Uncontrolled Diabetes as an Associated Factor with Dynapenia in Adults Aged 50 Years or Older: Sex Differences

BACKGROUND: Epidemiological studies demonstrate an association between diabetes and low neuromuscular strength (NMS). However, none have grouped participants into non-diabetics (ND), undiagnosed diabetics (UDD), controlled diabetics (CD) and uncontrolled diabetics (UCD) or investigated what glycated hemoglobin levels (HbA1c) are associated with low NMS (dynapenia) by sex. METHODS: We analyzed the association between UDD, CD and UCD and dynapenia, the extent to which the different groupings of these individuals modifies this association and the association between HbA1c levels and NMS, by sex, in a cross-sectional study involving 5,290 participants ≥ 50 years from the ELSA study. In the first two analyses, logistic regression models were used with dynapenia (grip strength < 26kg in men and < 16kg in women) as outcome and diabetes [ND, UDD, CD and UCD] as exposure. Next, linear regression was performed with grip strength as outcome and the participants classified based on HbA1c level as exposure. The models were adjusted by sociodemographic, behavioral and clinical characteristics. RESULTS: Compared to ND only UCD was associated with dynapenia (men OR=2.37 95% CI 1.36-4.14; women OR=1.67 95% CI 1.01-2.79). This association was less clear, particularly in women, when CD and UCD groups were merged. HbA1c ≥ 6.5% in men and ≥ 8.0% in women were associated with lower NMS. CONCLUSIONS: UCD increases the chance of dynapenia in both sexes. The different groupings based on diabetes status modify the association between UCD and dynapenia. The threshold of HbA1c associated with reduced NMS is lower in men compared to women

Host hindrance to HIV-1 replication in monocytes and macrophages

Monocytes and macrophages are targets of HIV-1 infection and play critical roles in multiple aspects of viral pathogenesis. HIV-1 can replicate in blood monocytes, although only a minor proportion of circulating monocytes harbor viral DNA. Resident macrophages in tissues can be infected and function as viral reservoirs. However, their susceptibility to infection, and their capacity to actively replicate the virus, varies greatly depending on the tissue localization and cytokine environment. The susceptibility of monocytes to HIV-1 infection in vitro depends on their differentiation status. Monocytes are refractory to infection and become permissive upon differentiation into macrophages. In addition, the capacity of monocyte-derived macrophages to sustain viral replication varies between individuals. Host determinants regulate HIV-1 replication in monocytes and macrophages, limiting several steps of the viral life-cycle, from viral entry to virus release. Some host factors responsible for HIV-1 restriction are shared with T lymphocytes, but several anti-viral mechanisms are specific to either monocytes or macrophages. Whilst a number of these mechanisms have been identified in monocytes or in monocyte-derived macrophages in vitro, some of them have also been implicated in the regulation of HIV-1 infection in vivo, in particular in the brain and the lung where macrophages are the main cell type infected by HIV-1. This review focuses on cellular factors that have been reported to interfere with HIV-1 infection in monocytes and macrophages, and examines the evidences supporting their role in vivo, highlighting unique aspects of HIV-1 restriction in these two cell types