Horm Metab Res 2004; 36(10): 667-673
DOI: 10.1055/s-2004-826012
Original Basic
© Georg Thieme Verlag KG Stuttgart · New York

Short-term Fasting and Lipolytic Activity in Rat Adipocytes

T.  Szkudelski1 , M.  Lisiecka1 , E.  Nowicka1 , A.  Kowalewska1 , L.  Nogowski1 , K.  Szkudelska1
  • 1Department of Animal Physiology and Biochemistry · University of Agriculture · 60-637 Wolyñska 35 · Poznañ · Poland
Further Information

Publication History

Received 22 January 2004

Accepted after revision 22 June 2004

Publication Date:
03 November 2004 (online)

Abstract

The aim of this experiment was to study the influence of 18-hour food deprivation on basal and stimulated lipolysis in adipocytes obtained from young male Wistar rats. Fat cells from fed and fasted rats were isolated from the epididymal adipose tissue by collagenase digestion. Adipocytes were incubated in Krebs-Ringer buffer (pH 7.4, 37 °C) without agents affecting lipolysis and with different lipolytic stimulators (epinephrine, forskolin, dibutyryl-cAMP, theophylline, DPCPX, amrinone) or inhibitors (PIA, H-89, insulin). After 60 min of incubation, glycerol and, in some cases, also fatty acids released from adipocytes to the incubation medium were determined. Basal lipolysis was substantially potentiated in cells of fasted rats in comparison to adipocytes isolated from fed animals. The inhibition of protein kinase A activity by H-89 partially suppressed lipolysis in both groups of adipocytes, but did not eliminate this difference. The agonist of adenosine A1 receptor also did not suppress fasting-enhanced basal lipolysis. The epinephrine-induced triglyceride breakdown was also enhanced by fasting. Similarly, the direct activation of adenylyl cyclase by forskolin or protein kinase A by dibutyryl-cAMP resulted in a higher lipolytic response in cells derived from fasted animals. These results indicate that the fasting-induced rise in lipolysis results predominantly from changes in the lipolytic cascade downstream from protein kinase A. The antagonism of the adenosine A1 receptor and the inhibition of cAMP phosphodiesterase also induced lipolysis, which was potentiated by food deprivation. Moreover, the rise in basal and epinephrine-stimulated lipolysis in adipocytes of fasted rats was shown to be associated with a diminished non-esterified fatty acids/glycerol molar ratio. This effect was presumably due to increased re-esterification of triglyceride-derived fatty acids in cells of fasted rats. Comparing fed and fasted rats for the antilipolytic effect of insulin in adipocytes revealed that short-term food deprivation resulted in a substantial deterioration of the ability of insulin to suppress epinephrine-induced lipolysis.

References

T. Szkudelski

Department of Animal Physiology and Biochemistry, University of Agriculture ·

60-637 Wolyñska 35 · Poznañ · Poland

Phone: +48(61)84871 96

Fax: +48(61)8487196 ·

Email: [email protected]