Interleukin 6 stimulates hepatic glucose release from prelabeled glycogen pools
- Shriners Burns Institute, Galveston, TX (USA)
Cytokines, derived from a wide variety of cell types, are now believed to initiate many of the physiological responses accompanying the inflammatory phase that follows either Gram-negative septicemia or thermal injury. Because hypoglycemia (after endotoxic challenge) and hyperglycemia (after thermal injury) represent well-characterized responses to these injuries, we sought to determine whether hepatic glycogen metabolism could be altered by specific cytokines. Cultured adult rat hepatocytes were prelabeled with ({sup 14}C)glucose for 24 h, a procedure that resulted in the labeling of hepatic glycogen pools that subsequently could be depleted (with concomitant ({sup 14}C)glucose release) by either glucagon or norepinephrine. After the addition of a highly concentrated human monocyte-conditioned medium (MCM) or various cytokines to these prelabeled cells, ({sup 14}C)glucose release was stimulated by MCM and recombinant human interleukin 6 (IL-6) but was not stimulated by other cytokines tested. Furthermore, only antisera to IL-6 were capable of reducing the glucose-releasing factor activity found in MCM. These data therefore suggest a novel glucoregulatory role for IL-6.
- OSTI ID:
- 7026900
- Journal Information:
- American Journal of Physiology; (USA), Vol. 258; ISSN 0002-9513
- Country of Publication:
- United States
- Language:
- English
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HEMIC DISEASES
HYPERGLYCEMIA
INTERFERON
LIVER
MONOCYTES
RATS
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550501* - Metabolism- Tracer Techniques