7. C A R B O H Y D R A T E A N D E N E R G Y M E T A B O L I S M
267
the glucose concentration in the medium is different in the L cell and
HeLa cell (Danes et al., 1963).
B. G L Y C O L Y S I S IN " N O R M A L " A N D " M A L I G N A N T " C E L L S
The previous discussion naturally leads to this topic, which is discussed fully in another chapter but which must be mentioned briefly in
the present context. Warburg (1930) and his colleagues observed that
tumours almost invariably exhibit a higher aerobic glycolysis than
normal tissues, i.e. a greater capacity to convert glucose to lactic acid
in the presence of air. Although this has been contested throughout the
years it is now agreed that in general the observation itself is correct.
However, Warburg's contention, based on this observation, that cancer
is due to an irreversible lesion ofthe respiratory pathways, has been and
still is seriously challenged and since it has been found that glycolysis
very rapidly increases when tissues are explanted (Paul and Pearson,
1957a, b ; Warburg et al., 1958; Suschny et al., 1958) most authors have
expressed doubts concerning its validity. There are currently two
general schools of thought among those who are prepared to agree that
tumour cells on the whole have higher rates of glycolysis than normal
ones. One of these maintains that the differences obtained may be due
to the conditions to which the tumour cell is exposed in situ (Agol,
1960b, c ; Paul, 1961). Evidence for this is provided by the observation
that when cells are grown in conditions of lowered oxygen tension they
may exhibit lowered respiration for 24-48 h after being placed in normal
oxygen tension again (Danes and Paul, 1961b; Paul, 1961). Since
tumours in situ nearly always have an inadequate blood supply
(Goldacre and Sylven, 1959) this may well explain the phenomenon.
The other school maintains that there is a persistent difference in the
carbohydrate metabolism of normal and malignant cells. Some of the
best evidence arises from the work of Burk and his colleagues who claim
to have demonstrated a correlation between high tumour-producing
capacity, high glycolytic capacity and reduced sensitivity of the
insulin-anti-insulin mechanism of the cell (Woods, Wight and Burk,
1953; Woods et al., 1959).
It is not impossible that both explanations are partially correct.
However, because of the difficulty of obtaining normal tissues strictly
comparable with given tumour tissues and the inadequacy of our
knowledge of the environmental factors which could affect carbohydrate
metabolism no conclusive results have yet been obtained. Recently
most of the environmental factors have been defined reasonably well
and it is possible to transform cells from low-tumour to high-tumour
types rapidly by means of oncogenic viruses. Consequently a definite
267
the glucose concentration in the medium is different in the L cell and
HeLa cell (Danes et al., 1963).
B. G L Y C O L Y S I S IN " N O R M A L " A N D " M A L I G N A N T " C E L L S
The previous discussion naturally leads to this topic, which is discussed fully in another chapter but which must be mentioned briefly in
the present context. Warburg (1930) and his colleagues observed that
tumours almost invariably exhibit a higher aerobic glycolysis than
normal tissues, i.e. a greater capacity to convert glucose to lactic acid
in the presence of air. Although this has been contested throughout the
years it is now agreed that in general the observation itself is correct.
However, Warburg's contention, based on this observation, that cancer
is due to an irreversible lesion ofthe respiratory pathways, has been and
still is seriously challenged and since it has been found that glycolysis
very rapidly increases when tissues are explanted (Paul and Pearson,
1957a, b ; Warburg et al., 1958; Suschny et al., 1958) most authors have
expressed doubts concerning its validity. There are currently two
general schools of thought among those who are prepared to agree that
tumour cells on the whole have higher rates of glycolysis than normal
ones. One of these maintains that the differences obtained may be due
to the conditions to which the tumour cell is exposed in situ (Agol,
1960b, c ; Paul, 1961). Evidence for this is provided by the observation
that when cells are grown in conditions of lowered oxygen tension they
may exhibit lowered respiration for 24-48 h after being placed in normal
oxygen tension again (Danes and Paul, 1961b; Paul, 1961). Since
tumours in situ nearly always have an inadequate blood supply
(Goldacre and Sylven, 1959) this may well explain the phenomenon.
The other school maintains that there is a persistent difference in the
carbohydrate metabolism of normal and malignant cells. Some of the
best evidence arises from the work of Burk and his colleagues who claim
to have demonstrated a correlation between high tumour-producing
capacity, high glycolytic capacity and reduced sensitivity of the
insulin-anti-insulin mechanism of the cell (Woods, Wight and Burk,
1953; Woods et al., 1959).
It is not impossible that both explanations are partially correct.
However, because of the difficulty of obtaining normal tissues strictly
comparable with given tumour tissues and the inadequacy of our
knowledge of the environmental factors which could affect carbohydrate
metabolism no conclusive results have yet been obtained. Recently
most of the environmental factors have been defined reasonably well
and it is possible to transform cells from low-tumour to high-tumour
types rapidly by means of oncogenic viruses. Consequently a definite