G. Cuatrecasas et al., INCREASED LEPTIN PRODUCTION IN-VIVO AND INSULIN CLEAVAGE BY THE OMENTAL ADIPOSE-TISSUE OF MORBIDLY OBESE PATIENTS, Clinical endocrinology, 48(2), 1998, pp. 181-185
OBJECTIVE The aim of this investigation was to assess the insulin clea
vage capacity in obese humans. Increased insulin degradation by viscer
al adipose tissue has previously been demonstrated in obese rats and c
ould be interpreted as a physiological response to hyperinsulinaemia.
The recent characterization of leptin receptors in pancreatic beta cel
ls, liver and muscle suggests that leptin may influence insulin functi
on and metabolism. Our study focuses on the possible relationship betw
een leptin secretion and adipose tissue insulin-degrading capacity, DE
SIGN AND PATIENTS Insulin and leptin were measured in arterial blood a
nd in the epiploic vein of morbidly obese (n=7) and non-obese patients
(n=7) who were undergoing abdominal surgery, Arteriovenous insulin di
fference (AV insulin) was considered an in vivo marker of insulin degr
adation by the omental fat tissue. Statistical comparison between veno
us and arterial leptin was used to assess endogenous leptin production
. MEASUREMENTS Insulin was measured using an oligoclonal IRMA and lept
in levels were determined by using a specific radioimmunoassay. RESULT
S Morbidly obese patients were hyperinsulinaemic compared to non-obese
patients according to arterial insulin levels (P=0.049) but not to ve
nous revels. Insulin cleavage capacity, nil in the control group, was
clearly significant in the morbidly obese patients (P=0.001). In the m
orbidly obese group, leptin levels in venous epiploic samples were sig
nificantly higher (P=0.028) than in the arterial samples, confirming i
n situ the synthesis of leptin by human white adipose tissue. We also
observed a correlation between insulin arterial levels and venous lept
in concentrations (P=0.009) which supports the chronic leptinogenic ef
fect of insulin suggested in previous works. Finally, our results show
that venous leptin levels are correlated with the extent of insulin c
leavage by omental tissue (P=0.033). CONCLUSIONS Morbidly obese patien
ts have a higher white adipose tissue insulin cleavage capacity, which
could partially diminish hyperinsulinaemia-derived adverse effects. H
igh leptin production, a consequence of high insulin levels, may act a
s a signal to the insulin-degrading tissues in order to lower insulina
emia.