5. THE ENDOCRINE PANCREAS
299
mains to be seen if the different reactions of Petromyzon and Myxine
result from scattered B-cell-like elements in the bile duct and possibly
also in the gut of the latter species (Falkmer and Matty, 1966a). Pancreatectomy in elasmobranchs causes hyperglycemia ( Diamare, 1906;
Diamare and Montuori, 1907), which can be alleviated by hypophysectomy Orias, 1932; Abramowitz et al., 1940). Removal of the compact
pancreas of the eel was followed by inconstant glucosuria (Caparelli,
1894). In teleosts removal of the Brockmann bodies leads to hyperglycemia, glucosuria, and increase in liver lipids ( McCormick and Macleod,
1925; Simpson, 1926; Falkmer, 1961; Falkmer and Matty, 196613). However, in Cottus scorpius the occurrence of hyperglycemia is more evident
in fed than in starved animals; insulin alleviates hyperglycemia, while
hypophysectomy shows less consistent results ( Falkmer, 1961; Falkmer
and Matty, 1966b).
4. EFFECTS OF ISLET CYTOTOXINS
a. Alloxan. Ever since the observation that alloxan selectively destroys
the pancreatic B cells in the rabbit ( Dunn et al., 1943) , this compound
has been widely used to induce experimental diabetes or to support the
histological identification of the B cells. There is even a report of alloxan
“diabetes” in a clam (Kasinathan, 1964). Representatives of both groups
of the cyclostomes have been treated with alloxan. In lampreys (Petromyzon pluneri and Petromyzon fluviatilis), alloxan injection sometimes
causes B-cell destruction; however, very high doses are required, and
other organs (liver, kidney, and intestines) may also be damaged
(Ermisch, 1966; Winbladh, 1967). In Myxine glutinosu, extremely high
doses of alloxan led only to hyperglycemia and damage of B-cell groups
in a relatively small number of the experimental animals. There was no
correlation between B-cell destruction and hyperglycemia. These observations might result from special circulatory conditions, e.g., imperfect
mixing of blood and slow circulation. All animals, regardless of the state
of islet damage or glycemia, showed a very low hematocrit (Falkmer and
Winbladh, 1964b).
The reports on B-cell destruction by alloxan in the chondrichthyans
are rather controversial. After intraperitoneal injections, Saviano ( 1946,
1947a) finds an increase of blood sugar but no islet damage in sharks.
In highly hyperglycemic animals there was a remarkable development of
the A cells and a clear increase of the cytoplasmatic granules. Paradoxically, the exocrine pancreas was damaged by the drug. Even with
high intramuscular doses of alloxan, Kern (1966) was unable to produce
any alterations in the blood sugar level or the islet organ in Scylwrhinus
299
mains to be seen if the different reactions of Petromyzon and Myxine
result from scattered B-cell-like elements in the bile duct and possibly
also in the gut of the latter species (Falkmer and Matty, 1966a). Pancreatectomy in elasmobranchs causes hyperglycemia ( Diamare, 1906;
Diamare and Montuori, 1907), which can be alleviated by hypophysectomy Orias, 1932; Abramowitz et al., 1940). Removal of the compact
pancreas of the eel was followed by inconstant glucosuria (Caparelli,
1894). In teleosts removal of the Brockmann bodies leads to hyperglycemia, glucosuria, and increase in liver lipids ( McCormick and Macleod,
1925; Simpson, 1926; Falkmer, 1961; Falkmer and Matty, 196613). However, in Cottus scorpius the occurrence of hyperglycemia is more evident
in fed than in starved animals; insulin alleviates hyperglycemia, while
hypophysectomy shows less consistent results ( Falkmer, 1961; Falkmer
and Matty, 1966b).
4. EFFECTS OF ISLET CYTOTOXINS
a. Alloxan. Ever since the observation that alloxan selectively destroys
the pancreatic B cells in the rabbit ( Dunn et al., 1943) , this compound
has been widely used to induce experimental diabetes or to support the
histological identification of the B cells. There is even a report of alloxan
“diabetes” in a clam (Kasinathan, 1964). Representatives of both groups
of the cyclostomes have been treated with alloxan. In lampreys (Petromyzon pluneri and Petromyzon fluviatilis), alloxan injection sometimes
causes B-cell destruction; however, very high doses are required, and
other organs (liver, kidney, and intestines) may also be damaged
(Ermisch, 1966; Winbladh, 1967). In Myxine glutinosu, extremely high
doses of alloxan led only to hyperglycemia and damage of B-cell groups
in a relatively small number of the experimental animals. There was no
correlation between B-cell destruction and hyperglycemia. These observations might result from special circulatory conditions, e.g., imperfect
mixing of blood and slow circulation. All animals, regardless of the state
of islet damage or glycemia, showed a very low hematocrit (Falkmer and
Winbladh, 1964b).
The reports on B-cell destruction by alloxan in the chondrichthyans
are rather controversial. After intraperitoneal injections, Saviano ( 1946,
1947a) finds an increase of blood sugar but no islet damage in sharks.
In highly hyperglycemic animals there was a remarkable development of
the A cells and a clear increase of the cytoplasmatic granules. Paradoxically, the exocrine pancreas was damaged by the drug. Even with
high intramuscular doses of alloxan, Kern (1966) was unable to produce
any alterations in the blood sugar level or the islet organ in Scylwrhinus