5. THE ENDOCRINE PANCREAS
303
to hypoglycemic convulsibns and/or death. Insulin hypoglycemia was
provoked in cyclostomes (Bentley and Follett, 1965; Falkmer and Matty,
1966a; Plisetskaya, 1967; Leibson and Plisetskaya, 1967), in chondrichthyans (W. C. Grant, Jr., 1964; Leibson and Plisetskaya, 1967; Patent,
1968), and actinopterygians (Mann et al., 1924; Olmstedt, 1924; Collip,
1925; McCormick and Macleod, 1925; Simpson, 1926; Gray, 1928; Gray
and Hall, 1930; Root et al., 1931; Bruun and Hemmingsen, 1938; Vorhauer,
1938; Alghauhari, 1958; Falkmer, 1961; Leibson and Plisetskaya, 1967;
Yanni, 1964; Seshadri, 1967; Young and Chavin, 1967; Khanna and
Mehrotra, 196913). The data on duration and degree of hypoglycemia and
on the onset of hypoglycemic convulsions vary greatly. Most investigators
observed a slow response, the peak of hypoglycemia or convulsions
occurring 1 or 2 days after injection, or even later. This agrees with the
observations on insulin action in other poikilotherms (cf. Bern and Nandi,
1964). Seshadri ( 1967) reported a mammalianlike hypoglycemic response
in Ophicephalus striutus with return to normal blood sugar levels within
3 hr. Falkmer and Wilson (1967) observed a weak hypoglycemic response
even to species specific insulin in Cottus scorpius; Tashima and Cahill
(1964) failed to obtain any hypoglycemia in Opsanus tau at a very high
dosage of bovine insulin. Young and Chavin (1967) observed a moderate
hyperglycemia after lo00 U/kg and 5000 U/kg bonito insulin in the goldfish, while 1 U/ kg produced significant hypoglycemia.
b. Glycogen. In lampreys, mammalian insulin leads to an increase or
ambiguous behavior of liver glycogen; it causes little or no increase in
muscle glycogen (Bentley and Follet, 1965; Leibson and Plisetskaya,
1967). In Petromyzon, exogenous insulin causes a decrease of the high
glycogen content of the brain ( Plisetskaya, 1967). In Lampetra fluviuti2is
injection of insulin decreased the glucose 6-phosphatase activity in the
liver ( Plisetskaya and Ogorodnikova, 1967). In chondrichthyans, exogenous insulins have no effect on either liver or muscle glycogen or they
lead to an increase of glycogen in one or both organs (Leibson and
Plisetskaya, 1967; Patent, 1968). Insulin also increases the glucose uptake
of dogfish branchial muscle in vitro (Villee et al., 1950). In teleosts, the
effects of exogenous insulin on the glycogen content of liver and muscle
vary greatly. Root et al. (1931) found in Stenotomus chysops a transient
increase in liver glycogen, followed by hypoglycemia and an increased
glycogen deposition in muscles. Tashima and Cahill (1964) found no
effect on glucose incorporation into toadfish tissues in vitro. Seshadri
(1967) observed in Ophicephalus striatus a peak of both liver and muscle
glycogen deposition 90 min after injection, and returning to normal after
3 hr, while the blood sugar level showed an inverse response. Increased
dosage of insulin caused an increase in both liver and muscle glycogen. In
303
to hypoglycemic convulsibns and/or death. Insulin hypoglycemia was
provoked in cyclostomes (Bentley and Follett, 1965; Falkmer and Matty,
1966a; Plisetskaya, 1967; Leibson and Plisetskaya, 1967), in chondrichthyans (W. C. Grant, Jr., 1964; Leibson and Plisetskaya, 1967; Patent,
1968), and actinopterygians (Mann et al., 1924; Olmstedt, 1924; Collip,
1925; McCormick and Macleod, 1925; Simpson, 1926; Gray, 1928; Gray
and Hall, 1930; Root et al., 1931; Bruun and Hemmingsen, 1938; Vorhauer,
1938; Alghauhari, 1958; Falkmer, 1961; Leibson and Plisetskaya, 1967;
Yanni, 1964; Seshadri, 1967; Young and Chavin, 1967; Khanna and
Mehrotra, 196913). The data on duration and degree of hypoglycemia and
on the onset of hypoglycemic convulsions vary greatly. Most investigators
observed a slow response, the peak of hypoglycemia or convulsions
occurring 1 or 2 days after injection, or even later. This agrees with the
observations on insulin action in other poikilotherms (cf. Bern and Nandi,
1964). Seshadri ( 1967) reported a mammalianlike hypoglycemic response
in Ophicephalus striutus with return to normal blood sugar levels within
3 hr. Falkmer and Wilson (1967) observed a weak hypoglycemic response
even to species specific insulin in Cottus scorpius; Tashima and Cahill
(1964) failed to obtain any hypoglycemia in Opsanus tau at a very high
dosage of bovine insulin. Young and Chavin (1967) observed a moderate
hyperglycemia after lo00 U/kg and 5000 U/kg bonito insulin in the goldfish, while 1 U/ kg produced significant hypoglycemia.
b. Glycogen. In lampreys, mammalian insulin leads to an increase or
ambiguous behavior of liver glycogen; it causes little or no increase in
muscle glycogen (Bentley and Follet, 1965; Leibson and Plisetskaya,
1967). In Petromyzon, exogenous insulin causes a decrease of the high
glycogen content of the brain ( Plisetskaya, 1967). In Lampetra fluviuti2is
injection of insulin decreased the glucose 6-phosphatase activity in the
liver ( Plisetskaya and Ogorodnikova, 1967). In chondrichthyans, exogenous insulins have no effect on either liver or muscle glycogen or they
lead to an increase of glycogen in one or both organs (Leibson and
Plisetskaya, 1967; Patent, 1968). Insulin also increases the glucose uptake
of dogfish branchial muscle in vitro (Villee et al., 1950). In teleosts, the
effects of exogenous insulin on the glycogen content of liver and muscle
vary greatly. Root et al. (1931) found in Stenotomus chysops a transient
increase in liver glycogen, followed by hypoglycemia and an increased
glycogen deposition in muscles. Tashima and Cahill (1964) found no
effect on glucose incorporation into toadfish tissues in vitro. Seshadri
(1967) observed in Ophicephalus striatus a peak of both liver and muscle
glycogen deposition 90 min after injection, and returning to normal after
3 hr, while the blood sugar level showed an inverse response. Increased
dosage of insulin caused an increase in both liver and muscle glycogen. In