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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 hindbrain of rainbow trout.Further details as in legend of Fig 3.
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pone.0128603.g006: Activities of CPT-1 (A) and HOAD (D), and mRNA abundance of CPT1c (B), CPT1d (C), HOAD (E), COX4 (F), and UCP2a (G) in hindbrain of rainbow trout.Further details as in legend of Fig 3.

Mentions: The parameters associated with mitochondrial activity in hindbrain are shown in Fig 6. CPT-1 activity (Fig 6A) in normo-glycaemic fish was lower than that of hypo-glycaemic fish under HSD conditions whereas no changes were noted for fish under NSD. The mRNA abundance of CPT1c (Fig 6B) of hypo-glycaemic fish was higher than in the other two glycaemic conditions for fish under HSD while no changes occurred under NSD. The mRNA abundance of HOAD (Fig 6E) was lower in hyper-glycaemic than in normo-glycaemic fish under NSD conditions; no changes were noted under HSD. The mRNA abundance of UCP2a (Fig 6G) was higher in normo-glycaemic fish than in the other two conditions in fish under NSD whereas in fish under HSD the value was higher than that of hyper-glycaemic fish. Finally, no significant changes were noted for mRNA abundance of CPT1d (Fig 6C), HOAD activity (Fig 6D), and mRNA abundance of COX4 (Fig 6F).


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 hindbrain 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.g006: Activities of CPT-1 (A) and HOAD (D), and mRNA abundance of CPT1c (B), CPT1d (C), HOAD (E), COX4 (F), and UCP2a (G) in hindbrain of rainbow trout.Further details as in legend of Fig 3.
Mentions: The parameters associated with mitochondrial activity in hindbrain are shown in Fig 6. CPT-1 activity (Fig 6A) in normo-glycaemic fish was lower than that of hypo-glycaemic fish under HSD conditions whereas no changes were noted for fish under NSD. The mRNA abundance of CPT1c (Fig 6B) of hypo-glycaemic fish was higher than in the other two glycaemic conditions for fish under HSD while no changes occurred under NSD. The mRNA abundance of HOAD (Fig 6E) was lower in hyper-glycaemic than in normo-glycaemic fish under NSD conditions; no changes were noted under HSD. The mRNA abundance of UCP2a (Fig 6G) was higher in normo-glycaemic fish than in the other two conditions in fish under NSD whereas in fish under HSD the value was higher than that of hyper-glycaemic fish. Finally, no significant changes were noted for mRNA abundance of CPT1d (Fig 6C), HOAD activity (Fig 6D), and mRNA abundance of COX4 (Fig 6F).

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.