full and unique pattern of gene expression, regardless of their environment (33, 34, 35, 36) . Further research is required, particularly in equines, to evaluate the importance of the site of fat deposition and differences in metabolism of these fat
Antonia Ertelt, Ann-Kristin Barton, Robert R Schmitz, and Heidrun Gehlen
Lang Qin, Xiaoming Zhu, Xiaoxia Liu, Meifang Zeng, Ran Tao, Yan Zhuang, Yiting Zhou, Zhaoyun Zhang, Yehong Yang, Yiming Li, Yongfei Wang, and Hongying Ye
). These studies have suggested a cross-talk between lipid metabolism disorders and blood pressure regulation through nuclear hormone receptors. Blood pressure reduction has previously been reported with cholesterol reduction in hyperlipidemia patients
Britt J van Keulen, Conor V Dolan, Bibian van der Voorn, Ruth Andrew, Brian R Walker, Hilleke Hulshoff Pol, Dorret I Boomsma, Joost Rotteveel, and Martijn J J Finken
, there are no studies that have reported on HPA-axis activity across pubertal development. HPA-axis activity is determined by the net effect of cortisol production and metabolism. Cortisol is metabolized by various enzymes ( Fig. 1 ). The A
Kristin Godang, Karolina Lundstam, Charlotte Mollerup, Stine Lyngvi Fougner, Ylva Pernow, Jörgen Nordenström, Thord Rosén, Svante Jansson, Mikael Hellström, Jens Bollerslev, Ansgar Heck, and the SIPH Study Group
, lipids and glucose metabolism in mild PHPT. Materials and methods Subjects From 1999 to the end of inclusion by June 2005, the SIPH study (ClinicalTrials.gov: Nbib522028) included a total of 191 patients (26 men) with asymptomatic (mild) PHPT
Introduction White adipose tissue (WAT) is a metabolically active tissue that modifies systemic metabolism significantly by regulating the storage and release of lipids. Free fatty acids serve as a major fuel source during times of energy
Hong-Fa Yan, Zhao-Yu Liu, Zhi-Ang Guan, and Chuang Guo
hypoxia-inducible factor-1α (HIF-1α) activity, resulting in an increase in proteins related to lipid metabolism, including peroxisome proliferator-activated receptor-γ (PPARγ), PPARγ co-activator 1 alpha (PGC-1α) and uncoupling protein (UCP) 1 ( 10 ). Of
Fabian Eichelmann, Cornelia Weikert, Romina di Giuseppe, Ronald Biemann, Berend Isermann, Matthias B Schulze, Heiner Boeing, and Krasimira Aleksandrova
). Ten years later (in 2007) chemerin was re-discovered as a novel adipokine regulating adipogenesis and genes critical in glucose and lipid metabolism of adipocytes ( 3 ). Subsequent research characterized additional roles of chemerin in diverse
Selina Mäkinen, Neeta Datta, Yen H. Nguyen, Petro Kyrylenko, Markku Laakso, and Heikki A Koistinen
Objectives: Simvastatin use is associated with muscular side effects, and increased risk for type 2 diabetes (T2D). In clinical use, simvastatin is administered in inactive lipophilic lactone-form, which is then converted to active acid-form in the body. Here, we have investigated if lactone- and acid-form simvastatin differentially affect glucose metabolism and mitochondrial respiration in primary human skeletal muscle cells.
Methods: Muscle cells were exposed separately to lactone- and acid-form simvastatin for 48 h. After pre-exposure, glucose uptake and glycogen synthesis were measured using radioactive tracers; insulin signalling was detected with western blotting; and glycolysis, mitochondrial oxygen consumption and ATP production were measured with Seahorse XFe96 analyzer.
Results: Lactone-form simvastatin increased glucose uptake and glycogen synthesis, whereas acid-form simvastatin did not affect glucose uptake and decreased glycogen synthesis. Phosphorylation of insulin signalling targets Akt substrate 160 kDa (AS160) and glycogen synthase kinase 3β (GSK3β) was upregulated with lactone-, but not with acid-form simvastatin. Exposure to both forms of simvastatin led to a decrease in glycolysis and glycolytic capacity, as well as to a decrease in mitochondrial respiration and ATP production.
Conclusions: These data suggest that lactone- and acid-forms of simvastatin exhibit differential effects on non-oxidative glucose metabolism as lactone-form increases and acid-form impairs glucose storage into glycogen, suggesting impaired insulin sensitivity in response to acid-form simvastatin. Both forms profoundly impair oxidative glucose metabolism and energy production in human skeletal muscle cells. These effects may contribute to muscular side effects and risk for T2D observed with simvastatin use.
Maximilian Bielohuby, Martin Bidlingmaier, and Uwe Schwahn
, gastric emptying and glucose metabolism ( 31 , 32 , 33 ). In our hands and using a small set of samples collected from the tail vein with or without isoflurane anesthesia in C57BL/6J mice, plasma insulin concentrations were significantly ( P < 0
L Ghataore, I Chakraborti, S J Aylwin, K-M Schulte, D Dworakowska, P Coskeran, and N F Taylor
pathways stimulated by mitotane. Names shaded white are for steroids that show decreases after mitotane. The only reports of mitotane effects on extra-adrenal cortisol metabolism (10, 11, 13) note a rapid change in metabolism of administered cortisol