| 1. |
- Antonopoulou, Efthimia
(författare)
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Feedback control of reproduction in Atlantic salmon, Salmo salar, male parr
- 1998
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- In fish, as in other vertebrates, the gonads are stimulated by two pituitary gonadotropic hormones, follicle stimulating hormone (FSH) and luteinizing hormone (LH). LH and FSH secretion are regulated by the gonadal steroids acting either directly on the pituitary or indirectly via the hypothalamus. Both positive and negative gonadal feedback mechanisms are present in fishes. Plasma and pituitary LH and FSH levels are higher in Atlantic salmon parr males that have been sham-operated in spring than in castrated fish, when sampled in the periods of gonadal growth and breeding, indicated the existence of a physiological positive feedback involved in the control of LH and FSH secretion. However, for FSH also a physiological negative feedback controlling FSH secretion was found in the early phase of sexual maturation in early summer.The involvement of different steroids and the role of aromatization in feedback systems controlling reproduction has also been studied by administration of different androgens and aromatase inhibitors in vivo. Testosterone (T) stimulates LH by an aromatase-dependent positive feedback. Also 11-androgens exert a positive effect on LH, though weaker than T. FSH appears to be controlled both by a negative aromatase dependent feedback and a negative non-aromatase dependent T effect, as well as possibly a positive aromatase-dependent feedback. FSH is also controlled by both a negative and a positive feedback of 11-androgens. In addition, treatment with different aromatase inhibitors increased the proportion of fish maturing.Positive gonadal feedback eventually separate gonadotropic functions between rematuring high level and non-rematuring low level fish. However, FSH secretion appears not to be the only responsible factor for the onset of maturation in Atlantic salmon male parr, since immunoassayable plasma FSH levels are equally high in non-rematuring and rematuring fish during the onset of gonadal growth in early summer.The decline of androgens at the beginning of breeding season is not due to a suppressive action of elevated 17,20P at either the pituitary or testicular level in salmon.Moreover, administration of T at the end of spawning season diminished the postbreeding decline of 17,20P, testes weights, milt production and sperm motility, possibly via a positive feedback on LH secretion.
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| 2. |
- Eskilsson, Anna, et al.
(författare)
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Immune-Induced Fever Is Mediated by IL-6 Receptors on Brain Endothelial Cells Coupled to STAT3-Dependent Induction of Brain Endothelial Prostaglandin Synthesis
- 2014
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Ingår i: Journal of Neuroscience. - : Society for Neuroscience. - 0270-6474 .- 1529-2401. ; 34:48, s. 15957-15961
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Tidskriftsartikel (refereegranskat)abstract
- The cytokine IL-6, which is released upon peripheral immune challenge, is critical for the febrile response, but the mechanism by which IL-6 is pyrogenic has remained obscure. Herewegenerated mice with deletion of themembranebound IL-6 receptor alpha (IL-6R alpha) onneural cells, on peripheral nerves, on fine sensory afferent fibers, and on brain endothelial cells, respectively, and examined its role for the febrile response to peripherally injected lipopolysaccharide. We show that IL-6R alpha on neural cells, peripheral nerves, and fine sensory afferents are dispensable for the lipopolysaccharide-induced fever, whereas IL-6R alpha in the brain endothelium plays an important role. Hence deletion of IL-6R alpha on brain endothelial cells strongly attenuated the febrile response, and also led to reduced induction of the prostaglandin synthesizing enzyme Cox-2 in the hypothalamus, the temperature-regulating center in the brain, as well as reduced expression of SOCS3, suggesting involvement of the STAT signaling pathway. Furthermore, deletion of STAT3 in the brain endothelium also resulted in attenuated fever. These data show that IL-6, when endogenously released during systemic inflammation, is pyrogenic by binding to IL-6R alpha on brain endothelial cells to induce prostaglandin synthesis in these cells, probably in concerted action with other peripherally released cytokines.
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| 3. |
- Irachi, Shotaro, et al.
(författare)
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Photoperiodic regulation of pituitary thyroid-stimulating hormone and brain deiodinase in Atlantic salmon
- 2021
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Ingår i: Molecular and Cellular Endocrinology. - : Elsevier BV. - 0303-7207 .- 1872-8057. ; 519
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Tidskriftsartikel (refereegranskat)abstract
- © 2020 Seasonal timing is important for many critical life history events of vertebrates, and photoperiod is often used as a reliable seasonal cue. In mammals and birds, it has been established that a photoperiod-driven seasonal clock resides in the brain and pituitary, and is driven by increased levels of pituitary thyroid stimulating hormone (TSH) and brain type 2 iodothyronine deiodinase (DIO2), which leads to local increases in triiodothyronine (T3). In order to determine if a similar mechanism occurs in fish, we conducted photoperiod manipulations in anadromous (migratory) Atlantic salmon (Salmo salar) that use photoperiod to time the preparatory development of salinity tolerance which accompanies downstream migration in spring. Changing daylength from short days (light:dark (LD) 10:14) to long days (LD 16:8) for 20 days increased gill Na+/K+-ATPase (NKA) activity, gill NKAα1b abundance and plasma growth hormone (GH) levels that normally accompany increased salinity tolerance of salmon in spring. Long-day exposure resulted in five-fold increases in pituitary tshβb mRNA levels after 10 days and were sustained for at least 20 days. tshβb mRNA levels in the saccus vasculosus were low and not influenced by photoperiod. Increased daylength resulted in significant increases in dio2b mRNA levels in the hypothalamus and midbrain/optic tectum regions of the brain. The results are consistent with the presence of a photoperiod-driven seasonal clock in fish which involves pituitary TSH, brain DIO2 and the subsequent production of T3, supporting the hypothesis that this is a common feature of photoperiodic regulation of seasonality in vertebrates.
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| 4. |
- Luukkonen, Panu K., et al.
(författare)
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The PNPLA3 I148M variant increases ketogenesis and decreases hepatic de novo lipogenesis and mitochondrial function in humans
- 2023
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Ingår i: Cell Metabolism. - : Elsevier. - 1550-4131 .- 1932-7420. ; 35:11, s. 1887-1896.e5
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Tidskriftsartikel (refereegranskat)abstract
- The PNPLA3 I148M variant is the major genetic risk factor for all stages of fatty liver disease, but the underlying pathophysiology remains unclear. We studied the effect of this variant on hepatic metabolism in homozygous carriers and non-carriers under multiple physiological conditions with state-of-the-art stable isotope techniques. After an overnight fast, carriers had higher plasma b-hydroxybutyrate concentrations and lower hepatic de novo lipogenesis (DNL) compared to non-carriers. After a mixed meal, fatty acids were channeled toward ketogenesis in carriers, which was associated with an increase in hepatic mitochondrial redox state. During a ketogenic diet, carriers manifested increased rates of intrahepatic lipolysis, increased plasma b-hydroxybutyrate concentrations, and decreased rates of hepatic mitochondrial citrate synthase flux. These studies demonstrate that homozygous PNPLA3 I148M carriers have hepatic mitochondrial dysfunction leading to reduced DNL and channeling of carbons to ketogenesis. These findings have implications for understanding why the PNPLA3 variant predisposes to progressive liver disease.
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| 5. |
- Matsuwaki, Takashi, 1978-, et al.
(författare)
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Involvement of interleukin-1 type 1 receptors in lipopolysaccharide-induced sickness responses
- 2017
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Ingår i: Brain, behavior, and immunity. - : Elsevier. - 0889-1591 .- 1090-2139. ; 66, s. 165-176
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Tidskriftsartikel (refereegranskat)abstract
- Sickness responses to lipopolysaccharide (LPS) were examined in mice with deletion of the interleukin (IL)-1 type 1 receptor (IL-1R1). IL-1R1 knockout (1(0) mice displayed intact anorexia and HPA-axis activation to intraperitoneally injected LPS (anorexia: 10 or 120 mu g/kg; HPA-axis: 120 mu g/kg), but showed attenuated but not extinguished fever (120 g/kg). Brain PGE2 synthesis was attenuated, but Cox-2 induction remained intact. Neither the tumor necrosis factor-alpha (TNF alpha) inhibitor etanercept nor the IL -6 receptor antibody tocilizumab abolished the LPS induced fever in IL -1R1 KO mice. Deletion of IL -1R1 specifically in brain endothelial cells attenuated the LPS induced fever, but only during the late, 3rd phase of fever, whereas deletion of IL-1R1 on neural cells or on peripheral nerves had little or no effect on the febrile response. We conclude that while IL-1 signaling is not critical for LPS induced anorexia or stress hormone release, IL-1R1, expressed on brain endothelial cells, contributes to the febrile response to LPS. However, also in the absence of IL-1R1, LPS evokes a febrile response, although this is attenuated. This remaining fever seems not to be mediated by IL-6 receptors or TNFa, but by some yet unidentified pyrogenic factor.
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| 6. |
- Morini, Marina, et al.
(författare)
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Dynamic evolution of transient receptor potential vanilloid (TRPV) ion channel family with numerous gene duplications and losses
- 2022
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Ingår i: Frontiers in Endocrinology. - : Frontiers Media S.A.. - 1664-2392. ; 13
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Tidskriftsartikel (refereegranskat)abstract
- The transient receptor potential vanilloid (TRPV) ion channel family is involved in multiple sensory and physiological functions including thermosensing and temperature-dependent neuroendocrine regulation. The objective of the present study was to investigate the number, origin and evolution of TRPV genes in metazoans, with special focus on the impact of the vertebrate whole-genome duplications (WGD). Gene searches followed by phylogenetic and synteny analyses revealed multiple previously undescribed TRPV genes. The common ancestor of Cnidaria and Bilateria had three TRPV genes that became four in the deuterostome ancestor. Two of these were lost in the vertebrate ancestor. The remaining two genes gave rise to two TRPV subfamilies in vertebrates, consisting of subtypes 1, 2, 3, 4, 9 and 5, 6, 7, 8, respectively. This gene expansion resulted from the two basal vertebrate WGD events (1R and 2R) and three local duplications before the radiation of gnathostomes. TRPV1, 4 and 5 have been retained in all gnathostomes investigated, presumably reflecting important functions. TRPV7 and 8 have been lost independently in various lineages but are still retained in cyclostomes, actinistians (coelacanth), amphibians, prototherians and basal actinopterygians (Polypteridae). TRPV3 and 9 are present in extant elasmobranchs, while TRPV9 was lost in the osteichthyan ancestor and TRPV3 in the actinopterygian ancestor. The coelacanth has retained the ancestral osteichthyan repertoire of TRPV1, 3, 4, 5, 7 and 8. TRPV2 arose in the tetrapod ancestor. Duplications of TRPV5 occurred independently in various lineages, such as cyclostomes, chondrichthyans, anuran amphibians, sauropsids, mammals (where the duplicate is called TRPV6), and actinopterygians (Polypteridae and Esocidae). After the teleost-specific WGD (3R) only TRPV1 retained its duplicate, whereas TRPV4 and 5 remained as single genes. Both 3R-paralogs of TRPV1 were kept in some teleost species, while one paralog was lost in others. The salmonid-specific WGD (4R) duplicated TRPV1, 4, and 5 leading to six TRPV genes. The largest number was found in Xenopus tropicalis with no less than 15 TRPV genes. This study provides a comprehensive evolutionary scenario for the vertebrate TRPV family, revealing additional TRPV types and proposing a phylogeny-based classification of TRPV across metazoans.
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| 7. |
- Rogoz, Katarzyna, et al.
(författare)
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VGLUT2-dependent glutamatergic transmission in primary afferents is required for intact nociception in both acute and persistent pain modalities
- 2012
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Ingår i: Pain. - : Ovid Technologies (Wolters Kluwer Health). - 0304-3959 .- 1872-6623. ; 153:7, s. 1525-1536
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Tidskriftsartikel (refereegranskat)abstract
- Glutamate is an essential transmitter in pain pathways. However, its broad usage in the central and peripheral nervous system prevents us from designing efficient glutamate-based pain therapies without causing harmful side effects. The discovery of vesicular glutamate transporters (VGLUT1-3) has been a crucial step in describing specific glutamatergic neuronal subpopulations and glutamate-dependent pain pathways. To assess the role of VGLUT2-mediated glutamatergic contribution to pain transmission from the entire primary sensory population, we crossed our Vglut2(f/f) line with the Ht-Pa-Cre line. Such Vglut2-deficient mice showed significantly decreased, but not completely absent, acute nociceptive responses. The animals were less prone to develop an inflammatory-related state of pain and were, in the partial sciatic nerve ligation chronic pain model, much less hypersensitive to mechanical stimuli and did not develop cold allodynia or heat hyperalgesia. To take advantage of this neuropathic pain-resistant model, we analyzed Vglut2-dependent transcriptional changes in the dorsal spinal cord after nerve injury, which revealed several novel candidate target genes potentially relevant for the development of neuropathic pain therapeutics. Taken together, we conclude that VGLUT2 is a major mediator of nociception in primary afferents, implying that glutamate is the key somatosensory neurotransmitter.
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| 8. |
- Schmitz, Monika, et al.
(författare)
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Silvering: Metamorphosis or Puberty?
- 2009
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Ingår i: Spawning migration of the European eel. - Dordrecht : Springer. - 1402090943
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Bokkapitel (refereegranskat)
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| 9. |
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| 10. |
- Trombley, Susanne, 1979-
(författare)
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Regulation of Leptin by Sexual Maturation and Energy Status in Male Atlantic Salmon (Salmo salar L.) Parr
- 2014
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Leptin is a peripheral adiposity signal and a key hormone in energy balance regulation in mammals, acting as a link between nutritional status and the endocrine reproductive axis. If this is also the role of leptin in fish is not fully understood. This thesis investigates how different components of the leptin system are affected by sexual maturation and seasonal changes in energy balance in male Atlantic salmon (Salmo salar L.) parr under fully fed and feed-restricted conditions. Moreover, the role of sex steroids as being one of the possible mechanisms by which sexual maturation interacts with leptin is explored.The salmon leptin-a genes, lepa1 and lepa2, were expressed mainly in liver and the leptin receptor (lepr) in brain and ubiquitously in peripheral tissues. Seasonal characterization of the lepa genes and lepr during the growth and reproductive season in one-year old males showed that hepatic lepa1 and lepa2 mRNA levels and plasma leptin levels were down-regulated concomitantly with an increase in weight and body fat. Feed restriction up-regulated hepatic leptin, and pituitary lepr expression as well as plasma leptin levels. Correlation between leptin levels and body lipid stores were either lacking or negative. These findings show that leptin and lepr are sensitive to changes in energy balance, but that leptin might not reflect adiposity in juvenile salmon.Hepatic lepa1 and lepa2, and testicular lepr expression increased during mid- to late spermatogenesis in early maturing males. This up-regulation was preceded by rapid gonadal growth and elevated pituitary follicle-stimulating hormone gene expression levels, whereas peak leptin levels coincided with peak pituitary luteinizing hormone expression and the presence of running milt in the testes. The sex steroids testosterone (T), 11-ketotestosterone and 17-β estradiol stimulated lepa1 and lepa2 gene expression in Atlantic salmon hepatocytes in vitro differentially depending on developmental stage. T was also able to stimulate hepatic lepa1 and pituitary lepa1 and lepr gene expression in immature male salmon in vivo. These results suggest that leptin plays a role in male fish reproduction during later stages of the maturational process and that the elevation of leptin expression during spermatogenesis could be caused by androgen stimulation.
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