Journal article
Participation of hindbrain AMP-activated protein kinase in glucoprivic feeding
Diabetes (New York, N.Y.), Vol.60(2), pp.436-442
02/2011
Handle:
https://hdl.handle.net/2376/114999
PMCID: PMC3028342
PMID: 21270255
Abstract
To examine the role of AMP-activated protein kinase (AMPK) in the control of glucoprivic feeding by hindbrain catecholamine neurons.
Micropunched hindbrain samples were collected from control and 2-deoxy-d-glucose (2DG)-injected rats for Western blot analysis of phosphorylated (activated) AMPK (pAMPK). Samples also were collected from 2DG-injected rats pretreated with anti-dopamine-β-hydroxylase conjugated to saporin to lesion hindbrain catecholamine neurons. In a second experiment, rats were given a fourth-ventricle injection of compound C (CC) or 5-aminoimidazole-4-carboxyamide ribonucleoside (AICAR), an inhibitor and activator of AMPK, to identify a role for AMPK in hindbrain neurons required for elicitation of 2DG-induced feeding.
Systemic 2DG stimulated food intake in controls but not in catecholamine-lesioned rats. In controls, but not catecholamine-lesioned rats, 2DG also increased phosphorylated Thr172 at AMPKα subunits (pAMPKα) in hindbrain micropunches containing catecholaminergic cell groups A1 through the middle region of C1 (A1-C1m). Increased pAMPKα was not observed in the adjacent noncatecholaminergic ventromedial medulla or in the A2-C2 catecholamine cell groups in the dorsal hindbrain. Fourth-ventricle injection of CC attenuated 2DG-induced feeding during the first 2 h of the test, and AICAR alone increased food intake only during the first 60 min of the 4-h test.
Results indicate that AMPK in catecholaminergic A1-C1m neurons is activated by glucoprivation. Therefore, AMPK may contribute to the glucose-sensing mechanism by which these neurons detect and signal a glucose deficit in the service of systemic glucoregulation.
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Details
- Title
- Participation of hindbrain AMP-activated protein kinase in glucoprivic feeding
- Creators
- Ai-Jun Li - Programs in Neuroscience, Washington State University, Pullman, Washington, USA. aijunli@vetmed.wsu.eduQing WangSue Ritter
- Publication Details
- Diabetes (New York, N.Y.), Vol.60(2), pp.436-442
- Academic Unit
- Integrative Physiology and Neuroscience, Department of
- Publisher
- United States
- Grant note
- R01 DK081546 / NIDDK NIH HHS DK040498 / NIDDK NIH HHS R01 DK040498 / NIDDK NIH HHS DK00345072 / NIDDK NIH HHS
- Identifiers
- 99900547604001842
- Language
- English
- Resource Type
- Journal article