Impact of Dietary Modifications on Plasma Sirtuins 1, 3 and 5 in Older Overweight Individuals Undergoing 12-Weeks of Circuit Training.

Sirtuins are nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases that regulate numerous pathways such as mitochondrial energy metabolism in the human body. Lower levels of these enzymes were linked to diseases such as diabetes mellitus and were also described as a result of aging. Sirtuins were previously shown to be under the control of exercise and diet, which are modifiable lifestyle factors.

Energy metabolism in umbilical endothelial cells from preterm and term neonates.

Aim: The aim of this study was to investigate the impact of gestational age on energy metabolism in human umbilical vein endothelial cells (HUVECs) of preterm and term neonates.

Methods: Activities of respiratory chain (RC) complexes I-V, citrate synthase (CS), overall mitochondrial fatty acid oxidation (FAO), carnitine palmitoyltransferase 2 (CPT2), glycolytic enzymes as well as energy-rich phosphates in HUVECs from uncomplicated term and preterm pregnancies were measured. Neonatal acylcarnitine profiles were analyzed postpartum.

Effect of tacrolimus on energy metabolism in human umbilical endothelial cells.

Background: Tacrolimus has a wide spectrum of adverse effects, including neurotoxic and vascular events. Vascular dysfunction due to interference of tacrolimus with mitochondrial function in endothelial cells may contribute to these adverse reactions.

Material/methods: We evaluated the impact of clinically relevant tacrolimus concentrations after 48 hours on energy metabolism in cultured human umbilical vein endothelial cells (HUVEC): Global fatty acid oxidation (FAO), activities of respiratory chain complexes I-V (RC), citratesynthase (CS), glycolytic enzymes and energy rich phosphates were measured.

Cyclosporine A: impact on mitochondrial function in endothelial cells.

Introduction: Although cyclosporine A (CSA) is considered to be an efficient immunosuppressive compound in transplantation, vascular side effects like arterial hypertension, neurologic complications and other adverse reactions occur. Interference of CSA with mitochondrial function may be responsible for these side effects.

Methods: We evaluated the effect of CSA on mitochondrial and glycolytic function by measuring fatty acid oxidation (FAO), activities of respiratory chain complexes (RC) and citratesynthase (CS), lactate/pyruvate-ratios, energy-rich phosphates as well as activities of some glycolytic enzymes in human umbilical vein endothelial cells.

Preeclampsia and HELLP syndrome: impaired mitochondrial function in umbilical endothelial cells.

Preeclampsia (PE) and hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome have been linked to congenital fetal disorders of mitochondrial fatty acid oxidation (FAO). Different incidences may argue for the association of noncongenital alterations of mitochondrial energy metabolism with PE/HELLP syndrome. We studied human umbilical vein endothelial cells [HUVEC] as selected part of the feto-placental unit from uncomplicated (n = 46) and diseased (n = 27; 17 PE and 10 HELLP) pregnancies by measuring the overall FAO, carnitine palmitoyltransferase 2 (CPT2), respiratory chain (RC) complexes I-V, citratesynthase (CS), lactatedehydrogenase (LDH), hexokinase (HK), phosphofructokinase (PFK), and energy rich phosphates.