ObjectivesWith the use of potent antiretroviral therapy in patients with HIV disease, changes in lipid parameters and glucose homeostasis have been noted. However, these effects have been difficult to interpret because of the varied demographic and treatment characteristics of the cohorts and the complexity of differentiating the effect of HIV disease from that of the drugs used in its treatment. This study was designed to explore these issues. MethodsDemographic information and fasting blood samples were collected from 419 antiretroviral-naïve HIV-1-infected patients. ResultsThe average age of the participants was 38.2 years, with 21% being female, 60% being African American, and 14% having a history of injection drug use. The mean CD4 lymphocyte count was 216 cells/mL, the mean baseline log 10 HIV viral load was 4.98 HIV-1 RNA copies/mL, and 26% of patients had a history of AIDS-defining events. Women and African Americans had significantly higher levels of high-density lipoprotein (HDL) cholesterol, and older age was associated with higher total cholesterol levels. Lower CD4 lymphocyte counts and higher HIV RNA levels were independently associated with lower HDL cholesterol levels. Additionally, higher HIV RNA level was associated with lower levels of low-density lipoprotein (LDL) cholesterol and higher levels of very-low-density lipoprotein (VLDL) cholesterol and triglycerides. A history of AIDS-defining events was associated with higher total cholesterol, VLDL cholesterol and triglyceride concentrations. With respect to glucose homeostasis, a higher CD4 lymphocyte count was associated with less evidence of insulin resistance. However, a higher body mass index was associated with higher lipid levels and with more evidence of insulin resistance. ConclusionsBoth HIV disease and demographic characteristics were found to influence lipid values and glucose homeostasis in the absence of antiretroviral treatment. More advanced HIV disease was associated with less favourable lipid and glucose homeostatic profiles. The independent association between HIV RNA levels and various lipid parameters suggests that viral replication had a direct effect on lipid levels. Interpretation of the effects of various HIV treatment regimen and drugs on metabolic parameters must take into account the stage of HIV disease and the demographic characteristics of the population studied.

Significant differences exist in the prevalence of various components of the metabolic syndrome even within an urban environment and this appears to be influenced by socioeconomic status.

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Objective: Few dietary surveys have been done with reference to chronic diseases, such as diabetes, in India, which is considered to be the diabetes capital of the world. We report on the dietary intake of urban adults living in Chennai, South India. Design: A population-based cross-sectional study. Setting: A representative population of urban Chennai in southern India. Subjects: The study population comprised 2042 individuals aged $20 years selected from the Chennai Urban Rural Epidemiological Study (CURES). Dietary intake was measured using a validated and previously published interviewer-administered semi-quantitative meal-based FFQ. Results: The mean daily energy intake was 10 393 (SD 2347) kJ (male: 10 953 (SD 2364) kJ v. female: 9832 (SD 233) kJ). Carbohydrates were the major source of energy (64 %), followed by fat (24 %) and protein (12 %). Refined cereals contributed to the bulk of the energy (45?8 %), followed by visible fats and oils (12?4 %) and pulses and legumes (7?8 %). However, energy supply from sugar and sweetened beverages was within the recommended levels. Intake of micronutrient-rich foods, such as fruit and vegetable consumption (265 g/d), and fish and seafoods (20 g/d), was far below the FAO/WHO recommendation. Dairy and meat products intake was within the national recommended intake. Conclusions: The diet of this urban South Indian population consists mainly of refined cereals with low intake of fish, fruit and vegetables, and all of these could possibly contribute to the risk of non-communicable diseases such as diabetes in this population. At the end of 20th century, India had rapid progress in controlling communicable diseases and the socioeconomic status of people has shown marked improvement. However, ageing of the population and altered lifestyles (unhealthy diets and physical inactivity) have contributed to the increase in the prevalence of chronic non-communicable diseases such as diabetes, obesity and CVD (1) . According to recent estimates, India leads the world with the largest number of persons with type 2 diabetes (50?8 million) (2) . In all, 53 % of all deaths and 44 % of disability-adjusted life-years lost in India in 2005 could be attributed to chronic disease (including cancer, coronary artery disease, CVD, hypertension and diabetes) (3) . The common factors with regard to diabetes and its rising prevalence rates are increased insulin resistance, stronger genetic factors and environmental factors, particularly those associated with urbanisation (4) . Although genetic factors (5) and physical inactivity (6) have been shown to explain, at least in part, the diabetes epidemic, there is paucity of data on the dietary intake of the population. In many developing countries, food-related policies continue to focus only on undernutrition, and do not address the prevention of chronic diseases, which are primarily due to overnutrition (7,8) . Moreover, large national surveys such as National Sample Survey Organization do not provide an insight into the actual dietary intak...

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We have developed a direct and efficient route for the synthesis of ciclamycin 0 using the sulfoxide glycosylation reaction to form the glycosidic linkages. In the course of completing the synthesis of ciclamycin 0, we developed new glycosylation conditions that improve the outcome of the sulfoxide reaction. The conditions involve the addition of agents that scavenge phenylsulfenyl triflate, a highly reactive byproduct that forms following activation of anomeric sulfoxides with triflic anhydride.

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