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- Isaksson, B, et al.
(författare)
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Chronically administered islet amyloid polypeptide in rats serves as an adiposity inhibitor and regulates energy homeostasis
- 2005
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Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 5:1, s. 29-36
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Tidskriftsartikel (refereegranskat)abstract
- Aims/Hypothesis: Islet amyloid polypeptide ( IAPP) reduces food intake and body weight in laboratory animals. In addition, IAPP appears to regulate nutrient metabolism. In the present studies, we investigated the effect of chronic IAPP treatment on different aspects of energy homeostasis. Methods: IAPP was infused ( 25 pmol/kg/min) from subcutaneous osmotic pumps for 2 - 7 days. Rats in 2 saline-infused control groups were fed ad libitum (AF) or pair-fed (PF) against the IAPP-treated rats. Results: As expected, the IAPP infusion reduced food intake and body weight gain. In addition, the IAPP treatment decreased the epididymal fat pad ( vs. PF rats, p < 0.05) and lowered circulating levels of triglycerides (vs. PF rats, p < 0.05), free fatty acids ( vs. PF rats, p < 0.05), leptin ( vs. both AF and PF rats, p < 0.05) and insulin ( vs. AF rats, p < 0.05). In contrast, glucose and protein metabolism in the IAPP-treated rats was largely unchanged, as shown in results regarding serum glucose, glucose transport in skeletal muscle, blood urea nitrogen, and glycogen and protein content in the liver and in skeletal muscle. Conclusion/Interpretation: In summary, chronic IAPP exposure led to a changed lipid metabolism, which was characterized by decreased adiposity, hypolipidemia and hypoleptinemia, and to unchanged glucose and protein homeostasis. These results were similar to those seen in rodents during chronic exposure to another satiety/adiposity regulator, leptin. In conclusion, chronically administered IAPP plays a role as a satiety and adiposity signal in rats, and helps regulate energy homeostasis.
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| 2. |
- Kroos, G., et al.
(författare)
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Gene expression of angiogenic factors in muscle tissue during age-related development of hypertension in spontaneously hypertensive rats
- 2008
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Ingår i: Abstracts 25th Conference of the European Society for Microcirculation. - Basel : S. Karger. - 9783805586368 ; , s. 120-120
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Konferensbidrag (refereegranskat)abstract
- Essential hypertension has been associated with capillary rarefaction but little is known about the cellular mechanisms underlying this process. We examined the gene expression of angiogenic factors during age-related development of hypertension in spontaneously hypertensive rats (SHR). Wild-type Wistar Kyoto (WKY) rats served as controls. White gastrocnemius muscle was obtained and blood pressure was monitored at 5, 10 and 15 weeks of age. In the SHR group, systolic blood pressure increased from 5 to 10 and 15 weeks of age and the levels were higher than in the WKY group at 10 and 15 weeks (~70%; P<0.05). The mRNA content for MMP-2 was overall lower (P<0.05) in SHR compared to WKY. VEGFmRNA increased (p<0.05) from 5 to 10 weeks in SHR and there was a general increase (P<0.05) in the VEGF receptor flt-1. There was a trend for a lower content of eNOS and CYP 2C11 in the SHR than in WKY group. There were no alterations in the mRNA content of KDR, AMP 5'- nucleotidase, or Cytochrome P450 4A. The results show that the age-related development of hypertension from 5 to 15 weeks in SHR rats is not associated with major changes in mRNA content of the herein included angiogenic factors.
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| 3. |
- Marx, James O, et al.
(författare)
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Scaling of skeletal muscle shortening velocity in mammals representing a 100,000-fold difference in body size
- 2006
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Ingår i: Pflügers Archiv. - Heidelberg : Springer. - 0031-6768 .- 1432-2013. ; 452:2, s. 222-230:452, s. 222-230
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Tidskriftsartikel (refereegranskat)abstract
- To fully understand the effect of scaling on skeletal muscle shortening velocity (V 0), it is important to know which phenotypic characteristics drive the changes between species. The purpose of the current investigation was to compare the effects of body mass and femur length, as an estimate of total limb length, on V 0 in species that cover a 100,000-fold range of body masses. Using the slack test procedure, V 0 was determined for fibers expressing types I and IIa myosin heavy chain (MyHC) isoforms in the mouse, rat, dog, human, horse, and rhinoceros under identical experimental conditions. A significant scaling effect on V 0 was detected when compared to body mass (type I fibers, r=0.95, p<0.01; type IIa fibers, r=0.83, p<0.05). However, the horse's V 0 for both fiber types was faster than the human's, despite having a 5-fold greater body mass than the human. When V 0 was scaled vs limb length, the strength of the relationships improved in fibers expressing both types I and IIa MyHC (r=0.98, p<0.001, and r=0.89, p<0.05, respectively) and scaled with the expected relationship, with the species with the shorter femur, the horse, having the faster V 0. A similar effect can be seen with stride frequency scaling more closely with limb length than body mass. These results suggest that limb length, not body mass, is a more relevant factor driving the scaling effect on skeletal muscle shortening velocity.
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