In obese hypertensives cholecalciferol inhibits circulating TH17 cells but not macrophage infiltration on adipose tissue

Standard Doses of Cholecalciferol Reduce Glucose and Increase Glutamine in Obesity-Related Hypertension: Results of a Randomized Trial

“…In the case of short-lived Th17 cells that mostly rely on aerobic glycolysis and glutaminolysis for ATP production [ 39 ], increased glutamine may be responsible for Th17 cell stability and the modulation of reactive oxygen species synthesis and oxidative stress [ 39 ]. Although our trial was not designed to evaluate specific metabolic pathways or, specifically, the uptake of glutamine at the cellular level, we previously documented a restrictive effect of cholecalciferol on Th17 cell expansion in obese hypertensives [ 22 ]. In type 2 diabetics, for example, a profound inhibition of aerobic glycolysis in human T cells under the effect of vitamin D was also observed, contributing to a shift in the metabolic fate of immune cells from an activated state to an oligo-secreting state [ 40 ].…”

“…The results presented here are part of a prospective, single-center, randomized clinical trial conducted in patients with obesity-associated hypertension. The detailed study design has been published elsewhere [ 22 ]. Briefly, 36 patients routinely followed in the hypertension consultation with simultaneous obesity or metabolic syndrome diagnoses were recruited to a phase 2, open, parallel-group trial designed to explore the effects of cholecalciferol on the serum metabolome.…”

“…Here, we present an expanded dataset from a previously described cohort in which we analyzed the immunomodulatory effects of vitamin D [ 22 ]. Since immune cells depend on the nutrients available in their environment, it is plausible that modifications in the serum metabolome can affect immune cell populations.…”