scholarly journals Functional Characterization of Facilitative Glucose Transporter 4 With a Delay Responding to Plasma Glucose Level in Blunt Snout Bream (Megalobrama amblycephala)

2020 ◽  
Vol 11 ◽  
Author(s):  
Hualiang Liang ◽  
Sahya Maulu ◽  
Ke Ji ◽  
Xianping Ge ◽  
Mingchun Ren ◽  
...  
Keyword(s):  
Glucose Level ◽  
Plasma Glucose ◽  
Plasma Glucose Level ◽  
Glucose Transporter ◽  
Functional Characterization ◽  
Megalobrama Amblycephala ◽  
Glucose Transporter 4 ◽  
Blunt Snout Bream ◽  
Facilitative Glucose Transporter

The role of glucose uptake and metabolism in hyperglycemic exacerbation of neurological deficit in the paraplegic rat

1989 ◽  
Vol 71 (4) ◽  
pp. 594-600 ◽  
Author(s):  
Daniel R. LeMay ◽  
Gerald B. Zelenock ◽  
Louis G. D'Alecy
Keyword(s):  
Lower Extremity ◽  
Glucose Uptake ◽  
Glucose Level ◽  
Plasma Glucose ◽  
Neurological Deficit ◽  
Neurological Outcome ◽  
Plasma Glucose Level ◽  
Glucose Transporter ◽  
Neurological Deficits ◽  
Sprague Dawley

✓ Previous studies indicate that hyperglycemia, particularly that induced by exogenous glucose administration, exacerbates neurological deficits in the rat spinal cord ischemic model. The effect of inhibition of glucose uptake (glucose transporter) and initial metabolism (hexokinase) on neurological outcome was evaluated in the present investigation using the competitive inhibitors 2-deoxyglucose (2-DG) and 3-O-methylglucose (3-OMG). Sprague-Dawley rats, weighing 200 to 300 gm each, received either 0.25, 1, or 2 gm/kg 2-DG; 2 gm/kg 3-OMG; 2 gm/kg glucose; or an equivalent volume of 0.9% saline intraperitoneally. Rats were intubated and ventilated with 1% to 1.5% halothane. The aortic arch was exposed and snares were placed on the right and left subclavian arteries and the aorta distal to the left subclavian artery. The three vessels were occluded for 10, 11, 12, or 13 minutes. Lower-extremity neurological deficits were evaluated at 1, 4, 18, and 24 hours postocclusion based on a 15-point scale (normal = 0, severe deficit =15). Lower-extremity neurological deficits were significantly less severe in the groups treated with 2-DG (0.25 and 1 gm/kg) at 18 and 24 hours postocclusion (p < 0.05 for 0.25 gm/kg and p < 0.005 for 1 gm/kg, Student's t-test with Bonferroni correction). The lower 2-DG dose of 0.25 gm/kg did not significantly increase the plasma glucose level, suggesting that the glucose transporter was not markedly inhibited, and that the improved neurological outcome was more likely due to inhibition of hexokinase. The higher 2-DG dose of 1 gm/kg afforded protection despite significantly increasing the plasma glucose level, implying a strong inhibition of both the glucose transporter and hexokinase. Administration of 3-OMG, which only inhibits glucose uptake and not hexokinase, actually worsened the neurological deficit in a manner similar to that observed in rats treated with glucose. The authors conclude that the activity of the glucose transporter by itself does not significantly contribute to hyperglycemic exacerbation of neurological deficits. In contrast, the hexokinase step, at least in combination with the transporter and possibly alone, plays a significant role in hyperglycemic exacerbation of the lower-extremity neurological deficit in the paraplegic rat.

Validity of the operational equation of the 14C-deoxyglucose method modified for changing arterial plasma glucose level.

1987 ◽  
Vol 36 (2) ◽  
pp. 217-222
Author(s):  
Kortaro Tanaka ◽  
Fumio Gotoh ◽  
Shintaro Gomi ◽  
Shutaro Takashima ◽  
Ban Mihara
Keyword(s):  
Glucose Level ◽  
Plasma Glucose ◽  
Plasma Glucose Level ◽  
Operational Equation ◽  
Arterial Plasma ◽  
Deoxyglucose Method

scholarly journals Molecular Characterization of PGC-1β (PPAR Gamma Coactivator 1β) and its Roles in Mitochondrial Biogenesis in Blunt Snout Bream (Megalobrama amblycephala)

2020 ◽  
Vol 21 (6) ◽  
pp. 1935 ◽  
Author(s):  
Kangle Lu ◽  
Tomas Policar ◽  
Xiaojun Song ◽  
Samad Rahimnejad
Keyword(s):  
Molecular Characterization ◽  
Mitochondrial Biogenesis ◽  
Phylogenetic Analyses ◽  
Ppar Gamma ◽  
Megalobrama Amblycephala ◽  
Fat Intake ◽  
High Fat ◽  
Blunt Snout Bream ◽  
Mitochondria Biogenesis

This study aimed at achieving the molecular characterization of peroxisome proliferator-activated receptor-gamma coactivator 1β (PGC-1β) and exploring its modulatory roles in mitochondria biogenesis in blunt snout bream (Megalobrama amblycephala). A full-length cDNA of PGC-1β was cloned from liver which covered 3110 bp encoding 859 amino acids. The conserved motifs of PGC-1β family proteins were gained by MEME software, and the phylogenetic analyses showed motif loss and rearrangement of PGC-1β in fish. The function of PGC-1β was evaluated through overexpression and knockdown of PGC-1β in primary hepatocytes of blunt snout bream. We observed overexpression of PGC-1β along with enhanced mitochondrial transcription factor A (TFAM) expression and mtDNA copies in hepatocytes, and its knockdown led to slightly reduced NRF1 expression. However, knockdown of PGC-1β did not significantly influence TFAM expression or mtDNA copies. The alterations in mitochondria biogenesis were assessed following high-fat intake, and the results showed that it induces downregulation of PGC-1β. Furthermore, significant decreases in mitochondrial respiratory chain activities and mitochondria biogenesis were observed by high-fat intake. Our findings demonstrated that overexpression of PGC-1β induces the enhancement of TFAM expression and mtDNA amount but not NRF-1. Therefore, it could be concluded that PGC-1β is involved in mitochondrial biogenesis in blunt snout bream but not through PGC-1β/NRF-1 pathway.

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