Ds. Weigle et al., LEPTIN DOES NOT FULLY ACCOUNT FOR THE SATIETY ACTIVITY OF ADIPOSE TISSUE-CONDITIONED MEDIUM, American journal of physiology. Regulatory, integrative and comparative physiology, 44(4), 1998, pp. 976-985
To determine whether leptin alone accounts for the satiety activity se
creted by native adipose tissue, we prepared culture media conditioned
by microdissected adipose tissue from overfed Long-Evans rats, fa/fa
rats, or db/db mice (media A, B, and C, respectively). Medium A signif
icantly suppressed food intake following intracerebroventricular deliv
ery to Long-Evans rats (2-h chow intake = 68 +/- 5% of baseline, P < 0
.001). Media B and C significantly suppressed food intake following in
traperitoneal delivery to ob/ob mice (24-h chow intake = 56 +/- 7% of
baseline for medium B, P = 0.001; 4-day chow intake = 78 +/- 3% of bas
eline for medium C, P = 0.004). Using a leptin receptor-based bioassay
, we determined that the leptin concentration of medium C was 392 +/-
.18 ng/ml. This concentration was 20-fold lower than the concentration
of recombinant murine leptin required to produce a similar degree of
feeding suppression following 5 days of administration to ob/ob mice.
Neither medium conditioned by adipose tissue from ob/ob mice nor mediu
m conditioned by adipose tissue from fa/fa rats and subsequently immun
odepleted of leptin had significant satiety activity. We conclude that
leptin is necessary but not sufficient to account for the satiety act
ivity of native adipose tissue, perhaps due to the production by adipo
cytes of a cofactor that augments the ability of leptin to suppress fe
eding.