| 1. |
|
|
| 2. |
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
|
|
| 7. |
- Abbott, Michael C., et al.
(författare)
-
Dyonic Giant Magnons in CP3 : Strings and Curves at Finite J
- 2009
-
Ingår i: Physical Review D. Particles and fields. - 0556-2821 .- 1089-4918. ; 80:2, s. 026005-
-
Tidskriftsartikel (refereegranskat)abstract
- This paper studies giant magnons in AdS4×CP3 using both the string sigma model and the algebraic curve. We complete the dictionary of solutions by finding the dyonic generalization of the CP1string solution, which matches the “small” giant magnon in the algebraic curve, and by pointing out that the solution recently constructed by the dressing method is the “big” giant magnon. We then use the curve to compute finite-J corrections to all cases, which for the nondyonic cases always match the Arutyunov-Frolov-Zamaklar result. For the dyonic RP3 magnon we recover the S5answer, but for the small and big giant magnons we obtain new corrections.
|
|
| 8. |
|
|
| 9. |
- Bohlooly-Yeganeh, Mohammad, 1966, et al.
(författare)
-
Growth hormone overexpression in the central nervous system results in hyperphagia-induced obesity associated with insulin resistance and dyslipidemia.
- 2005
-
Ingår i: Diabetes. - 0012-1797 .- 1939-327X. ; 54:1, s. 51-62
-
Tidskriftsartikel (refereegranskat)abstract
- It is well known that peripherally administered growth hormone (GH) results in decreased body fat mass. However, GH-deficient patients increase their food intake when substituted with GH, suggesting that GH also has an appetite stimulating effect. Transgenic mice with an overexpression of bovine GH in the central nervous system (CNS) were created to investigate the role of GH in CNS. This study shows that overexpression of GH in the CNS differentiates the effect of GH on body fat mass from that on appetite. The transgenic mice were not GH-deficient but were obese and showed increased food intake as well as increased hypothalamic expression of agouti-related protein and neuropeptide Y. GH also had an acute effect on food intake following intracerebroventricular injection of C57BL/6 mice. The transgenic mice were severely hyperinsulinemic and showed a marked hyperplasia of the islets of Langerhans. In addition, the transgenic mice displayed alterations in serum lipid and lipoprotein levels and hepatic gene expression. In conclusion, GH overexpression in the CNS results in hyperphagia-induced obesity indicating a dual effect of GH with a central stimulation of appetite and a peripheral lipolytic effect.
|
|
| 10. |
- de la Cour, Charlotta, et al.
(författare)
-
Ghrelin treatment reverses the reduction in weight gain and body fat in gastrectomised mice.
- 2005
-
Ingår i: Gut. - : BMJ. - 0017-5749 .- 1468-3288. ; 54:7, s. 907-13
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND AIMS: The gastric hormone ghrelin has been reported to stimulate food intake, increase weight gain, and cause obesity but its precise physiological role remains unclear. We investigated the long term effects of gastrectomy evoked ghrelin deficiency and of daily ghrelin injections on daily food intake, body weight, fat mass, lean body mass, and bone mass in mice. METHODS: Ghrelin was given by subcutaneous injections (12 nmol/mouse once daily) for eight weeks to young female mice subjected to gastrectomy or sham operation one week previously. RESULTS: Gastrectomy reduced plasma concentrations of total ghrelin (octanoylated and des-octanoylated) and active (octanoylated) ghrelin by approximately 80%. Immediately after injection of ghrelin, the plasma concentration was supraphysiological and was still elevated 16 hours later. Daily food intake was not affected by either gastrectomy or ghrelin treatment. The effect of ghrelin on meal initiation was not studied. At the end point of the study, mean body weight was 15% lower in gastrectomised mice than in sham operated mice (p<0.001); daily ghrelin injections for eight weeks partially prevented this weight loss. In sham operated mice, ghrelin had no effect on body weight. The weight of fat was reduced in gastrectomised mice (-30%; p<0.01). This effect was reversed by ghrelin, enhancing the weight of fat in sham operated mice also (+20%; p<0.05). Gastrectomy reduced lean body mass (-10%; p<0.01) and bone mass (-20%; p<0.001) compared with sham operated mice. Ghrelin replacement prevented the gastrectomy induced decrease in lean body mass but did not affect bone. In sham operated mice, ghrelin affected neither of these two parameters. CONCLUSIONS: Ghrelin replacement partially reversed the gastrectomy induced reduction in body weight, lean body mass, and body fat but not in bone mass. In sham operated mice, ghrelin only increased fat mass. Our results suggest that ghrelin is mainly concerned with the control of fat metabolism and that ghrelin replacement therapy may alleviate the weight loss associated with gastrectomy.
|
|
