Body composition analysis: A snapshot across the perimenopause.

During the perimenopause, estrogen concentrations gradually decrease, and this is associated with changes to women's energy expenditure and intake. These changes result in weight gain and altered body fat distribution, with increased abdominal fat deposition and cardiometabolic risk via insulin resistance. Body composition analysis is a useful clinical tool in outpatient settings, as it is simple, not expensive and provides information on body mass index, skeletal mass, fat mass, fat percentage and basal metabolic rate. This review discusses body composition analysis as part of a health assessment for healthy women during the perimenopause and investigates the associations between body composition and cardiometabolic profile.

Modulation of endogenous antioxidant defense and the progression of kidney disease in multi-heritage groups of patients with type 2 diabetes: PRospective EValuation of Early Nephropathy and its Treatment (PREVENT).

BACKGROUND: Diabetes is the western world's leading cause of end-stage renal disease. Glucose-dependent, oxidative stress is linked to the development of renal inflammation and sclerosis, which, in animal models of diabetes, can be prevented by anti-oxidative treatment. Patients of non-Caucasian heritage have low activity of the selenoprotein, antioxidant enzyme, glutathione peroxidase (GPx) and its co-factor vitamin E, which may be linked to their increased propensity to developing end-stage renal disease. RESEARCH DESIGN AND METHODS: We have designed a double-blind, randomized, placebo controlled study with selenium and/or vitamin E versus placebo as the interventions for patients with type 2 diabetes and chronic kidney disease (CKD) stages 1-3. A 2 × 2 factorial design will allow a balanced representation of the heritage groups exposed to each intervention. The primary biochemical outcome is change in GPx activity, and clinical outcome measure is the actual, rate of-and/or percentage change in estimated glomerular filtration rate (eGFR) from baseline. Analysis will be with a marginal model for longitudinal data using Generalized Estimating Equations corrected for measures of baseline serum antioxidant enzyme activities (GPx, superoxide dismutase and catalase), micronutrient levels (vitamins E and C), measures of inflammation (interleukin 6, c-reactive protein and monocyte chemoattractant protein-1) and markers of oxidative damage (plasma 8-isoprostaglandin F2α and urinary 8-hydroxydeoxyguanosine). EXPECTED RESULTS: The study will assess the relationship between GPx activity, oxidative stress, inflammation and eGFR. It will test the null hypothesis that antioxidant therapy does not influence the activity of GPx or other antioxidant enzymes and/or alter the rate of change in eGFR in these patient groups. CONCLUSIONS: Outcome data on the effect of antioxidants in human diabetic renal disease is limited. Previous post hoc analyses have not shown a beneficial effect of vitamin E on renal function. A recent trial of a pharmaceutical antioxidant agent, improved eGFR, but in patients with advanced diabetes-related chronic kidney disease its use was associated with an increased incidence of cardiovascular events. We will explore whether the nutritional antioxidants, vitamin E and selenium alone, or in combination in patients at high risk of renal disease progression, forestalls a reduction in eGFR. The study will describe whether endogenous antioxidant enzyme defenses can be safely modified by this intervention and how this is associated with changes in markers of oxidative stress. Trial registration ISRCTN 97358113. Registered 21st September 2009.

Estrogen plus progestin treatment: effect of different progestin components on serum markers of apoptosis in healthy postmenopausal women.

One hundred healthy postmenopausal women were randomly assigned to receive 17ß-E2 1 mg/drospirenone 2 mg or 17ß-E2 1 mg/norethisterone acetate 0.5 mg for 6 months, and circulating soluble Fas, soluble Fas ligand, and cytochrome c were measured at baseline and at 6 months in 87 women who completed the study. Although cytochrome c levels were undetectable, circulating soluble Fas/soluble Fas ligand ratio decreased in both groups, suggesting a decrease in ligand-mediated apoptosis.

Apoptosis in atherosclerosis: a mini-review.

Apoptosis in atherosclerotic lesions is triggered by inflammatory processes, both via cell-cell contact and by cytokines and oxidized lipids. The role of apoptosis in atherogenesis is dual, depending on the stage of the plaque: In early stages, apoptotic death of smooth muscle--and inflammatory cells, such as lymphocytes and macrophages--may delay atherosclerotic process. However, once the plaque is formed, apoptosis may lead to plaque rupture and thrombosis.