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BackgroundSodium-glucose co-transporter-2 inhibitors (SGLT2i) reduce glucose levels, body weight, and blood pressure, possibly resulting in cardiovascular protection. In phase III trials, SGLT2i were shown to increase HDL cholesterol. We aimed to evaluate whether the SGLT2i dapagliflozin affects HDL function in a randomized placebo-controlled trial.MethodsThirty-three type 2 diabetic patients were randomized to receive dapagliflozin 10 mg or placebo for 12 weeks on top of their glucose lowering medications. The primary end-point was the change in cholesterol efflux capacity (CEC) from macrophages at study end versus baseline. Secondary endpoints were changes in: distribution of HDL subfractions, lipid profile, activity of enzymes that mediate HDL antioxidant properties (PON1 and ARE) and cholesterol metabolism (CETP), HbA1c, body weight and composition.ResultsThirty-one patients completed the study, n = 16 in the placebo group and n = 15 in the dapagliflozin group. Patients randomized to dapagliflozin were older and had lower adiposity indexes, although these differences disappeared after correction for multiple testing. Therapy with dapagliflozin reduced HbA1c by 0.9% and body weight by 3.1 kg, mainly attributable to reduction of body water and lean mass. As compared to placebo, dapagliflozin reduced CEC (−6.7 ± 2.4 versus 0.3 ± 1.8%; p = 0.043), but this effect was no longer significant after adjusting for age and BMI. No change was detected in HDL cholesterol, HDL subfractions, activity of PON1, ARE, and CETP.ConclusionsDespite improvements in glucose control and reduction in body weight, therapy with dapagliflozin exerted no significant effect on HDL cholesterol levels and HDL functionality. Trial registration EudraCT 2014-004270-42; NCT02327039Electronic supplementary materialThe online version of this article (doi:10.1186/s12933-017-0529-3) contains supplementary material, which is available to authorized users.

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Objectives Institutionalized older adults have a high prevalence of frailty and disability, which may make them more vulnerable to the negative consequences of COVID-19. We investigated the impact of COVID-19 on the level of frailty, physical and cognitive performance in nursing home residents. Design Nested case-control study. Setting and participants. The study included nursing home residents who were infected with COVID-19 ( case group , n=76), matched by age to a control group (n=76). Methods Participants’ sociodemographic and medical data were collected, and they were also assessed for physical function (handgrip and walking speed), cognitive performance (Mini-Mental State Examination [MMSE]) and frailty (Frail-NH scale) before the first wave of the COVID-19 pandemic (October to December 2019, "pre-COVID-19") and after (June to July 2020, "post-COVID-19"). COVID-19 symptoms and clinical course were recorded for the cases . Results Between the pre- and post-COVID-19 assessments, we found a 19% greater deterioration in handgrip, a 22% greater increase in walking speed, and a 21% greater increase in Frail-NH scores in cases compared with controls. In both cases and controls, on the other hand, there was a significant 10% decrease in MMSE scores over the study period. Multivariable logistic regression showed that COVID-19 survivors had a four-fold increased chance of developing frailty compared with controls (OR = 4.95, 95% CI: 1.13-21.6, p =0.03), but not cognitive decline. Conclusions and implications COVID-19 can accelerate the aging process of institutionalized older adults in terms of physical performance and frailty by around 20%. However, we found similar levels of decline in cognitive performance in both cases and controls, likely due to the burden of social isolation and containment measures on neuropsychological health.