594
I L S E
L A S N I T Z K I
normal mouse mammary tissue but did not influence that of the mammary carcinoma. A comparison of glucose utilization and glycolysis in
insulin-treated human-skin fibroblasts and human cancer cells (Leslie,
Fulton and Sinclair, 1957) showed that glycolysis was considerably
higher in the tumour cells. The hormone reduced the rate of total acid
production in the embryonic cells and increased it in the cancer cells.
In chick-heart fibroblasts (Leslie, 1952) a combination of insulin with
growth hormone gave results similar to those seen after insulin alone,
but growth hormone alone added in concentrations of 0-1-0-5 mg/ml
medium inhibited cell growth by 25°/o while the cell composition
remained unchanged.
On the other hand M o o n and St. Vincent (1957) reported a growthpromoting effect of a pituitary growth hormone on a strain of rat
fibroblasts. Cell counts made after 96 h incubation in a medium
containing 20-200 ju,g/ml, were greater than those in control medium
and the total tyrosine content measured by the method of Ogaya and
Eagle (1956) was consistently higher. It seems difficult to reconcile
these two results, but it must be remembered that Leslie (1952) and
Leslie and Davidson (1951) used fresh explants, while Moon and St.
Vincent's results (1957) were obtained with a long-established cell
strain; it is possible that changes in the enzymic pattern during prolonged cultivation may alter the response to the growth hormone.
In experiments designed to shed more light on the mechanisms
involved in the action of insulin and growth hormone on carbohydrate
metabolism Bullough (1954b) studied the effect o f t h e two hormones
on epidermal mitosis in fragments of mouse ears kept in a non-growthpromoting medium supplemented with three different sugars. In
earlier work, Bullough and Johnson (1951) had shown that the rate of
mitosis in mouse epidermis depended on the rate of entry of glucose
into the cells and its subsequent conversion to energy.
The addition of insulin to the medium of ear fragments of male mice
(1-25-12-5 /ug/ml) almost doubled the mitotic rate when glucose was
used as a substrate. This effect was, no doubt, due to an increased
consumption of glucose as Overell, Condon and Petrov (1960) had
shown that the hormone stimulated glucose uptake in fragments of
mouse skin in vitro. Insulin was, however, ineffective if either L-lactate
or fructose were substituted for glucose. O n the other hand, L-lactate
or fructose alone induced a significantly higher mitotic rate than
glucose. The author concluded that insulin stimulates a reaction in
glucose metabolism which takes place before the pyruvate stage and is
most probably the reaction: glucose->glucose-6-phosphate.
Addition of pituitary-growth hormone to the medium depressed
the mitotic rate in the ear fragments in the presence of glucose but
I L S E
L A S N I T Z K I
normal mouse mammary tissue but did not influence that of the mammary carcinoma. A comparison of glucose utilization and glycolysis in
insulin-treated human-skin fibroblasts and human cancer cells (Leslie,
Fulton and Sinclair, 1957) showed that glycolysis was considerably
higher in the tumour cells. The hormone reduced the rate of total acid
production in the embryonic cells and increased it in the cancer cells.
In chick-heart fibroblasts (Leslie, 1952) a combination of insulin with
growth hormone gave results similar to those seen after insulin alone,
but growth hormone alone added in concentrations of 0-1-0-5 mg/ml
medium inhibited cell growth by 25°/o while the cell composition
remained unchanged.
On the other hand M o o n and St. Vincent (1957) reported a growthpromoting effect of a pituitary growth hormone on a strain of rat
fibroblasts. Cell counts made after 96 h incubation in a medium
containing 20-200 ju,g/ml, were greater than those in control medium
and the total tyrosine content measured by the method of Ogaya and
Eagle (1956) was consistently higher. It seems difficult to reconcile
these two results, but it must be remembered that Leslie (1952) and
Leslie and Davidson (1951) used fresh explants, while Moon and St.
Vincent's results (1957) were obtained with a long-established cell
strain; it is possible that changes in the enzymic pattern during prolonged cultivation may alter the response to the growth hormone.
In experiments designed to shed more light on the mechanisms
involved in the action of insulin and growth hormone on carbohydrate
metabolism Bullough (1954b) studied the effect o f t h e two hormones
on epidermal mitosis in fragments of mouse ears kept in a non-growthpromoting medium supplemented with three different sugars. In
earlier work, Bullough and Johnson (1951) had shown that the rate of
mitosis in mouse epidermis depended on the rate of entry of glucose
into the cells and its subsequent conversion to energy.
The addition of insulin to the medium of ear fragments of male mice
(1-25-12-5 /ug/ml) almost doubled the mitotic rate when glucose was
used as a substrate. This effect was, no doubt, due to an increased
consumption of glucose as Overell, Condon and Petrov (1960) had
shown that the hormone stimulated glucose uptake in fragments of
mouse skin in vitro. Insulin was, however, ineffective if either L-lactate
or fructose were substituted for glucose. O n the other hand, L-lactate
or fructose alone induced a significantly higher mitotic rate than
glucose. The author concluded that insulin stimulates a reaction in
glucose metabolism which takes place before the pyruvate stage and is
most probably the reaction: glucose->glucose-6-phosphate.
Addition of pituitary-growth hormone to the medium depressed
the mitotic rate in the ear fragments in the presence of glucose but