Normal number and kinase activity of insulin receptors in liver of genetically fat chickens.

Genetically fat (FL) chickens exhibit an increase in liver lipogenesis and, in the fasting state, insulin sensitivity compared with genetically lean (LL) chickens. Liver insulin receptor number and insulin receptor kinase (IRK) activity were studied at 5 wk. In the fasting (16 h) and fed state, insulin binding to liver membranes and insulin receptor affinity (50% inhibition of tracer binding, range: 5-7 ng/mL at 4 degrees C) were very similar in fat and lean chickens. Insulin degrading activity of membranes was negligible for both genotypes. Following solubilization with Triton X-100, liver receptors were purified either on wheat germ agglutinin (WGA receptors) or on lentil then wheat germ lectins (lentil receptors). Both types of purified receptors exhibited the same binding affinity, independent of the genotype or the nutritional state. Autophosphorylation and IRK activity toward artificial substrate poly(Glu, Tyr)4:1 were not different between genotypes. Basal IRK (i.e., in the absence of insulin) was decreased by the overnight fast. Fattening of genetically fat chickens cannot be accounted for by an increase in the number or the kinase activity of liver insulin receptors. Steps following the binding or the receptor kinase may be involved.