Possible mediators of metabolic endotoxemia in women with obesity and women with obesity-diabetes in The Gambia.

Aims/hypothesis: Translocation of bacterial debris from the gut causes metabolic endotoxemia (ME) that results in insulin resistance, and may be on the causal pathway to obesity-related type 2 diabetes. To guide interventions against ME we tested two hypothesised mechanisms for lipopolysaccharide (LPS) ingress: a leaky gut and chylomicron-associated transfer following a high-fat meal.

Methods: In lean women (n = 48; fat mass index (FMI) 9.

Rapid growth is a dominant predictor of hepcidin suppression and declining ferritin in Gambian infants.

Iron deficiency and iron deficiency anemia are highly prevalent in low-income countries, especially among young children. Hepcidin is the major regulator of systemic iron homeostasis. It controls dietary iron absorption, dictates whether absorbed iron is made available in circulation for erythropoiesis and other iron-demanding processes, and predicts response to oral iron supplementation.

Host iron status and erythropoietic response to iron supplementation determines susceptibility to the RBC stage of falciparum malaria during pregnancy.

Anaemia and malaria are both common in pregnant women in Sub-Saharan Africa. Previous evidence has shown that iron supplementation may increase malaria risk. In this observational cohort study, we evaluated P.

Elevated Hepcidin Is Part of a Complex Relation That Links Mortality with Iron Homeostasis and Anemia in Men and Women with HIV Infection.

Background: Early and chronic inflammation is a hallmark of HIV infection, and inflammation is known to increase hepcidin expression. Consequently, hepcidin may be a key determinant of the iron homeostasis and anemia associated with poorer HIV prognoses.

Objective: The objective of this study was to understand how hepcidin is related to anemia, iron homeostasis, and inflammation at HIV diagnosis and to investigate associations between hepcidin and all-cause mortality in HIV infection.

Measuring lymphocyte kinetics in tropical field settings.

Studies involving in-vivo labelling of lymphocyte DNA with 6,6-2H2-glucose to track T-cell turnover have contributed to understanding lymphocyte homeostasis in health and disease. Applying such studies in tropical settings (where diseases that affect T-cells are prevalent) requires protocol modifications including non-intravenous label administration, applicability in outpatient facilities, and T-cell sorting methods independent of a fluorescence activated cell sorter (FACS). Such protocols were validated in UK pilot studies and applied in The Gambia.