TY - JOUR
T1 - Leptin inhibits insulin binding in isolated rat adipocytes
AU - Walder, K.
AU - Filippis, A.
AU - Clark, S.
AU - Zimmet, P.
AU - Collier, G. R.
PY - 1997/12
Y1 - 1997/12
N2 - Leptin is secreted from adipose tissue, and is thought to act as a 'lipostat', signalling the body fat levels to the hypothalamus resulting in adjustments to food intake and energy expenditure to maintain body weight homeostasis. In addition, plasma leptin concentrations have been shown to be related to insulin sensitivity independent of body fat content, suggesting that the hyperleptinemia found in obesity could contribute to the insulin resistance. We investigated the effects of leptin on insulin binding by isolated adipocytes. Adipocytes isolated from Sprague-Dawley rats exhibited a dose-dependent reduction in the uptake of 125I-labelled insulin when incubated with various concentrations of exogenous leptin. For example, addition of 150 nM leptin reduced total insulin binding in isolated adipocytes by 19% (P<0.05). Analysis of displacement curve binding data suggested that leptin reduced maximal insulin binding in a dose- dependent manner, but had no significant effect on the affinity of insulin for its binding site. We conclude that leptin directly inhibited insulin binding by adipocytes, and the role of leptin in the development of insulin resistance in obese individuals requires further investigation.
AB - Leptin is secreted from adipose tissue, and is thought to act as a 'lipostat', signalling the body fat levels to the hypothalamus resulting in adjustments to food intake and energy expenditure to maintain body weight homeostasis. In addition, plasma leptin concentrations have been shown to be related to insulin sensitivity independent of body fat content, suggesting that the hyperleptinemia found in obesity could contribute to the insulin resistance. We investigated the effects of leptin on insulin binding by isolated adipocytes. Adipocytes isolated from Sprague-Dawley rats exhibited a dose-dependent reduction in the uptake of 125I-labelled insulin when incubated with various concentrations of exogenous leptin. For example, addition of 150 nM leptin reduced total insulin binding in isolated adipocytes by 19% (P<0.05). Analysis of displacement curve binding data suggested that leptin reduced maximal insulin binding in a dose- dependent manner, but had no significant effect on the affinity of insulin for its binding site. We conclude that leptin directly inhibited insulin binding by adipocytes, and the role of leptin in the development of insulin resistance in obese individuals requires further investigation.
UR - http://www.scopus.com/inward/record.url?scp=0030782649&partnerID=8YFLogxK
U2 - 10.1677/joe.0.155R005
DO - 10.1677/joe.0.155R005
M3 - Article
C2 - 9488006
AN - SCOPUS:0030782649
SN - 0022-0795
VL - 155
SP - R5-R7
JO - Journal of Endocrinology
JF - Journal of Endocrinology
IS - 3
ER -