standard laboratory diet and tap water. Sucrose group (SG) received the same laboratory diet and water enriched with 50% w/v of sucrose. Body weight, food, macronutrient and total caloric intake were determined. After intervention period, blood samples, hepatic and aortic tissues were collected. Glucose, insulin, total cholesterol, triglycerides, very low‐density lipoprotein cholesterol, low‐density lipoprotein cholesterol and high‐density lipoprotein cholesterol levels were determined in serum. Insulin resistance was calculated and total hepatic cholesterol was measured. Histopathological analysis was made for liver and aortic tissues. Results of parametric tests were expressed as mean values ± standard errors of the mean and for non‐parametric tests, results were expressed as medians and ranks. A p value of < 0.05 was considered significant.
Results
Sucrose‐enriched diet‐fed rats showed a decrease in food, lipids and protein intake as well as in serum total cholesterol levels, an increase in carbohydrates intake, glucose, insulin, triglycerides, very low‐density lipoprotein cholesterol and high‐density lipoprotein cholesterol levels, the development of insulin resistance, a higher percentage of steatosis and a greater degree of non‐alcoholic steatohepatitis. No significant differences were found in body weight, total caloric intake, low‐density lipoprotein cholesterol and hepatic cholesterol between the experimental groups. In aortic tissue samples, both groups showed a slight wall thickening.
Conclusion
Our results show that sucrose‐enriched diet consumption during twenty five weeks contribute to the development of risk factors associated to type 2 diabetes, atherosclerosis and non‐alcoholic fatty liver disease in male Wistar rats.
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