Glycogen Stores in Glucagon-Treated Rats. I. Time Factors.

Abstract

Glucagon is believed to cause hyperglycemia by promoting glycogenolysis in the liver. This is based on the following evidence which has been reviewed in detail recently (1) and which is largely indirect: 1) the hyperglycemic response to glucagon is decreased or absent in fasting, untreated diabetes, severe liver disease (2) and after evisceration ( 3 ) when the amount of liver glycogen is presumably low or absent; 2 ) glucagon is more effective when injected into the portal vein than by any other route of administration and is ineffective after occlusion of the liver circulation(2) ; 3) glucagon causes a sharp increase in splanchnic glucose production. as measured by venous catheterization in man ( 4 ) : 4) destruction of the pancreatic alpha cells, presumably accompanied by the liberation of preformed glucagon, causes an immediate hyperglycemia with a decrease in liver glycogen( 5 ) ; 5) glucagon promotes liver glycogenolysis in vitru by activating the phosphorylase system ( 6 ) . Although these findings would lead one to expect a decrease of liver glycogen in intact animals treated with glucagon, this effect has not been clearly demonstrated. Burger and Kramer(2) first reported a decrease in liver glycogen in dogs treated with glucagon. However, these pioneering results were obtained with crude preparations of glucagon heavily contaminated with insulin. Furthermore liver glycogen was determined in samples obtained by means of repeated biopsies, a traumatizing technic which may cause glycogenolysis in itself. Similarly, using an impure preparation of glucagon, Heard et a L ( 7 ) obtained a decrease in liver glycogen in normal rats, while Milman et al.(8) obtained similar results in vit. E-deficient rats. In contrast with these findings, the

Efeitos do Glucagon no metabolismo glicídico de Chrysemys d'orbignyi (Reptilia, Chelonia) sob a influência das variações estacionais

“…Em Alligator mississipensis, por exemplo, há necessidade de glicemia elevada por vários dias afim de aparecer um aumento significativo no teor de glicogênio hepático (Coulson e H er nandez, 1964). Costa et al (1956) haviam observado que, em ratos tratad o s com glucagon, há, inicialmente, diminuição do glicogênio hepático e, seeundàriamente, aumento acima dos níveis normais. Sugerem êstes autores que êste efeito secun dário se deve a um aumento da secreção de insulina ou de hor mônios corticais, ou de ambos.…”

“…2). Milman et al (1954) e Costa et al (1956, verificaram aumento oca sional do glicogênio m uscular em animais tratad o s com gluca gon. Porém, para êstes autores, o pequeno aumento não pa rece ser um efeito direto e específico do glucagon m as um re sultado da secreção de insulina.…”

“…Em ratos normais, a redução do glicogênio hepático é pas sageira, e 24 horas depois está mais alto (Costa et al, 1956;Foà et al, 1957;Okuno, 1960). Em ratos tratad o s por longo período com glucagon, o glicogênio do fígado pode estar nor m al ou aum entado Okuno, 1980;Saiter, 1960).…”