Action of insulin on the glycogen content of liver and muscle of the murrel,Ophicephalus striatus (Bloch)

Seshadri, B.

doi:10.1007/bf02144173

Cited by 3 publications

(1 citation statement)

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“…Pancreatectomy, isletectomy or treatment with islet cytotoxins leads to fasting hyperglycaemia (McCormick & MacLeod, 1925;Siinpson, 1926;Falkmer, 1961 ;Epple, 1969). Exogenous insulin exerts a hypoglycaemic effect (Phillips et al, 1948 ;Seshadri, 1967;Leibson & Plisetskaya, 1967). Although high glucose concentrations promote insulin release from toadfish islet tissue in vitro (Watkins et al, 1964), it is evident from the incidence of pronounced hyperglycaeinia following glucose administration, that the capacity for such release in vivo is low.…”

Section: Introductionmentioning

confidence: 99%

Studies on oral glucose intolerance in fish

Palmer

Ryman

1972

Journal of Fish Biology

199

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The oral glucose tolerance test, a diagnostic procedure used in the detection of human diabetes, was used to study carbohydrate metabolism in rainbow trout, Sulmo guirdneri (Richardson). Fish exhibited pronounced and persistent hyperglycaemia on oral glucose administration. Hyperglycaemia was accompanied by decrease in blood amino acids, serum free fatty acids and cholesterol and marked increase in hepatic storage of glycogen. The incidence of oral glucose intolerance results, at least in part from insufficient circulating insulin. Exogenous insulin exerts a hypoglycaemic action and effectively abolishes the hyperglycacmia resulting from glucose administration. Tolbutamidc, the sulphonylurea hypoglycaemic drug, is without effect. Possibly as an indirect result of hyperadrenocorticism, oral glucose tolerance is markedly improved in the pre-spawning female. Longterm feeding of high carbohydrate diet to goldfish Cnrussiirs aurutus (L.) resultcd in gross hepatomegaly due to excessive hepatic glycogen accumulation and, possibly, fatty change of the liver. Protein metabolism was impaired as evidenced by protein depletion. Such degenerative changes in liver metabolism are probably a direct result of oral glucose intolerance and reflcct a metabolism adapted to diets normally low in available carbohydrate.

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Section: Introductionmentioning

confidence: 99%