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S U Jayasinghe, S J Torres, C A Nowson, A J Tilbrook and A I Turner

to psychological stress can be influenced by the physiological status of an individual (2) . Obesity (a state of elevated adiposity) has reached epidemic proportions in the Western world (16) . As such, an understanding of the influence of obesity

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Shenglong Le, Leiting Xu, Moritz Schumann, Na Wu, Timo Törmäkangas, Markku Alén, Sulin Cheng and Petri Wiklund

substantially during puberty ( 6 , 7 ). Along these lines, low serum SHBG level has been associated with increased adiposity and insulin resistance in children and adolescents ( 3 , 8 , 9 , 10 , 11 , 12 ); therefore, it has been hypothesized that SHBG

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Shane M Regnier, Andrew G Kirkley, Daniel Ruiz, Wakanene Kamau, Qian Wu, Kurunthachalam Kannan and Robert M Sargis

have shown that TF augments adipogenesis in vitro ( 18 ) and promotes insulin resistance in rodent and human adipose tissues exposed ex vivo ( 19 ). These effects are postulated to result from activation of adipocytic glucocorticoid receptor (GR

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Meena Asmar, Ali Asmar, Lene Simonsen, Flemming Dela, Jens Juul Holst and Jens Bülow

Introduction The regulation of subcutaneous adipose tissue blood flow (ATBF) is crucial in lipid homeostasis ( 1 , 2 ). It has long been recognized that the ATBF is tightly coupled to adipose tissue metabolism ( 3 , 4 , 5 , 6 ). In

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Julia H Goedecke, Mehreen Tootla and Dheshnie Keswell

comprises both visceral (VAT) and subcutaneous adipose tissue (SAT), is commonly associated with increased cardiometabolic risk, whereas lower-body gluteo-femoral fat accumulation may be protective ( 4 , 5 ). Within adipose tissue, aromatase ( CYP19A1

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N Bergmann, F Gyntelberg and J Faber

Introduction The metabolic syndrome (MES) is a cluster of risk factors including male adiposity, dyslipidemia, reduced glucose tolerance and hypertension. MES is highly prevalent and increasing in most parts of the world (1) . A meta-analysis has

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Julie Smith, Jan Fahrenkrug, Henrik L Jørgensen, Christina Christoffersen and Jens P Goetze

Introduction Mammalian hearts release natriuretic hormones that regulate renal natriuresis and intravascular fluid homeostasis (1, 2) . More recently, an effect on adipose tissue has also been established in which hormone binding to the

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Monika Karczewska-Kupczewska, Agnieszka Nikołajuk, Magdalena Stefanowicz, Natalia Matulewicz, Irina Kowalska and Marek Strączkowski

systemic chemerin and insulin resistance has been reported ( 11 , 12 , 15 , 16 ); however, not all studies confirm this relationship ( 17 , 18 ). Furthermore, data regarding the correlations between adipose tissue (AT) chemerin expression and insulin

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Monika Karczewska-Kupczewska, Agnieszka Nikołajuk, Radosław Majewski, Remigiusz Filarski, Magdalena Stefanowicz, Natalia Matulewicz and Marek Strączkowski

complications ( 1 ). Adipose tissue (AT) function and the balance between lipid storage and mobilization play an important role in regulating insulin action. Inability of AT to store fat leads to free fatty acids (FFA) overflow to other tissues and to insulin

Open access

Emmely M de Vries, Hermina C van Beeren, Albert C.w.a. van Wijk, Andries Kalsbeek, Johannes A Romijn, Eric Fliers and Anita Boelen

Fasting induces profound changes in the hypothalamus-pituitary-thyroid axis and peripheral thyroid hormone (TH) metabolism, ultimately leading to lower serum thyroid hormone (TH) concentrations. In the present study, we aimed to investigate the regulation of type 3 deiodinase (D3) during fasting in two metabolic tissues: liver and white adipose tissue (WAT). To this end, we studied the effect of modulation of the mammalian target of rapamycin (mTOR) and hypoxia inducible factor 1α (HIF1α) on D3 expression in a primary rat hepatocytes and in 3T3-L1 adipocytes. In addition, we studied the role of the constitutive androstane receptor (CAR) on liver TH metabolism using primary hepatocytes and CAR-/- mice. Twenty-four hour fasting increased liver D3 expression in mice. Inhibition of mTOR using mTOR inhibitors markedly induced D3 mRNA expression in primary hepatocytes; this increase was accompanied by a small increase in D3 activity. Stimulation of these cells with a CAR agonist induced both D3 mRNA expression and activity. Fasting increased hepatic D3 expression in WT but not in CAR-/- mice. In WAT, D3 mRNA expression increased 5-fold after 48h fasting. Treatment of 3T3-L1 adipocytes with mTOR inhibitors induced D3 mRNA expression, whereas stimulation of these cells with cobalt chloride, a compound that mimics hypoxia and stabilizes HIF1α, did not induce D3 mRNA expression. In conclusion, our results indicate an important role of mTOR in the upregulation of D3 in WAT and liver during fasting. Furthermore, CAR plays a role in the fasting induced D3 increase in the liver.