Glucose utilization and glucose transporter proteins GLUT-1 and GLUT-3 in brains of diabetic (db/db) mice

Susan J. Vannucci, E. Michael Gibbs, Ian A. Simpson

Research output: Contribution to journalArticle

78 Citations (Scopus)

Abstract

This study describes the effects of diabetes on brain growth, cerebral glucose utilization (CGU), and the glucose transporter proteins GLUT-1 and GLUT-3 in the genetically diabetic db/db mouse. Mice were studied at 5 and 10 wk of age and compared with age-matched nondiabetic littermates. At 5 wk, db/db mice were not yet hyperglycemic, but their body weights were 27.5% greater than those of their nondiabetic littermates. By 10 wk, db/db mice were both hyperglycemic (blood glucose values of 39.3 ± 4.3 vs. 12.1 ± 2.1 mmol/l for db/db and control, respectively) and obese, with a twofold increase in body weight. Significant reductions in brain weight were observed at 5 wk (15% decrease in brain wet wt), and no further brain growth was observed, such that by 10 wk, brains of db/db mice were 25% smaller than those of control mice; brain wet weight-to-dry weight ratios were slightly reduced. Global rates of CGU, as determined with 2-[14C]deoxyglucose, were significantly reduced in the 10-wk diabetic mice. Levels of brain glucose and brain-to-blood glucose ratios were increased in 5- and 10-wk db/db mice, reflecting adequate glucose delivery to the brain. Blood-brain barrier GLUT- 1 levels were unchanged, and mRNA levels were regionally increased. The expression of the neuronal glucose transporter GLUT-3 was not reduced to a significant extent in brains of db/db mice. The results of this study indicate that the db/db mouse has markedly decelerated brain growth accompanied by global reductions in glucose metabolism that are not due to reductions in glucose transport capacity.

Original languageEnglish (US)
Pages (from-to)E267-E274
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume272
Issue number2 35-2
StatePublished - Feb 1 1997

Fingerprint

Glucose Transporter Type 1
Facilitative Glucose Transport Proteins
Glucose
Brain
Weights and Measures
Blood Glucose
Growth
Body Weight
Deoxyglucose
Blood-Brain Barrier

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Physiology (medical)

Cite this

@article{211dca8e00cd435296e62b79e6a43b36,
title = "Glucose utilization and glucose transporter proteins GLUT-1 and GLUT-3 in brains of diabetic (db/db) mice",
abstract = "This study describes the effects of diabetes on brain growth, cerebral glucose utilization (CGU), and the glucose transporter proteins GLUT-1 and GLUT-3 in the genetically diabetic db/db mouse. Mice were studied at 5 and 10 wk of age and compared with age-matched nondiabetic littermates. At 5 wk, db/db mice were not yet hyperglycemic, but their body weights were 27.5{\%} greater than those of their nondiabetic littermates. By 10 wk, db/db mice were both hyperglycemic (blood glucose values of 39.3 ± 4.3 vs. 12.1 ± 2.1 mmol/l for db/db and control, respectively) and obese, with a twofold increase in body weight. Significant reductions in brain weight were observed at 5 wk (15{\%} decrease in brain wet wt), and no further brain growth was observed, such that by 10 wk, brains of db/db mice were 25{\%} smaller than those of control mice; brain wet weight-to-dry weight ratios were slightly reduced. Global rates of CGU, as determined with 2-[14C]deoxyglucose, were significantly reduced in the 10-wk diabetic mice. Levels of brain glucose and brain-to-blood glucose ratios were increased in 5- and 10-wk db/db mice, reflecting adequate glucose delivery to the brain. Blood-brain barrier GLUT- 1 levels were unchanged, and mRNA levels were regionally increased. The expression of the neuronal glucose transporter GLUT-3 was not reduced to a significant extent in brains of db/db mice. The results of this study indicate that the db/db mouse has markedly decelerated brain growth accompanied by global reductions in glucose metabolism that are not due to reductions in glucose transport capacity.",
author = "Vannucci, {Susan J.} and Gibbs, {E. Michael} and Simpson, {Ian A.}",
year = "1997",
month = "2",
day = "1",
language = "English (US)",
volume = "272",
pages = "E267--E274",
journal = "American Journal of Physiology",
issn = "0193-1849",
publisher = "American Physiological Society",
number = "2 35-2",

}

Glucose utilization and glucose transporter proteins GLUT-1 and GLUT-3 in brains of diabetic (db/db) mice. / Vannucci, Susan J.; Gibbs, E. Michael; Simpson, Ian A.

In: American Journal of Physiology - Endocrinology and Metabolism, Vol. 272, No. 2 35-2, 01.02.1997, p. E267-E274.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Glucose utilization and glucose transporter proteins GLUT-1 and GLUT-3 in brains of diabetic (db/db) mice

AU - Vannucci, Susan J.

AU - Gibbs, E. Michael

AU - Simpson, Ian A.

PY - 1997/2/1

Y1 - 1997/2/1

N2 - This study describes the effects of diabetes on brain growth, cerebral glucose utilization (CGU), and the glucose transporter proteins GLUT-1 and GLUT-3 in the genetically diabetic db/db mouse. Mice were studied at 5 and 10 wk of age and compared with age-matched nondiabetic littermates. At 5 wk, db/db mice were not yet hyperglycemic, but their body weights were 27.5% greater than those of their nondiabetic littermates. By 10 wk, db/db mice were both hyperglycemic (blood glucose values of 39.3 ± 4.3 vs. 12.1 ± 2.1 mmol/l for db/db and control, respectively) and obese, with a twofold increase in body weight. Significant reductions in brain weight were observed at 5 wk (15% decrease in brain wet wt), and no further brain growth was observed, such that by 10 wk, brains of db/db mice were 25% smaller than those of control mice; brain wet weight-to-dry weight ratios were slightly reduced. Global rates of CGU, as determined with 2-[14C]deoxyglucose, were significantly reduced in the 10-wk diabetic mice. Levels of brain glucose and brain-to-blood glucose ratios were increased in 5- and 10-wk db/db mice, reflecting adequate glucose delivery to the brain. Blood-brain barrier GLUT- 1 levels were unchanged, and mRNA levels were regionally increased. The expression of the neuronal glucose transporter GLUT-3 was not reduced to a significant extent in brains of db/db mice. The results of this study indicate that the db/db mouse has markedly decelerated brain growth accompanied by global reductions in glucose metabolism that are not due to reductions in glucose transport capacity.

AB - This study describes the effects of diabetes on brain growth, cerebral glucose utilization (CGU), and the glucose transporter proteins GLUT-1 and GLUT-3 in the genetically diabetic db/db mouse. Mice were studied at 5 and 10 wk of age and compared with age-matched nondiabetic littermates. At 5 wk, db/db mice were not yet hyperglycemic, but their body weights were 27.5% greater than those of their nondiabetic littermates. By 10 wk, db/db mice were both hyperglycemic (blood glucose values of 39.3 ± 4.3 vs. 12.1 ± 2.1 mmol/l for db/db and control, respectively) and obese, with a twofold increase in body weight. Significant reductions in brain weight were observed at 5 wk (15% decrease in brain wet wt), and no further brain growth was observed, such that by 10 wk, brains of db/db mice were 25% smaller than those of control mice; brain wet weight-to-dry weight ratios were slightly reduced. Global rates of CGU, as determined with 2-[14C]deoxyglucose, were significantly reduced in the 10-wk diabetic mice. Levels of brain glucose and brain-to-blood glucose ratios were increased in 5- and 10-wk db/db mice, reflecting adequate glucose delivery to the brain. Blood-brain barrier GLUT- 1 levels were unchanged, and mRNA levels were regionally increased. The expression of the neuronal glucose transporter GLUT-3 was not reduced to a significant extent in brains of db/db mice. The results of this study indicate that the db/db mouse has markedly decelerated brain growth accompanied by global reductions in glucose metabolism that are not due to reductions in glucose transport capacity.

UR - http://www.scopus.com/inward/record.url?scp=0030951430&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030951430&partnerID=8YFLogxK

M3 - Article

C2 - 9124334

AN - SCOPUS:0030951430

VL - 272

SP - E267-E274

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0193-1849

IS - 2 35-2

ER -