“…Although in cirrhosis basal hepatic glucose production is lower than normal (Myers, 1950;Reichle et al, 1978;Proietto et al, 1980;Owen et al, 1981) and suppresses to very low levels with physiological increments of insulin (Proietto et al, 1980), overall resistance to both endogenous (Megyesi et al, 1967;Stocks & Powell, 1973;Collins & Crofford, 1969) and exogenous (Stocks & Powell, 1973;West et al, 1975;Perez ef al., 1978) insulin has been clearly demonstrated. Numerous causes for this insulin resistance have been suggested and include elevated levels of ammonia (Klassen et al, 1969), growth hormone (Conn & Daughaday, 1970) and free fatty acids (Stocks & Powell, 1973), the presence ofcirculating inhibitors of insulin action (Dzurikova et al, 1972). and reduced insulin receptor binding (Piniewski et al, 1980;Teng et al, 1982;Blei e f al., 1982).…”