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4

PROCEEDINGS

OF THE

ROYAL SOCIETY

OF

QUEENSLAND

FOR 1952

VOL. LX1V.

ISSUED 5th APRIL, 1954.

PRICE: TWENTY-FIVE SHILLINGS.

Printed for the Society
by

A. H. TUCKER, Government Printer, Brisbane.

The Royal Society* of Qyeensland.

Patron :

HIS EXCELLENCY LIEUT-GENEEAL SIE JOHN D. LAVAEACK, C.B.,

C.M.G., D.S.O., C. de G., K.B.E.

OFFICERS, 1952.

President :

I. M. MACKEEEAS, F.E.A.C.P.

Vice-President :

S. T. BLAKE, M.Sc.

Hon. Treasurer :

E. N. MAEKS, M.Sc., Pli.D.

Hon. Secretary :

DOEOTHEA F. SANDAES, M.Sc.

Hon. Librarian:
F. S. COLLIVEE

Hon. Editor:
GEOEGE MACK, B.Sc.

Members of Council:

. EOBINSON, M.Sc., Professor W. STEPHENSON, B.Sc., Pli.D., Professor
L. J. H. TEAKLE, B.Sc.Agr., M.S., Ph.D., J. H. SIMMONDS, M.B.E., M.Sc.,
Professor M. SHAW, M.E., M.I.Mec.E.

Hon. Auditor:

L. P. HEEDSMAN

Trustees :

F. BENNETT, B.Sc., Professor W. H. BEYAN, M.C., D.Sc.,
E. O. MAEKS, M.D., B.A., B.E.

CONTENTS.

6

Vol. LXIY.

Pages.

NIo. 1. — Some Biochemical Aspects of Reactions to Heat and Cold.

By H. J. G. Hines. (Issued separately, 16th November, 1953) 1-14

No. 2. — Volcanic Rocks of Aitape, New Guinea. By George Baker.

(Issued separately, 22nd March, 1953) . . . . . . . . 15-44

No. 3. — The Identity of Spadella moretonensis Johnston and Taylor.

By J. M. Thomson. (Issued separately, 22nd March, 1953) . . 45-49

No. 4. — Two New Species of Dipetalonema (Nematoda, Filarioidea) from
Australian Marsupials. By M. J. Mackerras. (Issued

separately, 22nd March, 1953) . . . . . . . . . . 51-56

No. 5. — Memorial Lecture. Professor T. Harvey Johnston: First Professor

of Biology in the University of Queensland. By Dorothea F.

Sandars. (Issued separately, 22nd March, 1953) . . . . 57-68

Report of Council . . . . . . . . . . . . . . . . . . v.

Abstract of Proceedings . . . . . . . . . . . . vii.

List of Members . . . . . . . • - ■ • • . • . . . . xiv.

«»

ft

PROCEEDINGS

OF THE

ROYAL SOCIETY

OF

QUEENSLAND

FOR 1952

VOL. LXIV.

PRICE: TWENTY-FIVE SHILLINGS.

Printed for the Society
by

A. H. TUCKER, Government Printer, Brisbane.

NOTICE TO AUTHORS

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Bagnold, It. A., 1937. The Transport of Sand by Wind. Geogr. J., 89,
409-438.

Kelley, T. L., 1923. Statistical Method. New York, Macmillan Company.
XI + 390 pp., 24 fig.

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Bagnold (1937), (Bagnold, 1937), Bagnold (1937, p. . . .), or (Bagnold
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Vol. LX IV., No. 1.

Proceedings of the Royal Society of

Queensland.

PRESIDENTIAL ADDRESS.

SOME BIOCHEMICAL ASPECTS OF
REACTIONS TO HEAT AND COLD.

By H. J. G. Hines, Department of Physiology and Biochemistry,

University of Queensland.

( Delivered before the Royal Society of Queensland, 31 st March, 1952.;

The department with which I am associated has, since its inception
in 1936, made the study of the reactions of man and animals to
environmental conditions its special business (Yeates, Lee and
Hines, 1941). It is the business of the physiologist to study the
working of animals and plants as a whole. To do this he must often
study the functions of parts whether in situ or detached from the
animals. It is the function of the biochemist to study the events of the
living process at the molecular level. There is often a considerable
gap between these two processes since the working out of biochemical
details usually lags behind the general overall picture of physiological
behaviour.

I shall therefore endeavour to show how this gap is being filled,
as yet, of course, incompletely, with respect to the effects of climatic
conditions on man and animals. I can assume that we are all familiar
with the distinction between warm-blooded and cold-blooded animals,
or to use more technical jargon, the homoiotherms and the poikilotherms.
The former group, which comprises the mammals and bird's, is able to
maintain a relatively constant internal temperature which is usually
above that of the environment, while the internal temperature of the
poikilotherms rises and falls with that of the surroundings. I want to
concern myself with homoiothermic animals, the maintenance of whose
internal temperature requires the generation of sufficient heat to balance
that which is lost to the environment, and also requires mechanisms to
regulate the production and loss of heat. The main features of this
process were clearly established during the nineteenth century, and
accounts given in text books written fifty years ago can still be read
with profit.

The production of animal heat was, of course, a mystery to the
ancients and its true nature had to await the investigations of Lavoisier
in Prance and of Crawford in Scotland in the latter part of the
eighteenth century. With the discovery of the true nature of combustion,
Lavoisier was quick to recognise the essential similarity between
combustion and respiration, the consumption of oxygen and the output
of carbon dioxide. He was able to measure the gaseous exchange quite
accurately and went on to measure the heat output of small animals with
his ice calorimeter. He realised the defects of this apparatus and in

2

PROCEEDINGS OF THE ROYAL SOCIETY OF QUEENSLAND.

particular noted that the heat output of the animal increased in the
cold. Crawford, and later Duboy and Despretz were able to make
improved measurements. Animal heat was clearly produced in the
process of oxidation of the food consumed. During the succeeding
century nearly every physiologist of note had something to say of this
problem, touching as it did on almost all aspects of physiology, and
the investigations of the great German physiologists, Yoit, Pettenkofer
and Rubner clearly established the energetic equivalence of food
consumed and heat and work produced. Throughout this time, the
nature of the oxidative process remained a mystery. Lavoisier thought
that combustion took place in the lungs, but later experiments showed
that oxygen was consumed and carbon dioxide was produced in all
parts of the body and that the amounts were greatly increased by
muscular exertion. A recent calculation gives the following estimate of
the heat produced by the tissues of a man under basal conditions.

TABLE I*.

Weight of
Organ and
(Proportion of
Body Weight).

Oxygen Consumption
of Organ. Litres
0 2 /24 in’, and
Proportion of Total
Oxygen Consumption.

Heat Produced
Kg. Cal./24 hr. /Kg.
Tissue.

Whole Body . .

70 Kg.

356

23-5

(100%)

(100%)

Heart . .

0-33 Kg.

37

520

(0-47%)

(10%)

Kidneys

0-33 Kg.

31

440

(0-47%)

(9%)

Liver . .

1-6 Kg.

115

335

(2*3%)

(32%)

Brain . .

1-4 Kg.

68-5

225

(2%)

(19%)

3-66 Kg.

251-5

(5*24%)

(70%)

Rest of Body (by difference)

66-3 Kg.

105

7-4

(94-7%)

(30%)

Muscles

29-5 Kg.

58-5

9-2

(42%)

(16%)

* This table is taken from Mr. Hedley Marston’s Liversidge Lecture
(Marston 1951).

The term ' basal conditions’ used in this connection may require
a little explanation. When an animal fasts, the food in its alimentary
canal is quickly used up and it is forced to live on its own reserves, the
protein and fat of its tissues. Oxygen consumption, carbon dioxide
production, and with them heat production, fall to a minimum value
which forms an important base line, the 'basal metabolism,’ well
known in all nutritional studies. Under external conditions, generally
spoken of as thermoneutral, the basal metabolism is held to represent
the minimum energy expenditure necessary to sustain life.

The table shows that most of the energy exchange under these
conditions occurs in a central 'core’. Particularly noteworthy is
the high oxygen consumption of liver and brain. Organs which between
them constitute only five per cent, of the body weight, are responsible
for seventy per cent, of the heat production. The liver, of course, is
the great factory and warehouse, receiving most of the products of

SOME BIOCHEMICAL ASPECTS OF REACTIONS TO HEAT AND COLD. 3

digestion and converting them into products suitable for use in other
tissues. The multiplicity of its chemical functions makes it a happy
hunting ground for the biochemical investigator.

The way in which oxidation is effected in the tissues remained
unknown in the nineteenth century. Quite obviously, the change from
such a substance as sugar to carbon dioxide and water was not sudden.
The patient unravelling of the mechanisms of oxidation in the tissues
has been a major occupation of biochemists during the past thirty
years. The operation proceeds stepwise through a series of inter-
mediates. Linked with these steps is another process, the transfer of
phosphoric acid. The energy released by the dismutation and oxidation
of sugars, fats, and other substances is transferred to compounds of
phosphoric acid, and in particular is used in forming the substance
adenosine triphosphate. The anhydride linkages in this substance serve
as a kind of energy currency. Simple hydrolysis of the linkage merely
dissipates chemical energy as heat, but the energy of fission can be
directly utilized for a variety of purposes ; the contraction of muscle,
the generation of electricity, the movement of substances along
concentration gradients, the synthesis of complex molecules, all derive
the necessary energy through transfer of phosphoric acid from these
(instable compounds of phosphoric acid. The process appears universal
in plants and animals, and its discovery is one of the major biochemical
achievements of the past twenty-five years. Animals therefore are not
beat engines. They do not convert heat energy into mechanical energy,
but achieve the transfer of chemical energy in a variety of ways. In all
such transfers a part of the energy is lost as heat energy, and if the
animal is not performing external work, eventually all the energy

QC

'b

O

>

N.

Cc

uj

Cl

Co

Ui

o

N?

u

Fig. 1. Comparison of the heat production of fasting albino rats with that of
animals receiving feed at different environmental temperatures.

4

PROCEEDINGS OF THE ROYAL SOCIETY OF QUEENSLAND.

resulting from oxidation appears as heat. Such heat energy is useful
to the animal only in so far as it serves to maintain body temperature
above that of the surroundings.

From the earliest investigations it was made clear that down to a
certain environmental temperature (the critical temperature), the body
temperature could be maintained without increasing the metabolism,
simply by increasing the insulation (so called physical heat, regulation).
Below the critical temperature, the body temperature could be main-
tained only by increasing the heat production (so-called metabolic or
‘chemical 7 heat regulation). A great many experiments have been
conducted to determine this critical temperature for a variety of animals.
A typical experiment with that favourite laboratory animal, the albino
rat, is shown in Fig. 1 (Black and Swift, 1943).

In this rather pampered animal, the range of thermoneutrality is
limited to a degree or so, and the heat production rises linearly with
decrease in temperature. Note that above the critical temperature, or
critical thermal environment, heat production also rises.

Fig. 2. Influence of environmental temperature on heat production.

Figure 2 (Brody, 1945) serves to illustrate features common to
all homoiotherms. If the environmental conditions are such that heat
production can no longer keep pace with heat loss, and ‘body tempera-
ture’ falls and the animal may die. In man, a rectal temperature
of 25° C. seems to be the lowest consistent with survival, but other
animals can drop to still lower temperatures and survive. The

SOME BIOCHEMICAL ASPECTS OF REACTIONS TO HEAT AND COLD. 5

hibernating animals during hibernation resemble cold-blooded animals
and the rectal temperature may fall to as low as 2°C. with metabolism
almost at a standstill.

Strictly speaking then, the term homoiotherm as applied to
mammals and birds is a misnomer. Life can continue over quite a range
of temperature, but the range is greater below the critical temperature
than above it.

At this stage I should like to draw your attention to the compre-
hensive studies on arctic and tropical birds and mammals recently
published by Scholander (1950) and his associates. They were able
to carry out experiments at Point Barrow, Alaska, latitude 71°N., and
in the Panama Canal zone at latitude 9°N. Metabolic rates for a
number of animals were determined at different environmental tempera-
tures, and striking differences were shown in the behaviour of the
arctic and tropical groups. The arctic animals were able to maintain
constant body temperatures without increase in metabolic rate. There
is no evidence of adaptive low body temperature in arctic mammals and
birds, or high body temperature in the tropical species. There are no
signs so far that body temperatures of mammals and birds are adaptive
to the different climates on earth. A logical corollary of this is that
they cannot have been adaptive to the overall climatic conditions on
earth. It seems then that the narrow band of body temperatures on
which both birds and mammals operate is a fundamental, non-adaptive
constant in their biochemical set-up. This shows that the striking
differences in critical temperatures, and increased rates of heat produc-
tion below critical temperatures, are largely a matter of insulation in the
broad sense, that is, in resistance to heat dissipation (Pig. 3).

Fig. 3. Heat regulation and temperature sensitivity in arctic and tropical mammals.

With the facilities available at the Arctic Research Laboratory at
Point Barrow, Scholander was unable to reach the critical temperature
for foxes or eskimo dogs. It is believed that their critical temperature
is somewhere between — 45° C. and — 50° C. In Panama it was observed
that the tropical mammals and birds responded with an increase in
metabolism starting at only a few degrees below the ambient air
temperature, producing strikingly steep curves compared with those
of the arctic animals.

6

PROCEEDINGS OF THE ROYAL SOCIETY OF QUEENSLAND.

The critical temperature in naked man is known to be around 27° C.
to 29 °C., which places him among the more temperature sensitive
of the tropical mammals. The Australian aboriginal however, seems
to be exceptional in that he can apparently lie naked and at rest at
temperatures near to freezing point without increasing his metabolic
rate. There appears to be a fall in body temperature, however, and
the aborigine’s behaviour on waking bears some resemblance to that of
a hibernating animal. The point that emerges from these investigations
is that the basal metabolic rate of terrestrial mammals from tropics
to arctic is fundamentally determined by a size relation according to
the formula Cal. /day =70 Kg«, and is phylogenetically non-adaptive
to external temperature conditions. Equally non-adaptive is the body
temperature, and the phylogenetic adaptation to cold therefore rests
entirely upon the plasticity of the factors which determine the heat loss.

The basal heat production we have seen, arises largely from the
activity of the visceral organs and the brain. The muscles contribute
a relatively small amount. Below the critical temperature, however,
when conditions are no longer basal, the extra heat production is
brought about largely through muscular movement, both voluntary and
involuntary. The survival of an animal exposed to cold obviously
depends on whether this extra heat production can balance the heat
loss, and the duration of this extra heat production will determine
survival. This in turn will depend on the rate supply of nutrients to
the metabolising tissues and the rate of utilization. The rapidity with
which liver glycogen is used by pigeons subjected to cold is shown by
the following table (adapted from Streicher, Hackel and Fleischmann,
1950).

TABLE II.

Duration of
Experiment
in Hours.

At — 40°C.

At 23°-

-25°C.

Liver

Glycogen %.

Blood Sugar
mg.m/lOOml.

Liver

Glycogen %.

Blood Sugar
mg.m/lOOml.

1

1-48

147

1*31

152

3

0-84

143

1*54

147

8

005

158

0-76

154

24

0002

135

0043

154

48

0015

129

0108

141

72

0-0

159

0005

151

In eight hours the liver glycogen of the birds kept fasting at — 40°C.
was almost exhausted. After 24 hours that of the control group was
almost zero. The metabolic rate of the birds exposed to cold was
approximately three times that of the birds in the control group.
The blood sugar on the other hand stays constant, and this implies the
efficient conversion of non-sugars to sugar. The survival of the birds
will depend on the availability of body reserves of protein and fat and
the rate at which they can be oxidised.

That metabolic demand may outstrip exogeneous supply in fully
fed animals is also shown by the experiments of Black and Swift
(1943) on rats. With decreasing external temperatures, their experi-
ments showed that the respiratory quotient fell as the metabolic rate
rose. A curious point is that the respiratory quotient also fell with
the rise in metabolic rate above the critical temperature. The following
table is taken from their paper.

SOME BIOCHEMICAL ASPECTS OF REACTIONS TO HEAT AND COLD. 7

TABLE III.

Temperature.

Respiratory Quotient.

Total Heat /hr.

•c.

12

0-837

3-00

18

0-859

2-40

24

0-902

1-79

28

0-948

1-59

30

0-946

1-50

31

0-951

1.38

32

0-942

1-38

33

0-915

1-45

34

0-918

1*61

DAYS

Fig. 4. Survival of clipped rats at 1*5 °C. after periods of previous exposure.

8

PROCEEDINGS OF THE ROYAL SOCIETY OF QUEENSLAND.

A respiratory quotient of unity in an experiment lasting 7-J hours
may be taken to indicate that carbohydrate is being consumed whilst
the R.Q. of fat is 0.7.

It has been shown, however, that rats can gradually undergo
adaptive changes to cold which increase their resistance to this form
of stress. The 1 acclimatisation, ’ if such it can be called, is related
to the ability of the animal to maintain a high level of metabolic
activity for prolonged periods. This relationship has been shown by
clipping the fur of normal and acclimatised rats and exposing them
to cold. Acclimatised animals survive and maintain greatly increased
metabolic rates for significantly longer periods than do animals which
are unaccustomed to lowered environmental temperatures. The effects
of varying exposure on survival time are shown in figure 4 (Sellers,
Reichman and Thomas, 1951).

The conclusions drawn from these figures are that the process of
acclimatisation to cold is gradual. No effect is noticed before two
weeks of exposure, but it is fully developed after four to five weeks
and does not increase further. The altered metabolic state is not
permanent and may be rapidly lost after a return to a warm
environment.

There is ample evidence that hormonal factors are implicated in
some of the changes which take place during exposure to cold. The
pituitary, the adrenal and the thyroid glands all undergo alterations
in size and in function during exposure. Indeed, there is evidence
that survival at temperatures near zero is dependent on the presence
of these glands. The relationship of the endocrine glands to acclimatisa-
tion is not a simple one, however, for it has been shown that acclimatised
animals subjected to adrenalectomy survive longer in the cold than
do non-acclimatised adrenalectomised controls. A similar relationship
has also been established with respect to the exposure of thyroidectomised
animals to cold. These observations, taken in conjunction with the
finding that acclimatisation develops gradually, suggest that metabolic
tissues themselves undergo some adaptive alteration, perhaps in response
to a general controlling influence. Note that these changes are temporary
and are not to be confused with phylogenetic adaption to temperature.
Sellers, Reichmann and Thomas (1951) attempted to prolong survival
‘artificially’ by pretreatment with cortisone and thyroxine and with
other substances. The use of a combination of cortisone and thyroxine
given before clipping and exposure to cold significantly increased
survival (Fig. 5).

The recognition of the part played by the hormones of the sup-
rarenal in the maintenance of homeostasis has been one of the most
striking features of the physiology of the past decade. Earlier emphasis
on the sympatho-adrenal system has been followed by the discover}'
of the even more ubiquitous part played by the pituitary and adrenal
cortex. “The sympatho-adrenal system actively drives organs and
organ systems to increased functional activity in emergencies, whereas
the pituitary-adrenocortical system plays a passive role, making cortical
hormone available in quantities appropriate for the varying needs of
the organism. In other words, the sympatho-adrenal system initiates,
whereas the pituitary-adrenocortical system supports cellular activities.”

SOME BIOCHEMICAL ASPECTS OF REACTIONS TO HEAT AND COLD.

9

/on

c -*■

PRE- T RE A TM ENT

Wtfh:

controls

43 rais

y/ucose

/o

y/ucose insulin

to

cortisone <&. insulin

to “

DC A

9 -

ascorbic Odd

IO "

so/me controls 2-S6/ 0 4* -

fhyroxme, 200 mM-

! O "

ihyroxi ne ‘50m/u,.

23 »

A. C. T. H

3/

corfisone

36 "

cortisone £ thyroxine

79 '■

Fig. 5. Effect of various substances on the survival of clipped non-aeclimatised

rats exposed to cold.

Sayers (1950), whom I have quoted above, illustrates current
conceptions of cortical behaviour by means of the accompanying
diagrams (Figs. 6 and 7).

According to this concept then, the increased metabolism, in response
to exposure to cold may be initiated by impulses to the hypothalamus,
but the metabolic response is sustained by increased output from the
adrenal cortex. The stimulus to this is derived from the pituitary which
may simply respond to diminished levels of cortical hormone in the
venous blood.

I want to draw attention to one other consequence of the metabolic
adaptation to cold, and that is the increased demand for vitamin C,
ascorbic acid, under such conditions. Ascorbic acid is stored in the

10

PROCEEDINGS OF THE ROYAL SOCIETY OF QUEENSLAND.

A DEN OH Y POP H YS IS

PERIPHERAL Cor he a/ ADRENAL

T ISSUES hormone C ORT EX

Fig. C. Self-regularatory system (Peripheral — humoral concept).

Sfimu/ue

Afferent nervous
pathways

Ep/nephnt

)nne

Sympafh / n
Acelylcholn

ne

H YPO THALAMUS

ADENOHYPOPH YS/S

ACTH

Y

ADRENAL CORTEX

Corf ICO’
hormone

PERIPHERAL 7 ISSUES

Fig. 7. Centrally driven system (Central — neural concept).

suprarenal and disappears when the suprarenal is stimulated by stress
conditions. Dugal and Therien (1947) in an impressive series of
experiments were able to show that ascorbic acid was necessary for
resistance and adaption to cold by guinea pigs, animals which like man
are unable to synthesise vitamin C. The resemblance between scurvy
and certain features of adrenal insufficiency has been noted, but ii
seems certain that ascorbic acid is not concerned in the synthesis of
adrenocortical hormones. It appears more likely that both cortical
hormone and ascorbic acid are required to support cellular activity
and that the demand for both is roughly parallel. Either may prove

SOME BIOCHEMICAL ASPECTS OF REACTIONS TO HEAT AND COLD. 11

a limiting factor in cellular activity if the demand is great and the
supply restricted. Classical scurvy, although probably a multiple
deficiency, occurred most frequently in men performing strenuous
muscular work in cold environments. Scurvy generally occurred among
crews of sailing vessels after a strenuous rounding of Cape Horn, and
it was the bugbear of polar explorers.

I have said that hormones, such as those of the adrenal cortex and
such substances as vitamin C, are necessary for the support of cellular
activities. In spite of the fact that adrenalin has been known for close
on fifty years, there is still no clear idea of its action and the same holds
true for other hormones. Their general effect on metabolic processes
has been explored extensively, but their connection with specific reactions
occurring in cells remains obscure. With the vitamins however, which
may be looked upon as exogenous hormones, there has been more success.
The members of the vitamin B group have all been shown to be connected
with specific stages of cellular metabolism and to be components of the
catalysts accelerating cellular reactions, the enzymes. It is almost an
article of faith with biochemists that both vitamins and hormones will
ultimately be linked with the promotion of enzyme activity. Some recent
publications support this view. Ascorbic acid, vitamin C, has been
shown to be required for the oxidation of tyrosine in liver, a process
which also requires the presence of a-keto-glutaric acid. Hormones have
rarely been found to affect appropriate cell-free enzymes directly.
Special importance therefore attaches to a recent paper by Knox (1951).
Enzyme adaptation, that is, increased activity in a particular enzyme
produced by treatment with the substrate of the enzyme and indepen-
dent of the growth of selection of the cells, is well established for
micro-organisms. Knox claims that the same phenomenon is demonstrable
in liver with the enzyme tryptophane peroxidase and that it can be
demonstrated both in slices and in cell-free preparations after treat-
ment with the substrate tryptophane. He goes on to show that treatment
of the animal with small doses of adrenalin or histamine will elicit a
similar response which can be attributed to increased cortical hormone
release. You and Sellers (1951) have also shown that after rats have
been exposed to a cold environment for more than sixteen days, the
oxygen consumption of liver slices, and the succinoxidase activity of
liver homogenates is significantly increased. They point out therefore
that increased activity of non-mnscular tissues must contribute to the
increased heat production brought on by exposure to cold.

I want now to turn to another factor which affects the production
of heat by the animal, the influence of food. It has long been known
that giving food to a fasting animal increases its heat production and
that this effect varies with the kind of food given. This action of
nutrients was called by Rubner the “specific dynamic action”, and the
additional heat produced by a given quantity of food became known as
the heat increment. Lusk (1930) defined this action in the following
way: — “If what we now call the basal metabolism of a typical animal
be 100 calories per day and if 100 calories be administered to the
animal in each of the several foodstuffs on different days, then the
heat production of the animal after receiving meat protein will rise
to about 130 calories, after glucose to about 106 calories, and after fat
to about 104 calories”. The large heat increment observed with protein
feeding could also be observed with amino acids, and according to Grafe
(1915), even with ammonium salts. Lusk goes on to say: — “Just as the