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Effects of endothelin-1 and nitric oxide on glucokinase activity in isolated rat hepatocytes.

L D Monti¹, G Valsecchi, S Costa

¹Istituto Scientifico H. San Raffaele, Cattedra di Clinica Medica, Medicina I, Università di Milano, Italy.

Metabolism: Clinical and Experimental

|January 26, 2000

Summary

Endothelin-1 (ET-1) reduces nitric oxide (NO) levels, inhibiting glucokinase (GK) activity and glycogen synthesis in rat hepatocytes. This effect is mediated by NO signaling pathways, not ET-1 receptors directly.

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Area of Science:

Biochemistry
Endocrinology
Cellular Metabolism

Background:

Endothelin-1 (ET-1) and nitric oxide (NO) are key regulators of cellular functions.
Their precise interaction in modulating glucokinase (GK) activity and glycogen metabolism remains to be fully elucidated.
Understanding these pathways is crucial for metabolic disease research.

Purpose of the Study:

To investigate the opposing roles of ET-1 and NO on glucokinase (GK) activity and glycogen content in isolated rat hepatocytes.
To determine the involvement of specific ET-1 receptors (ETB, ETA-ETB) in this process.
To elucidate the signaling mechanisms, particularly the role of cyclic guanosine monophosphate (cGMP).

Main Methods:

Isolated rat hepatocytes were treated with ET-1, L-NAME (NO synthase inhibitor), L-arginine (NO precursor), and receptor antagonists (BQ 788, PD 142893).
Measurements included GK activity, intracellular cGMP, and glycogen content.
NO levels (as NO2-/NO3-) and glucose in the medium were also determined.

Main Results:

High ET-1 levels decreased NO, cGMP, GK activity, and glycogen content, while increasing medium glucose.
L-NAME mimicked ET-1's inhibitory effects on GK and glycogen, reducing cGMP.
ET-1's effects were abolished by ET receptor antagonists, with no change in NO or cGMP levels.
L-arginine partially counteracted ET-1's inhibitory effects.

Conclusions:

The NO pathway, via cGMP, is a significant regulator of GK activity and glycogen content.
ET-1 does not act directly but exerts its effects through a reduction in NO levels.
ET-1 receptor antagonists block the observed effects, indicating receptor-mediated signaling is essential for ET-1's influence on NO levels.