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Abstract
Changes in extracellular osmolality, and thus in the cellular hydration state, appear
to directly influence cell metabolism. The metabolic changes associated with cell
swelling are inhibition of glycogenolysis, glycolysis, and proteolysis. Recent studies
in our laboratory demonstrated diminished whole-body protein breakdown in humans during
an acute hypoosmolar state. Because of the close interrelationship between carbohydrate
and fat metabolism, we speculated that adipose tissue lipolysis and fatty acid oxidation
are regulated by changes in extracellular osmolality. Therefore, we investigated the
effect of artificially induced hypoosmolality on whole-body lipolysis and fat oxidation
in seven healthy young men. Hypoosmolality was induced by intravenous administration
of desmopressin, liberal ingestion of water, and infusion of hypotonic (0.45%) saline
solution. Lipolysis was assessed by a stable-isotope method (2-[13C]-glycerol infusion). The glycerol rate of appearance (Ra), reflecting whole-body
lipolysis, was higher under hypoosmolar compared with isoosmolar conditions (2.35
± 0.40 v 1.68 ± 0.21 μmol/kg/min, P = .03). This was even more pronounced when lipolysis was suppressed during hyperinsulinemia
and euglycemic clamping (0.90 ± 0.08 v 0.61 ± 0.03 μmol/kg/min, P = .002). However, plasma free fatty acid (FFA), glycerol, ketone body, insulin, and
glucagon concentrations and carbohydrate and lipid oxidation measured by indirect
calorimetry were not significantly altered by hypoosmolality. Plasma norepinephrine
concentrations were lower under hypoosmolar conditions (P < .01 v control). In conclusion, hypoosmolality in vivo results in increased whole-body lipolysis,
which is not due to changes in major lipolysis regulating hormones.
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Article info
Publication history
Accepted:
October 22,
1998
Received:
April 24,
1998
Footnotes
☆Supported by Grant No. 32-39747.93 from the Swiss National Science Foundation, and by the “Wissenschaftlicher Kredit” of the Kantonsspital Basel.
Identification
Copyright
© 1999 Published by Elsevier Inc.
