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The effects of cold and glucagon on lipolysis, glycogenolysis and oxygen consumption in young chicks
Comp. Biochem. Physiol., 1973, Vol. 45A, pp. 489 to 495. Pergmnon Press. Printed in Great Britain
THE EFFECTS OF COLD AND GLUCAGON ON LIPOLYSIS, GLYCOGENOLYSIS AND OXYGEN CONSUMPTION IN YOUNG CHICKS R. PALOKANGAS,
V. VIHKO
and I. NUUJA
Department of Biology, University of Jyvlskylzi, 40100 Jyvlskyll_lO,
Finland
(Received 19 September 1972) To study the possible role of glucagon in avian thermoregulation the effects of cold exposure and glucagon on lipolysis, glycogenolysis and oxygen consumption were measured in young chicks. 2. Cold exposure (+ 1O’C) and glucagon injection (0.3 mg/kg, i.p. at + 30°C) both caused a marked increase in the plasma FFA and a decrease in the liver glycogen content. 3. It is suggested that glucagon possibly acts in the avian thermoregulation by producing at least lipolysis and glycogenolysis during cold exposure.
Abstract-l.
INTRODUCTION
COLD exposure
increases the oxygen consumption of several species of young ducklings (Koskimies & Lahti, 1964), of chicks (Freeman, 1967) and of young black-headed gulls (Palokangas & Hissa, 1971). Plasma-free fatty acid (FFA) levels are also higher in cold-exposed chicks than in those kept at a thermoneutral zone (Freeman, 1967, 1970). The increased oxygen consumption in chicks during cold exposure has been suggested by Freeman (1967) to be the result of an intensive lipid metabolism. Glucagon is known to be a strongly lipolytic and glycogenolytic agent in birds (Grande & Prigge, 1970; Freeman & Manning, 1971). Freeman (1970) has even suggested that chemical thermogenesis might be mediated by glucagon in birds. The purpose of this study was to investigate the possible role of glucagon in the thermoregulation of young chicks. The lipid and carbohydrate metabolisms were studied during cold exposure and after glucagon administration. The measured variables were the most common individual plasma-free fatty acids, blood glucose, liver glycogen, oxygen consumption and body temperature near the thermoneutral zone (at + 30°C) and d uring or after cold exposure (at + 10°C). MATERIALS
AND METHODS
Two-day-old White Leghorn chicks, weighing 40-50 g, were used in the experiments. The chicks were obtained from a commercial hatchery. The birds were kept overnight at an ambient temperature (T,) of + 30°C with water and commercial chick feed ad lib. The experiments were always performed between 0900 and 1200 hr. 489
R. PALOKANGAS, V. VIHKOANDI. NIJUJA
490 Cold exposure
One group of chicks was exposed to + 10°C for 30 min and another group for 60 min to the same temperature. Their simultaneous controls were kept at +3O”C for respective periods. To avoid huddling behavior the chicks were individually placed into plastic jars with blotting paper on the bottom to keep the birds dry and clean from moist feces during the experiment. Glucagon injections Glucagon (E. Lilly, Indianapolis, U.S.A.) was dissolved into 0.9% saline. Injections of glucagon (0.3 or O-6 mg/kg) were given intraperitoneally. The control birds were given a corresponding volume of saline. Oxygen consumfkm Oxygen consumption was measured with a Beckman E 2 Oxygen Analyzer as described earlier by Hissa & Palokangas (1970). M easurements were done every fifth minute during 60 min at + 10°C and at + 30°C. The body temperature (T,,) was measured from the cloaca with a thermocouple (Ellab) before and after the experiments. Each bird was used only once. Chemical analyses The birds were killed by decapitation and blood was collected into test-tubes which contained dried heparin. The individual free fatty acids in plasma were determined by gas chromatography using a Perkin-Elmer 990 gas chromatograph as described earlier by Palokangas & Vihko (1971). The following acids were quantified using n-heptadecanoic acid as an internal standard: pahnitic (C16:0), pahnitoleic (C16:1), stearic (C18:O) and the combined amount of oleic (C18:1), linoleic (C18:2) and linolenic (C18:3) acids (C18:U = unsaturated). The whole blood glucose was determined enzymatically using Biochemica Boehringer’s test packings (TBAP, Boehringer GmbH, Mannheim) and a Perkin-Elmer 124 spectrophotometer. The liver glycogen content was estimated by the method of Kemp & Kits van Heijningen (1954). All chemical determinations were performed as double assays. RESULTS
Cold exposure Cold exposure
of + 10°C
for 30 min caused
a significant
increase
in the level
acid (PC O*OOl), and in the total FFA (the sum of the concentration of acids determined) (P< O-05). Wh en cold exposure was extended to 60 min, the lipolysis was more prominent and the differences were statistically
of plasma-free
palmitic
more significant.
The levels of every acid studied increased
The mean blood glucose concentration but
the
decrease
decreased
was not
32 per cent during
exposure for 60 min. The oxygen consumption intensive
statistically
decreased significant.
the exposure of the chicks
significantly
(Table
The
liver
glycogen
content
for 30 min and 41 per cent during exposed
than that of the birds kept at +3O”C
1).
slightly due to cold exposure,
(Table
to cold (+ 10°C)
the
was more
4).
Glucagon injections
The results on plasma
FFA,
of the experiments blood
glucose
concerning
the effects of glucagon
and liver glycogen
are given in Table
injections 2.
The
Group
Control Test
Control Test
Exposure time (min)
30 30
60 60
P
NS
40 + 2.6 41 + 2.2
45 f 5.2 59 f. 3.7 P
C16:l
NS
257 + 19.5 282 + 15.2
230 z!z13.3 308 * 20.4 < 0.01
Cl6:O
TABLE'&--THEEFFECTOFGLUCAGONINJECTION
NS 270 + 10.5 420 k 23.8 < 0.001
314 f 20.0 341+ 27.2
cl8:u*
NS 172 + 6.2 204 + 8.7 < 0.01
139 f 7.7 142fll.4
C18:O
< 0.05 778 f 23.5 1034 + 46.8 < O*OOl
727 + 31.5 854 rt 53.5
“Total”
217f7.5 199 I!I17.9 NS
NS
351* 37.4 352 f 20.0
314rt 20.0 473 + 64.6 < 0.05
C18:U
FFA &-equiv/l.)
NS
173 f 10.6 190 + 6.4
139 zt 7.7 171 Z!I16.8 NS
Cl8:O
NS
821 f 69.1 864 i 32.9
727 f 31.5 1011 z!z100.7 < 0.025
“Total”
2lOfll*l 263 jz 32.9 < 0.05
230 % 12.6 281 + 3.9 < 0.05
Blood glucose (mg/lOO ml)
100 80
100 87
Relative liver glycogen (%)
100 59
100 68
230 f 12.6 206 f 10.2
NS
Relative liver glycogen (%)
Blood glucose (mg/lOO ml)
2-day-old
(0*3mg/kg) ONTHEPLASMA FFA, BLOODGLUCOSEANDLIVERGLYCOGENOFTHE 2-day-old CHICKS AT + 30°C (MEANf S.E.)
+30 +10
60 60
*U = unsaturated, see text.
< 0.001 292 f 12.2 353 * 15.2 < 0.005
NS 43 f 4.8 56fl.9 P <0.05
P
230 + 13.3 325 f 12.9
45 + 5.2 45 f 4.1
+30 +10
30 30
Cl6:O
Cl6:l
FFA &-equiv/l.)
EFFECTOFCOLDEXPOSURE(+~O~C)ONTHEPLASMA FFA, BLOODGLUCOSEANDLIVERGLYCOGENOFTHE CHICKs(MEANf S.E.)
Exposure time (min)
TABLEI-THE
7 6
7 7
NE
;
N
5
s
3
d
ZX
!2
2
P
-a
8
!I 2
492
‘R. PALOKKANGAS,V. VIHKOAND
I. NUUJA
intraperitoneal glucagon injection (O-3 mg/kg) caused a marked increase in the plasma FFA during the 30-min exposure. The total FFA was about 40 per cent higher in test birds than in control birds. The increase of Cl&unsaturated acids was about 50 per cent ‘and that of palmitic acid 34 per cent. Stearic acid concentration changed the least. The blood glucose level was also higher (PC 0.05) in birds treated with glucagon. Simultaneously the liver glycogen content of the glucagon-injected birds decreased more than that of control birds. Sixty min after injection of glucagon the plasma FFA concentration had already nearly diminished to the same level as in the control birds. In contrast, the concentration of blood glucose was still at a higher level in the test birds (PC 0.05). The liver glycogen content was 20 per cent lower in test than in control birds. The lipolytic effect of glucagon was not readily noticeable in birds which were given glucagon and simultaneously exposed to cold as compared to the coldexposed controls (Table 3). Only the concentration of the plasma-free palmitic acid was significantly higher in the tests (PC O-05). No remarkable changes were seen either in the blood glucose levels or in the liver glycogen contents. The smaller glucagon dose (0.3 mg/kg) d ecreased the oxygen consumption slightly at + 30°C during 60 min exposure. Simultaneously the Tb declined by 3~5°C (Table 4). The dose of 0.6 mg/kg caused a more noticeable decrease in oxygen consumption and the T,, decreased even more (4~4°C). At + 10°C the glucagon injection (0.3 mg/kg) decreased the oxygen consumption significantly (Table 4). The dose of 0.6 mg/kg also decreased the oxygen consumption. The decreases in Tb were also significantly greater in the glucagontreated groups than in the control groups.
DISCUSSION
Cold exposure caused a prominent lipolysis and a slight glycogenolysis in 2-day-old chicks. The previously observed increases in the oxygen consumption of young birds exposed to cold (Koskimies & Lahti, 1964; Palokangas & Hissa, 1971) might partially be related to an increased lipid metabolism as suggested by Romijn & Lokhorst (1955) and Freeman (1967). It is not known in detail how the lipid mobilization is mediated in birds. Catecholamines can probably be discarded in this respect, because they do not cause any lipolysis in birds (e.g. Carlson et al., 1964; Palokangas & Vihko, 1971). Glucagon, on the other hand, is known to be a lipolytic agent in birds (Grande & Prigge, 1970) and Freeman (1970) has suggested that it is involved in the thermogenesis of birds. After glucagon administration the plasma FFA concentration increased significantly during 30 min exposure. This lipolytic effect resembles the effect caused by cold exposure but it was completed 60 min after the glucagon injection. If glucagon is infused into ducks, lipolysis continues for at least 2 hr (Grande & Prigge, 1970). It may be possible, as suggested by Freeman (1970), that lipolysis induced by cold exposure might be mediated by endogenous glucagon.
EFFECTS OF COLD AND GLUCAGON ON YOUNG CHICKS
493
494
R. PALOKANGAS, V. VIHKO ANDI. NUUJA
Confirmation of this, however, demands for example the measurement of glucagon concentration in blood during cold exposure. The glycogenolytic effect of glucagon lasted longer than the lipolytic effect, i.e. at least for an hour. Both of these findings are in agreement with the results reported by Heald et al. (1965) and Freeman & Manning (1971). In cold-exposed chicks an additional glucagon administration did not stimulate the lipolytic effect much more (Table 3). In spite of these findings glucagon did not increase the oxygen consumption of the chicks, but, on the contrary, it seemed to cause a decrease in respiration and T,,. These oxygen consumption and the T,, decreasing effects of glucagon resemble those brought about by catecholamines (Freeman, 1970; Hissa & Palokangas, 1970). Further support to this effect of glucagon is given by the unpublished findings of Nuuja (1971) concerning the house sparrow, and Palokangas (1970) concerning the titmouse and black-headed gull. The reason for this decreased oxygen consumption is unknown. In rats, relatively small doses of glucagon given subcutaneously raise the metabolic rate linearly with the logarithm of the dose (Davidson et al., 1960) and the calorigenic action is rapid, reaching its maximum about 1 hr after the injection. It is known that in mammals the calorigenic action of glucagon depends upon the state of the thyroid, e.g. in thyroidectomized rats glucagon does not increase the oxygen consumption (Hoch, 1971). The importance of the thyroid in the thermoregulation of the neonate chick is also discussed by Freeman (1970, 1971). Why the exogenous glucagon does not interact with the possible active endogenous thyroid hormones to increase the oxygen consumption in birds cannot be answered here. Despite the reported lipolytic and glycogenolytic actions of glucagon, its role in avian thermoregulation still remains open. Possibly glucagon acts in avian thermoregulation by producing lipolysis and glycogenolysis in the cold, but further oxygen-demanding calorigenesis needs some other agents, e.g. thyroid hormones. REFERENCES CARLSONA. L., LILJEDAHL S.-O., VERDY M. & WIRSEN C. (1964) Unresponsiveness to the lipid mobilizing action of catecholamines in vivo and in vitro in the domestic fowl. Metabolism 13, 227-23 1. DAVIDSONI. W. F., SALTER J. M. & BEST C. H. (1960) The effect of glucagon on the metabolic rate of rats. Am.J. clin. Nutr. 8, 540-546. FREEMANB. M. (1967) Some effects of cold on the metabolism of the fowl during the perinatal period. Camp. Biochem. Physiol. 20, 179-193. FREEMANB. M. (1970) Thermoregulatory mechanisms of the neonate fowl. Corn@. Biochem. Physiol. 33, 219-230. FREEMANB. M. (1971) Impaired thermoregulation in the thio-uracil-treated fowl. Corn@. Biochem. Physiol. 4OA, 553-555. FFEMAN B. M. & MANNINGA. C. C. (1971) Glycogenolysis and lipolysis in Gallus domesticus during the perinatal period. Comp. gen. Pharmac. 2, 198-204. GRANDE F. & PRIGGE W. F. (1970) Glucagon infusion, plasma FFA and triglycerides, blood sugar and liver lipids in birds. Am. J. Physiol. 218, 1406-1411.
EFFECTSOF COLDANDGLUCAGON ON YOUNGCHICKS
495
HEALDP. J., MCLACHLAN P. M. & ROOKLEDGE K. A. (1965) The effects of insulin, glucagon and adrenocorticotrophic hormone on the plasma glucose and free fatty acids of the domestic fowl. J. Endocr. 33, 83-95. HISSA R. Sz PALOKANGAS R. (1970) Thermoregulation in the titmouse (Parus major L.). Comp. Biochem. Physiol. 33, 941-953. HOCH F. L. (1971) Energy Transformations in Mammals: Regulatory Mechanisms. Saunders, Philadelphia. KEMP A. & KITS VANHEIJNINGENM. J. A. (1954) A calorimetric micro-method for the determination of glycogen in tissues. Biochem. J. 56, 646-648. KOSKIMIE~J. & LAHTI L. (1964) Cold-hardiness of the newly hatched young in relation to ecology and distribution in ten species of European ducks. Auk 81, 281-307. PALOKANGAS R. & HISSA R. (1971) Thermoregulation in young black-headed gull (Larus ridibundus L.). camp. Biochem. Physiol. 38A, 743-750. PALOKANGAS R. & VIHKO V. (1971) On the effects of noradrenaline, propranolol and corticosterone on the concentration of free fatty acids in the plasma of the titmouse (Purus major L.). Comp. Biochem. Physiol. 4OB, 813-818. ROMIJN C. & LOKHOR~TW. (1955) Chemical heat regulation in the chick embryo. Poult. Sci. 34, 649-654. Key Word Index-Avian thermoregulation; chick; glucagon; oxygen consumption; glycogen; body temperature; cold exposure.
17
FFA;
blood glucose;
THE EFFECTS OF COLD AND GLUCAGON ON LIPOLYSIS, GLYCOGENOLYSIS AND OXYGEN CONSUMPTION IN YOUNG CHICKS R. PALOKANGAS,
V. VIHKO
and I. NUUJA
Department of Biology, University of Jyvlskylzi, 40100 Jyvlskyll_lO,
Finland
(Received 19 September 1972) To study the possible role of glucagon in avian thermoregulation the effects of cold exposure and glucagon on lipolysis, glycogenolysis and oxygen consumption were measured in young chicks. 2. Cold exposure (+ 1O’C) and glucagon injection (0.3 mg/kg, i.p. at + 30°C) both caused a marked increase in the plasma FFA and a decrease in the liver glycogen content. 3. It is suggested that glucagon possibly acts in the avian thermoregulation by producing at least lipolysis and glycogenolysis during cold exposure.
Abstract-l.
INTRODUCTION
COLD exposure
increases the oxygen consumption of several species of young ducklings (Koskimies & Lahti, 1964), of chicks (Freeman, 1967) and of young black-headed gulls (Palokangas & Hissa, 1971). Plasma-free fatty acid (FFA) levels are also higher in cold-exposed chicks than in those kept at a thermoneutral zone (Freeman, 1967, 1970). The increased oxygen consumption in chicks during cold exposure has been suggested by Freeman (1967) to be the result of an intensive lipid metabolism. Glucagon is known to be a strongly lipolytic and glycogenolytic agent in birds (Grande & Prigge, 1970; Freeman & Manning, 1971). Freeman (1970) has even suggested that chemical thermogenesis might be mediated by glucagon in birds. The purpose of this study was to investigate the possible role of glucagon in the thermoregulation of young chicks. The lipid and carbohydrate metabolisms were studied during cold exposure and after glucagon administration. The measured variables were the most common individual plasma-free fatty acids, blood glucose, liver glycogen, oxygen consumption and body temperature near the thermoneutral zone (at + 30°C) and d uring or after cold exposure (at + 10°C). MATERIALS
AND METHODS
Two-day-old White Leghorn chicks, weighing 40-50 g, were used in the experiments. The chicks were obtained from a commercial hatchery. The birds were kept overnight at an ambient temperature (T,) of + 30°C with water and commercial chick feed ad lib. The experiments were always performed between 0900 and 1200 hr. 489
R. PALOKANGAS, V. VIHKOANDI. NIJUJA
490 Cold exposure
One group of chicks was exposed to + 10°C for 30 min and another group for 60 min to the same temperature. Their simultaneous controls were kept at +3O”C for respective periods. To avoid huddling behavior the chicks were individually placed into plastic jars with blotting paper on the bottom to keep the birds dry and clean from moist feces during the experiment. Glucagon injections Glucagon (E. Lilly, Indianapolis, U.S.A.) was dissolved into 0.9% saline. Injections of glucagon (0.3 or O-6 mg/kg) were given intraperitoneally. The control birds were given a corresponding volume of saline. Oxygen consumfkm Oxygen consumption was measured with a Beckman E 2 Oxygen Analyzer as described earlier by Hissa & Palokangas (1970). M easurements were done every fifth minute during 60 min at + 10°C and at + 30°C. The body temperature (T,,) was measured from the cloaca with a thermocouple (Ellab) before and after the experiments. Each bird was used only once. Chemical analyses The birds were killed by decapitation and blood was collected into test-tubes which contained dried heparin. The individual free fatty acids in plasma were determined by gas chromatography using a Perkin-Elmer 990 gas chromatograph as described earlier by Palokangas & Vihko (1971). The following acids were quantified using n-heptadecanoic acid as an internal standard: pahnitic (C16:0), pahnitoleic (C16:1), stearic (C18:O) and the combined amount of oleic (C18:1), linoleic (C18:2) and linolenic (C18:3) acids (C18:U = unsaturated). The whole blood glucose was determined enzymatically using Biochemica Boehringer’s test packings (TBAP, Boehringer GmbH, Mannheim) and a Perkin-Elmer 124 spectrophotometer. The liver glycogen content was estimated by the method of Kemp & Kits van Heijningen (1954). All chemical determinations were performed as double assays. RESULTS
Cold exposure Cold exposure
of + 10°C
for 30 min caused
a significant
increase
in the level
acid (PC O*OOl), and in the total FFA (the sum of the concentration of acids determined) (P< O-05). Wh en cold exposure was extended to 60 min, the lipolysis was more prominent and the differences were statistically
of plasma-free
palmitic
more significant.
The levels of every acid studied increased
The mean blood glucose concentration but
the
decrease
decreased
was not
32 per cent during
exposure for 60 min. The oxygen consumption intensive
statistically
decreased significant.
the exposure of the chicks
significantly
(Table
The
liver
glycogen
content
for 30 min and 41 per cent during exposed
than that of the birds kept at +3O”C
1).
slightly due to cold exposure,
(Table
to cold (+ 10°C)
the
was more
4).
Glucagon injections
The results on plasma
FFA,
of the experiments blood
glucose
concerning
the effects of glucagon
and liver glycogen
are given in Table
injections 2.
The
Group
Control Test
Control Test
Exposure time (min)
30 30
60 60
P
NS
40 + 2.6 41 + 2.2
45 f 5.2 59 f. 3.7 P
C16:l
NS
257 + 19.5 282 + 15.2
230 z!z13.3 308 * 20.4 < 0.01
Cl6:O
TABLE'&--THEEFFECTOFGLUCAGONINJECTION
NS 270 + 10.5 420 k 23.8 < 0.001
314 f 20.0 341+ 27.2
cl8:u*
NS 172 + 6.2 204 + 8.7 < 0.01
139 f 7.7 142fll.4
C18:O
< 0.05 778 f 23.5 1034 + 46.8 < O*OOl
727 + 31.5 854 rt 53.5
“Total”
217f7.5 199 I!I17.9 NS
NS
351* 37.4 352 f 20.0
314rt 20.0 473 + 64.6 < 0.05
C18:U
FFA &-equiv/l.)
NS
173 f 10.6 190 + 6.4
139 zt 7.7 171 Z!I16.8 NS
Cl8:O
NS
821 f 69.1 864 i 32.9
727 f 31.5 1011 z!z100.7 < 0.025
“Total”
2lOfll*l 263 jz 32.9 < 0.05
230 % 12.6 281 + 3.9 < 0.05
Blood glucose (mg/lOO ml)
100 80
100 87
Relative liver glycogen (%)
100 59
100 68
230 f 12.6 206 f 10.2
NS
Relative liver glycogen (%)
Blood glucose (mg/lOO ml)
2-day-old
(0*3mg/kg) ONTHEPLASMA FFA, BLOODGLUCOSEANDLIVERGLYCOGENOFTHE 2-day-old CHICKS AT + 30°C (MEANf S.E.)
+30 +10
60 60
*U = unsaturated, see text.
< 0.001 292 f 12.2 353 * 15.2 < 0.005
NS 43 f 4.8 56fl.9 P <0.05
P
230 + 13.3 325 f 12.9
45 + 5.2 45 f 4.1
+30 +10
30 30
Cl6:O
Cl6:l
FFA &-equiv/l.)
EFFECTOFCOLDEXPOSURE(+~O~C)ONTHEPLASMA FFA, BLOODGLUCOSEANDLIVERGLYCOGENOFTHE CHICKs(MEANf S.E.)
Exposure time (min)
TABLEI-THE
7 6
7 7
NE
;
N
5
s
3
d
ZX
!2
2
P
-a
8
!I 2
492
‘R. PALOKKANGAS,V. VIHKOAND
I. NUUJA
intraperitoneal glucagon injection (O-3 mg/kg) caused a marked increase in the plasma FFA during the 30-min exposure. The total FFA was about 40 per cent higher in test birds than in control birds. The increase of Cl&unsaturated acids was about 50 per cent ‘and that of palmitic acid 34 per cent. Stearic acid concentration changed the least. The blood glucose level was also higher (PC 0.05) in birds treated with glucagon. Simultaneously the liver glycogen content of the glucagon-injected birds decreased more than that of control birds. Sixty min after injection of glucagon the plasma FFA concentration had already nearly diminished to the same level as in the control birds. In contrast, the concentration of blood glucose was still at a higher level in the test birds (PC 0.05). The liver glycogen content was 20 per cent lower in test than in control birds. The lipolytic effect of glucagon was not readily noticeable in birds which were given glucagon and simultaneously exposed to cold as compared to the coldexposed controls (Table 3). Only the concentration of the plasma-free palmitic acid was significantly higher in the tests (PC O-05). No remarkable changes were seen either in the blood glucose levels or in the liver glycogen contents. The smaller glucagon dose (0.3 mg/kg) d ecreased the oxygen consumption slightly at + 30°C during 60 min exposure. Simultaneously the Tb declined by 3~5°C (Table 4). The dose of 0.6 mg/kg caused a more noticeable decrease in oxygen consumption and the T,, decreased even more (4~4°C). At + 10°C the glucagon injection (0.3 mg/kg) decreased the oxygen consumption significantly (Table 4). The dose of 0.6 mg/kg also decreased the oxygen consumption. The decreases in Tb were also significantly greater in the glucagontreated groups than in the control groups.
DISCUSSION
Cold exposure caused a prominent lipolysis and a slight glycogenolysis in 2-day-old chicks. The previously observed increases in the oxygen consumption of young birds exposed to cold (Koskimies & Lahti, 1964; Palokangas & Hissa, 1971) might partially be related to an increased lipid metabolism as suggested by Romijn & Lokhorst (1955) and Freeman (1967). It is not known in detail how the lipid mobilization is mediated in birds. Catecholamines can probably be discarded in this respect, because they do not cause any lipolysis in birds (e.g. Carlson et al., 1964; Palokangas & Vihko, 1971). Glucagon, on the other hand, is known to be a lipolytic agent in birds (Grande & Prigge, 1970) and Freeman (1970) has suggested that it is involved in the thermogenesis of birds. After glucagon administration the plasma FFA concentration increased significantly during 30 min exposure. This lipolytic effect resembles the effect caused by cold exposure but it was completed 60 min after the glucagon injection. If glucagon is infused into ducks, lipolysis continues for at least 2 hr (Grande & Prigge, 1970). It may be possible, as suggested by Freeman (1970), that lipolysis induced by cold exposure might be mediated by endogenous glucagon.
EFFECTS OF COLD AND GLUCAGON ON YOUNG CHICKS
493
494
R. PALOKANGAS, V. VIHKO ANDI. NUUJA
Confirmation of this, however, demands for example the measurement of glucagon concentration in blood during cold exposure. The glycogenolytic effect of glucagon lasted longer than the lipolytic effect, i.e. at least for an hour. Both of these findings are in agreement with the results reported by Heald et al. (1965) and Freeman & Manning (1971). In cold-exposed chicks an additional glucagon administration did not stimulate the lipolytic effect much more (Table 3). In spite of these findings glucagon did not increase the oxygen consumption of the chicks, but, on the contrary, it seemed to cause a decrease in respiration and T,,. These oxygen consumption and the T,, decreasing effects of glucagon resemble those brought about by catecholamines (Freeman, 1970; Hissa & Palokangas, 1970). Further support to this effect of glucagon is given by the unpublished findings of Nuuja (1971) concerning the house sparrow, and Palokangas (1970) concerning the titmouse and black-headed gull. The reason for this decreased oxygen consumption is unknown. In rats, relatively small doses of glucagon given subcutaneously raise the metabolic rate linearly with the logarithm of the dose (Davidson et al., 1960) and the calorigenic action is rapid, reaching its maximum about 1 hr after the injection. It is known that in mammals the calorigenic action of glucagon depends upon the state of the thyroid, e.g. in thyroidectomized rats glucagon does not increase the oxygen consumption (Hoch, 1971). The importance of the thyroid in the thermoregulation of the neonate chick is also discussed by Freeman (1970, 1971). Why the exogenous glucagon does not interact with the possible active endogenous thyroid hormones to increase the oxygen consumption in birds cannot be answered here. Despite the reported lipolytic and glycogenolytic actions of glucagon, its role in avian thermoregulation still remains open. Possibly glucagon acts in avian thermoregulation by producing lipolysis and glycogenolysis in the cold, but further oxygen-demanding calorigenesis needs some other agents, e.g. thyroid hormones. REFERENCES CARLSONA. L., LILJEDAHL S.-O., VERDY M. & WIRSEN C. (1964) Unresponsiveness to the lipid mobilizing action of catecholamines in vivo and in vitro in the domestic fowl. Metabolism 13, 227-23 1. DAVIDSONI. W. F., SALTER J. M. & BEST C. H. (1960) The effect of glucagon on the metabolic rate of rats. Am.J. clin. Nutr. 8, 540-546. FREEMANB. M. (1967) Some effects of cold on the metabolism of the fowl during the perinatal period. Camp. Biochem. Physiol. 20, 179-193. FREEMANB. M. (1970) Thermoregulatory mechanisms of the neonate fowl. Corn@. Biochem. Physiol. 33, 219-230. FREEMANB. M. (1971) Impaired thermoregulation in the thio-uracil-treated fowl. Corn@. Biochem. Physiol. 4OA, 553-555. FFEMAN B. M. & MANNINGA. C. C. (1971) Glycogenolysis and lipolysis in Gallus domesticus during the perinatal period. Comp. gen. Pharmac. 2, 198-204. GRANDE F. & PRIGGE W. F. (1970) Glucagon infusion, plasma FFA and triglycerides, blood sugar and liver lipids in birds. Am. J. Physiol. 218, 1406-1411.
EFFECTSOF COLDANDGLUCAGON ON YOUNGCHICKS
495
HEALDP. J., MCLACHLAN P. M. & ROOKLEDGE K. A. (1965) The effects of insulin, glucagon and adrenocorticotrophic hormone on the plasma glucose and free fatty acids of the domestic fowl. J. Endocr. 33, 83-95. HISSA R. Sz PALOKANGAS R. (1970) Thermoregulation in the titmouse (Parus major L.). Comp. Biochem. Physiol. 33, 941-953. HOCH F. L. (1971) Energy Transformations in Mammals: Regulatory Mechanisms. Saunders, Philadelphia. KEMP A. & KITS VANHEIJNINGENM. J. A. (1954) A calorimetric micro-method for the determination of glycogen in tissues. Biochem. J. 56, 646-648. KOSKIMIE~J. & LAHTI L. (1964) Cold-hardiness of the newly hatched young in relation to ecology and distribution in ten species of European ducks. Auk 81, 281-307. PALOKANGAS R. & HISSA R. (1971) Thermoregulation in young black-headed gull (Larus ridibundus L.). camp. Biochem. Physiol. 38A, 743-750. PALOKANGAS R. & VIHKO V. (1971) On the effects of noradrenaline, propranolol and corticosterone on the concentration of free fatty acids in the plasma of the titmouse (Purus major L.). Comp. Biochem. Physiol. 4OB, 813-818. ROMIJN C. & LOKHOR~TW. (1955) Chemical heat regulation in the chick embryo. Poult. Sci. 34, 649-654. Key Word Index-Avian thermoregulation; chick; glucagon; oxygen consumption; glycogen; body temperature; cold exposure.
17
FFA;
blood glucose;