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Evidence for the Presence of Glucosensor Mechanisms Not Dependent on Glucokinase in Hypothalamus and Hindbrain of Rainbow Trout (Oncorhynchus mykiss).

Otero-Rodiño C, Librán-Pérez M, Velasco C, López-Patiño MA, Míguez JM, Soengas JL - PLoS ONE (2015)

Bottom Line: Half of tanks were kept at a 10 Kg fish mass x m(-3) and denoted as fish under normal stocking density (NSD) whereas the remaining tanks were kept at a stressful high stocking density (70 kg fish mass x m(-3)) denoted as HSD.The results obtained in non-stressed rainbow trout provide evidence, for the first time in fish, that manipulation of glucose levels induce changes in parameters which could be related to putative glucosensor systems based on LXR, mitochondrial activity and sweet taste receptor in hypothalamus, and a system based on SGLT-1 in hindbrain.Stress altered the response of parameters related to these systems to changes in glycaemia.

View Article: PubMed Central - PubMed

Affiliation: Laboratorio de Fisioloxía Animal, Departamento de Bioloxía Funcional e Ciencias da Saúde, Facultade de Bioloxía, Universidade de Vigo, Vigo, Spain.

ABSTRACT
We hypothesize that glucosensor mechanisms other than that mediated by glucokinase (GK) operate in hypothalamus and hindbrain of the carnivorous fish species rainbow trout and stress affected them. Therefore, we evaluated in these areas changes in parameters which could be related to putative glucosensor mechanisms based on liver X receptor (LXR), mitochondrial activity, sweet taste receptor, and sodium/glucose co-transporter 1 (SGLT-1) 6 h after intraperitoneal injection of 5 mL x Kg(-1) of saline solution alone (normoglycaemic treatment) or containing insulin (hypoglycaemic treatment, 4 mg bovine insulin x Kg(-1) body mass), or D-glucose (hyperglycaemic treatment, 500 mg x Kg(-1) body mass). Half of tanks were kept at a 10 Kg fish mass x m(-3) and denoted as fish under normal stocking density (NSD) whereas the remaining tanks were kept at a stressful high stocking density (70 kg fish mass x m(-3)) denoted as HSD. The results obtained in non-stressed rainbow trout provide evidence, for the first time in fish, that manipulation of glucose levels induce changes in parameters which could be related to putative glucosensor systems based on LXR, mitochondrial activity and sweet taste receptor in hypothalamus, and a system based on SGLT-1 in hindbrain. Stress altered the response of parameters related to these systems to changes in glycaemia.

No MeSH data available.


Activities of CPT-1 (A) and HOAD (D), and mRNA abundance of CPT1c (B), CPT1d (C), HOAD (E), COX4 (F), and UCP2a (G) in hypothalamus of rainbow trout.Further details as in legend of Fig 3.
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pone.0128603.g005: Activities of CPT-1 (A) and HOAD (D), and mRNA abundance of CPT1c (B), CPT1d (C), HOAD (E), COX4 (F), and UCP2a (G) in hypothalamus of rainbow trout.Further details as in legend of Fig 3.

Mentions: The parameters associated with mitochondrial activity in hypothalamus are shown in Fig 5. CPT-1 activity (Fig 5A) increased in parallel with glycaemia in fish under NSD but no changes were noted in fish under HSD. The mRNA abundance of CPT1c (Fig 5B) in fish under NSD was higher in hyper-glycaemic than in normo-glycaemic fish whereas no changes were noted in fish under HSD. The mRNA abundance of CPT1d (Fig 5C) decreased with the increase in glycaemia in fish under HSD whereas no changes were noted for fish under NSD. HOAD activity (Fig 5D) increased in parallel with the increase in glycaemia in fish under NSD whereas in fish under HSD the value of normo-glycaemic fish was lower than in the other two glycaemic conditions. The mRNA abundance of HOAD (Fig 5E) in hyper-glycaemic fish was lower than that of normo-glycaemic fish under NSD conditions whereas in fish under HSD the value of normo-glycaemic fish was higher than in the other two glycaemic conditions. The mRNA abundance of COX4 (Fig 5F) decreased in parallel with the increase in glycaemia both under NSD and HSD conditions. Finally, the mRNA abundance of UCP2a decreased in parallel with the increase in glycaemia in fish under HSD while no changes were noted in fish under NSD.


Evidence for the Presence of Glucosensor Mechanisms Not Dependent on Glucokinase in Hypothalamus and Hindbrain of Rainbow Trout (Oncorhynchus mykiss).

Otero-Rodiño C, Librán-Pérez M, Velasco C, López-Patiño MA, Míguez JM, Soengas JL - PLoS ONE (2015)

Activities of CPT-1 (A) and HOAD (D), and mRNA abundance of CPT1c (B), CPT1d (C), HOAD (E), COX4 (F), and UCP2a (G) in hypothalamus of rainbow trout.Further details as in legend of Fig 3.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4440750&req=5

pone.0128603.g005: Activities of CPT-1 (A) and HOAD (D), and mRNA abundance of CPT1c (B), CPT1d (C), HOAD (E), COX4 (F), and UCP2a (G) in hypothalamus of rainbow trout.Further details as in legend of Fig 3.
Mentions: The parameters associated with mitochondrial activity in hypothalamus are shown in Fig 5. CPT-1 activity (Fig 5A) increased in parallel with glycaemia in fish under NSD but no changes were noted in fish under HSD. The mRNA abundance of CPT1c (Fig 5B) in fish under NSD was higher in hyper-glycaemic than in normo-glycaemic fish whereas no changes were noted in fish under HSD. The mRNA abundance of CPT1d (Fig 5C) decreased with the increase in glycaemia in fish under HSD whereas no changes were noted for fish under NSD. HOAD activity (Fig 5D) increased in parallel with the increase in glycaemia in fish under NSD whereas in fish under HSD the value of normo-glycaemic fish was lower than in the other two glycaemic conditions. The mRNA abundance of HOAD (Fig 5E) in hyper-glycaemic fish was lower than that of normo-glycaemic fish under NSD conditions whereas in fish under HSD the value of normo-glycaemic fish was higher than in the other two glycaemic conditions. The mRNA abundance of COX4 (Fig 5F) decreased in parallel with the increase in glycaemia both under NSD and HSD conditions. Finally, the mRNA abundance of UCP2a decreased in parallel with the increase in glycaemia in fish under HSD while no changes were noted in fish under NSD.

Bottom Line: Half of tanks were kept at a 10 Kg fish mass x m(-3) and denoted as fish under normal stocking density (NSD) whereas the remaining tanks were kept at a stressful high stocking density (70 kg fish mass x m(-3)) denoted as HSD.The results obtained in non-stressed rainbow trout provide evidence, for the first time in fish, that manipulation of glucose levels induce changes in parameters which could be related to putative glucosensor systems based on LXR, mitochondrial activity and sweet taste receptor in hypothalamus, and a system based on SGLT-1 in hindbrain.Stress altered the response of parameters related to these systems to changes in glycaemia.

View Article: PubMed Central - PubMed

Affiliation: Laboratorio de Fisioloxía Animal, Departamento de Bioloxía Funcional e Ciencias da Saúde, Facultade de Bioloxía, Universidade de Vigo, Vigo, Spain.

ABSTRACT
We hypothesize that glucosensor mechanisms other than that mediated by glucokinase (GK) operate in hypothalamus and hindbrain of the carnivorous fish species rainbow trout and stress affected them. Therefore, we evaluated in these areas changes in parameters which could be related to putative glucosensor mechanisms based on liver X receptor (LXR), mitochondrial activity, sweet taste receptor, and sodium/glucose co-transporter 1 (SGLT-1) 6 h after intraperitoneal injection of 5 mL x Kg(-1) of saline solution alone (normoglycaemic treatment) or containing insulin (hypoglycaemic treatment, 4 mg bovine insulin x Kg(-1) body mass), or D-glucose (hyperglycaemic treatment, 500 mg x Kg(-1) body mass). Half of tanks were kept at a 10 Kg fish mass x m(-3) and denoted as fish under normal stocking density (NSD) whereas the remaining tanks were kept at a stressful high stocking density (70 kg fish mass x m(-3)) denoted as HSD. The results obtained in non-stressed rainbow trout provide evidence, for the first time in fish, that manipulation of glucose levels induce changes in parameters which could be related to putative glucosensor systems based on LXR, mitochondrial activity and sweet taste receptor in hypothalamus, and a system based on SGLT-1 in hindbrain. Stress altered the response of parameters related to these systems to changes in glycaemia.

No MeSH data available.