We present a comprehensive statistical analysis of Swift X-ray light-curves of Gamma- Ray Bursts (GRBs) collecting data from more than 650 GRBs discovered by Swift and other facilities. The ...unprecedented sample size allows us to constrain the rest-frame X-ray properties of GRBs from a statistical perspective, with particular reference to intrinsic time scales and the energetics of the different light-curve phases in a common rest-frame 0.3-30 keV energy band. Temporal variability episodes are also studied and their properties constrained. Two fundamental questions drive this effort: i) Does the X-ray emission retain any kind of "memory" of the prompt γ-ray phase? ii) Where is the dividing line between long and short GRB X-ray properties? We show that short GRBs decay faster, are less luminous and less energetic than long GRBs in the X-rays, but are interestingly characterized by similar intrinsic absorption. We furthermore reveal the existence of a number of statistically significant relations that link the X-ray to prompt γ-ray parameters in long GRBs; short GRBs are outliers of the majority of these 2-parameter relations. However and more importantly, we report on the existence of a universal 3-parameter scaling that links the X-ray and the γ-ray energy to the prompt spectral peak energy of both long and short GRBs: E(sub X,iso)∝ E(sup 1.00+/-0.06)(sub γ,iso) /E(sup 0.60+/-0.10)(sub pk).
Stearoyl-CoA desaturase (SCD)1 converts saturated fatty acids into monounsaturated fatty acids. Using muscle overexpression, we sought to determine the role of SCD1 expression in glucose and lipid ...metabolism and its effects on exercise capacity in mice. Wild-type C57Bl/6 (WT) and SCD1 muscle transgenic (SCD1-Tg) mice were generated, and expression of the SCD1 transgene was restricted to skeletal muscle. SCD1 overexpression was associated with increased triglyceride (TG) content. The fatty acid composition of the muscle revealed a significant increase in polyunsaturated fatty acid (PUFA) content of TG, including linoleate (18:2n6). Untrained SCD1-Tg mice also displayed significantly increased treadmill exercise capacity (WT = 6.6 ± 3 min, Tg = 71.9 ± 9.5 min; P= 0.0009). SCD1-Tg mice had decreased fasting plasma glucose, glucose transporter (GLUT)1 mRNA, fatty acid oxidation, mitochondrial content, and increased peroxisome proliferator-activated receptor (PPAR)Δ and Pgc-1 protein expression in skeletal muscle. In vitro studies in C2C12 myocytes revealed that linoleate (18:2n6) and not oleate (18:1n9) caused a 3-fold increase in PPARΔ and a 9-fold increase in CPT-1b with a subsequent increase in fat oxidation. The present model suggests that increasing delta-9 desaturase activity of muscle increases metabolic function, exercise capacity, and lipid oxidation likely through increased PUFA content, which increases PPARΔ expression and activity. However, the mechanism of action that results in increased PUFA content of SCD1-Tg mice remains to be elucidated.
Background: Carbohydrate response element binding protein alpha (ChREBPα) is a transcription factor involved in carbohydrate (CHO) induced de novo lipogenesis. Recently, a novel isoform (ChREBPβ) has ...been discovered and the purpose of this study was to determine the effect of 1) obesity, and 2) different CHO on ChREBPβ induction and transcriptional activity.
Methods: For the effect of obesity, mice were fed a high‐fat diet for 12 weeks after which liver mRNA and protein expression of ChREBPα and –β were assessed. To determine the effect of dietary CHO on ChREBPα and –β, mice were fasted for 24 hours and refed a high glucose, sucrose, or fructose diet for 12 hours. Tissues were collected to assess changes in lipogenic induction as well as ChREBPα and ChREBPβ. HEK293 cells were transfected with either ChREBPα or ‐β and treated with either 25mM glucose or fructose for 24 hours and differences in lipogenic activity.
Results: ChREBPα mRNA was not affected by obesity, however ChREBPβ mRNA was 3.8±0.6 fold higher than chow‐fed mice. Unexpectedly, ChREBPα decreased after all three CHO diets whereas ChREBPβ increased in all tissues assessed except muscle. In liver, sucrose refeeding caused the largest increase in ChREBPβ expression followed by fructose, then glucose (24.4±11.1, 17.8±9.5, and 10.1±3.2). In HEK cells, ChREBPβ expression was also associated with glucose‐induced lipogenic gene expression and not ChREBPα.
Conclusions: ChREBPα and ChREBPb can be detected separately and their induction is detectible in the liver and other peripheral tissues of carbohydrate re‐fed mice. ChREBPβ expression appears to be responsible for carbohydrate‐induced lipogenic gene induction whereas ChREBPα is likely responsible for inducing ChREBPβ.
Grant Funding Source: Supported by Aniara Research Grant
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