Neural control of glucose uptake by skeletal muscle after central administration of NMDA

C. H. Lang, M. Ajmal, A. G S Baillie

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Intracerebroventricular injection of N-methyl-D-aspartate (NMDA) produces hyperglycemia and increases whole body glucose uptake. The purpose of the present study was to determine in rats which tissues are responsible for the elevated rate of glucose disposal. NMDA was injected intracerebroventricularly, and the glucose metabolic rate (R(g)) was determined for individual tissues 20-60 min later using 2-deoxy-D-[U- 14C]glucose. NMDA decreased R(g) in skin, ileum, lung, and liver (30-35%) compared with time-matched control animals. In contrast, R(g) in skeletal muscle and heart was increased 150-160%. This increased R(g) was not due to an elevation in plasma insulin concentrations. In subsequent studies, the sciatic nerve in one leg was cut 4 h before injection of NMDA. NMDA increased R(g) in the gastrocnemius (149%) and soleus (220%) in the innervated leg. However, R(g) was not increased after NMDA in contralateral muscles from the denervated limb. Data from a third series of experiments indicated that the NMDA-induced increase in R(g) by innervated muscle and its abolition in the denervated muscle were not due to changes in muscle blood flow. The results of the present study indicate that 1) central administration of NMDA increases whole body glucose uptake by preferentially stimulating glucose uptake by skeletal muscle, and 2) the enhanced glucose uptake by muscle is neurally mediated and independent of changes in either the plasma insulin concentration or regional blood flow.

Original languageEnglish (US)
Pages (from-to)R492-R497
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume268
Issue number2 37-2
StatePublished - Jan 1 1995

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N-Methylaspartate
aspartic acid
skeletal muscle
Skeletal Muscle
Glucose
glucose
Muscles
muscles
blood flow
Leg
legs
insulin
Insulin
injection
Injections
Regional Blood Flow
Sciatic Nerve
hyperglycemia
limbs (animal)
Ileum

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

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title = "Neural control of glucose uptake by skeletal muscle after central administration of NMDA",
abstract = "Intracerebroventricular injection of N-methyl-D-aspartate (NMDA) produces hyperglycemia and increases whole body glucose uptake. The purpose of the present study was to determine in rats which tissues are responsible for the elevated rate of glucose disposal. NMDA was injected intracerebroventricularly, and the glucose metabolic rate (R(g)) was determined for individual tissues 20-60 min later using 2-deoxy-D-[U- 14C]glucose. NMDA decreased R(g) in skin, ileum, lung, and liver (30-35{\%}) compared with time-matched control animals. In contrast, R(g) in skeletal muscle and heart was increased 150-160{\%}. This increased R(g) was not due to an elevation in plasma insulin concentrations. In subsequent studies, the sciatic nerve in one leg was cut 4 h before injection of NMDA. NMDA increased R(g) in the gastrocnemius (149{\%}) and soleus (220{\%}) in the innervated leg. However, R(g) was not increased after NMDA in contralateral muscles from the denervated limb. Data from a third series of experiments indicated that the NMDA-induced increase in R(g) by innervated muscle and its abolition in the denervated muscle were not due to changes in muscle blood flow. The results of the present study indicate that 1) central administration of NMDA increases whole body glucose uptake by preferentially stimulating glucose uptake by skeletal muscle, and 2) the enhanced glucose uptake by muscle is neurally mediated and independent of changes in either the plasma insulin concentration or regional blood flow.",
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Neural control of glucose uptake by skeletal muscle after central administration of NMDA. / Lang, C. H.; Ajmal, M.; Baillie, A. G S.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 268, No. 2 37-2, 01.01.1995, p. R492-R497.

Research output: Contribution to journalArticle

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