,,l,
.I
hi,W. BANNISTER
patible with present knowledge. Firstly, depletion of hepatic glycogen, leaving the bird with inadequate means of maintaining blood glucose concentration. Secondly, raised blood lactate (derived from muscular contraction) that cannot be disposed of normally, and that gives rise to a metabolic acidosis (Balnave rr al.. 1977a). The reduced glucose concentration stimulates adipose tissue lipolysis (hormonally mediated?) leading to elevated plasma free fatty acid concentration. These changes occur very rapidly, they are well established by 6 hr after precipitating the syndrome by removing food (Evans er al. 1977). indeed the hypoglycemia was becoming evident within 2.5 hr. The fatty acids are then taken up by a variety of tissues at a greater rate than they can be oxidised. The excess is esterified and formed into lipid droplets within the cells: this imposes a further burden on the diminishing amount of glucose present because of the requirement for glycerol 3-phosphate. The metabolic acidosis provides an additional threat to survival by altering blood pH and electrolyte balance. Furthermore the increased reductive capacity of hepatic cytoplasm, caused by elevated lactate, may inhibit gluconeogenesis from precursors such as glycerol leading to the observed complete collapse of this fundamental metabolic pathway. It is not known how some birds survive the clinical stage of FLKS. Perhaps, as mentioned earlier, the kidnewcompensate sufficiently to maintain glucose concentrations compatible with life and concomitantly remove lactate from the blood: how the liver subsequently regains its function is unknown. Other aspects of the syndrome are also less well understood for example, the origin and significance of elevated very-low-density lipoproteins in a proportion of affected chicks (Evans et al., 1975) and their possible contribution to fatty infiltration. There is also the appearance of elevated plasma urate levels in some birds (Balnave et al.. 1977a; Bannister et nl.. 1974) that might indicate renal failure despite the gluconeogenic function of the organs being maintained. Clearly then there is still much to be learned about this nutritionally-induced metabolic disorder, which is a fascinating example of interaction between major and micronutrients affecting the development of fundamental pathways. REFERENCES ACHUTAMURTHYP. N. & MISTRYS. P. (1972) Synthesis of biotindependent carboxvlases from their aoooroteins and biotin. 3. scienf. ind. R-es. 31, 554-563. ’ . BALNAVED. & JACKSONN. (1974) The influence of biotin and gonadal hormones on glutamate-metabolizing enzymes in the liver and oviduct of the immature female chick. Inr. J. Biochem. 5, 780-786. BALNAVED. & PEARCEJ. (1976) Aspects of lipid and carbohydrate metabolism, dietary biotin and fatty liver and kidney syndrome in broilers. Br. Pod?. Sci. 17, 627-636. BALNAVED., BERRYM. N. & GUMMINGR. B. (1977a) Clinical signi of fatty liver and kidney syndrome in broilers and their alleviation by the short-term use of biotin or animal tallow. Br. Pot&. Sci. 18, 749-753. BALNAVED.. GUMMINGR. B. & SUTHERLAND T. M. (1977b) A biochemical explanation for the fatty liver and kidney syndrome of broilers: its alleviation by the short-term use of dietary fat. Br. J. Nutr. 38, 319-328. BALNAVED., WOLFENDEN J., BALLF. M.. GUMMINGR. B. & LENG R. A. (1977~) Studies of fatty liver and kidney
syndrome in chickens: dynamics of glucose metabolism. Br. J. Nutr.
38, 329-334.
BANNISTERD. W. (1976a) Hepatic gluconeogenesis in chicks: effect of biotin on gluconeogenesis in biotin-deficiency and fatty liver and kidney syndrome. Camp. Biochrm. Phpsiol. 53B, 57>579. BANNISTERD. W. (1976b) The biochemistry of fatty liver and kidney syndrome: biotin-mediated restoration of hepatic gluconeogenesis in vitro and its relationship to pyruvate carboxylase activity. B&hem. J. 156, 167173. BANNISTERD. W. & EVANS A. J. (1974) The fatty liver and kidney syndrome in poultry: biochemical aspects. In Cosf/Eficrireness of Micro-Nutrient Supplementation, pp 63-70. Roche Symposium. BANNISTER D. W. & CLELANDM. E. (1977) The biochemistry of fatty liver and kidney syndrome of the fowl (Callus domesticus): reduced gluconeogenesis from precursors that are independent of pyruvate carboxylase. Inr. J. Biothem.
8, 869-875.
BANNISTER D. W. & CLELANDM. E. (1978) The biochemistry of fatty liver and kidney syndrome of the fowl (GUI/US domesticus): effects of fasting and fastinglre-reeding on renal gluconeogenesis in chicks fed on the syndromeinducing diet. Int. J. Biochem. 9, 531-537. BANNISTER D. W.. EVANSA. J. & WHITEHEAD C. C. (1975a) Evidence for a lesion in carbohydrate metabolism in fatty liver and kidney syndrome in chicks. Res. ret. Sci. 18, 149-156. BANNISTER D. W.. EVANSA. J. & WHITEHEAD C. C. (1975b) Carbohydrate absorption by chicks affected with the fatty liver and kidney syndrome. Res. ref. Sci. 19. 9C-92. BANNISTERD. W., BURNSA. B.. EVANSA. J. & MARTINDALEL. (1974) Interference by urate in the determination of plasma glucose. Br. Poulr: SC;. 15, 421-425. BAXTERR. M. & OUASTELJ. H. (1953) The enzymatic breakdown of d-biotin in vitro. J. hiol. Chek 201, 751-764. BELL D. J. (1971) Plasma glucose. In Physiology and Biochemisrrj, of rhe Domesric Fowl (Edited by BELL D. J. & FREEMANB. M.) Vol. 2, pp. 913-920. Academic Press, London. BHAGAVANH. N. & COURSIND. B. (1974) Nucleic acid incorporation of and protein contents, and L-[U-“Clleucine into proteins of brain and liver in biotin-deficient rats. Int. J. cit. Nutr. Res. 44, 363-369. BLAIR R.. BOLTONW. & DUFF R. H. (1969) Fatty liver and kidney disease in broiler chickens receiving diets with varying contents of protein. Vet. Rec. 84, 41-43. BLAIRR., WHITEHEADC. C. & TEAGUEP. W. (1975) The effect of dietary fat and protein levels. form and cereal type on fatty liver and kidney syndrome in chicks. Res. ref. SC;. 18, 76-81. BLAIR R.. WHITEHEADC. C.. BANNISTER D. W. & EVANS A. J. (1973) Involvement of diet in fatty liver and kidney syndrome in broiler chickens. Vet. Rec. 92, 118-l 19. BOECKX R. L. & DAKSHINAMURTIK. (1974) Biotinmediated protein biosynthesis. Biochem. J. 140, 549-556. BOECKXR. L. & DAKSHINAMURTt K. (1975) Effect of biotin on ribonucleic acid synthesis. Biochim. hiophys. Acrcr 383. 2X2-289.
DAKSH~NAMURTI K. & CHEAH-TAN C. (1968) Biotinmediated synthesis of hepatic glucokinase in the rat. Archs Biochem. Biophys. 127, 17-21. EVANSA. J. (1972) III ritro lipogenesis in the liver and adipose tissue of the female Aylesbury duck at different ages. Br. Pod?. Sri. 13, 59>602. EVANSA. J., BANNISTER D. W. & WHITEHEAD C. C. (1975) Some aspects of lipid metabolism in fatty liver and kidney synd’rome in chicks. Res. ref. Sci. 18. 2&31. EVANSA. J.. BANNISTER D. W.. WHITEHEADC: C.. SILLER W. G. & WIGH~ P. A. L. (1977) Changes in plasma lipid and glucose levels during the onset of fatty liver and kidney syndrome in chicks. Res. ret. Sri. 23, 275-279.
Recent GOODRIIXX A. G. (1968a)
advances
in avian
Citrate-cleavage enzyme. ‘malic’ enzyme and certain dehydrogenases in embryonic and growing chicks. Biorhem. J. 108, 663-666. GOODRIDGE A. G. (1968b) The effect of starvation and starvation followed by feeding on enzyme activity and the metabolism of [U-‘4C]glucose in liver from growing chicks. Biorhem. J. 108, 667-673. GOODRID~E A. G. & BALL E. G. (1966) Lipogenesis in the oieeon: in vitro studies. Am. J. Phvsiol. 211, 803-808. G&RIDC;E A. G. & BALL E. G. (196?) Lipogenesis in the pigeon: in ciao studies, Am. J. Physiol. 213, 245-249. HEMSLEY L. A. (1965) The fatty liver and kidney syndrome of young chickens. Vet. Rec. 77, 124-126. HEMSLEY L. A. (1973) The effect of sugar, molasses and litter age on the fatty liver and kidney syndrome of voune chickens. Vet. Rec. 93. 25&257. HOOD i. L., JOHNSON A. R.. FOC~ERTYA. C. & PEARSON J. A. (1976) Fatty liver and kidney syndrome in chicks. II. Biochemical role of biotin. Au.@. J. hid. Sci. 29, 429-44 I. JANSEN G. R.. HUT~HISON C. F. & ZANETTI M. E. (1966) Studies on lipogenesis in rice: effect of dietary fat or starvation on conversion of [‘4C]glucose into fat and turnover of newly synthesised fat. Biochem. J. 99, 323--33X KREBS H. A. (1972) The Pasteur effect and the relations between respiration and fermentation. In E.ssc~~s i!l Biochemistry (Edited by CAMPBELL P. N. & DICKENS F.) Vol. 8. pp. l-34. Academic Press. London. LAURSEN-JONES A. P. (1971) Fatty liver and kidney syndrome in chickens: a review. Proc. XIXrh W/d. Vet. Conp-. 3, 1165-l 168. LEvEtLLE G. A., ROMS~S D. R., YEH Y-Y. & O’HEA E. K. (1975) Lipid biosynthesis in the chick. A consideration of site of synthesis. influence of diet and possible regulatory mechanisms. Poulr. Sci. 54, 1075-1093. MAJERUS P. W. & KILBURN E. (1969) Acetyl-CoA carboxylase. The roles of synthesis and degradation in regulation of enzyme levels in rat liver. J. hid. Chem. 244. 6254-6262. O’H~A E. K. & LEVEILLE G. A. (1969) Lipid biosynthesis and transport in the domestic chick (Gullus domesticus). Camp. Biochem. Physiol. 30, 149-159. PAYNE C. G.. GILCHRIST P., PEARSON J. A. & HEMSLEY L. A. (1974) Involvement of biotin in the fatty liver and kidney syndrome of broilers. Br. Poulf. Sci. 15, 489-498. PEARCE J. (1975) The effects of choline and inositol on hepatic lipid metabolism and the incidence of the fatty liver and kidney syndrome in broilers. Br. Poult. Sci. 16, 565-570. PEARCE J. (1977) Minireview: some differences between avian and mammalian biochemistry. Int. J. Biochem. 8, 269-275. PEARCE J. & BROWN W. 0. (1971) Carbohydrate metabolism. In Physioloyy und Biochemistry sf the Domestic
biochemistry
I99
Fotil/ (Edited by BELL D. J. & FREIIMAN B. M.) Vol. I, pp. 295-319. Academic Press, London. PEARSON J., JOHNSON A. R.. HOOD R. L. & FO~;I.RTY A. C. (1976) Fatty liver and kidney syndrome in chicks. 1. EtTect of biotin in diet. Ausf. J. hid. Sci. 29. 4 19-428. RIDDELL C., OLSEN G. V. & GRIMSON R. E. (1971) Fatty liver and kidney syndrome in a broiler flock. Arictn t/is. 15, 398-405. ROLAND D. A. & EDWARDS H. M. (1971) Effect of essential fatty acid deficiency and type of dietary fat supplementation biotin-deficient chicks. J. Nutr. 101, 81 I -XIX. SHRAGO E.. GLENNON J. A. & GORDON E. S. (1971) Comparative aspects of lipogenesis in mammalian tissues. Mrruholism
20, 54-62.
SILLER W. G. & WIC;HT P. A. L. (1976) An ultrastructural study of the liver. kidney and myocardium in the fatty liver and kidney syndrome in the fowl. Res. WI. Ser. 21, 79-89. WHITEHEADC. C. (1975) Tissue
lipid composition in fatty liver and kidney syndrome. Res. wt. Sri. 18. 32-35. WHITEHEAD C. C. & BLAIR R. (1974a) Fatty liver and kidney syndrome in chicks: the involvement of dietary energy-protein ratio and house temperature. Rrs. ret. Sri. 17, 8690. WHtTEHEAD C. C. & BLAIR R. (1974b) The involvement of biotin in the fatty liver and kidney syndrome in broiler chickens. Wld. Poult. Sci. J. 30, 231. WHITEHEAD C. C.. BANNISTER D. W. & CLI..LANI) M. E. (1978) Metabolic changes associated with the occurrence of patty liver and kidney syndrome in chicks. Br. J. Nlrtv. 40. 22 I-234. WHITEHEAD C. C., BLAIR R., BANNISTER D. W. & EVANS A. J. (1975) The involvement of dietary fat and vitamins. stress, litter and starvation on the incidence of the Fatty liver and kidney syndrome in chicks. Res. ret. Sc,i. 18, lO&lO4. WHITEHEAD C. C., BANNISTER D. W.. EVANS A. J.. SII.LI:R W. G. 8~ WIGHT P. A. L. (1976a) Biotin deficiency and fatty liver and kidney syndrome in chicks given purified diets containing different fat and protein levels. Br. J. Nurr. 35, 115-125. WHITEHEAD C. C., BLAIR R.. BANNISTER D. W., EVANS A. J. & MORLEY JONES R. (1976b) The involvement of biotin in preventing the fatty liver and kidney syndrome in chicks. Res. ret. Sci. 20, 18&184. WIGHT P. A. L. (1975a) The neuropathology of the fatty liver and kidney syndrome of chicks. Neuroptrthol. upplied Neurohiol. I. 231-245. WIGHT P. A. L. (1975b) Histopathology of the adrenal glands in the fatty liver and kidney syndrome of chickens. J. romp. Poth. 85. 539-548. WIC;HT P. A. L. & ‘SILLERW. 6. (1975) The histopathology of fatty liver and kidney syndrome in chicks. Rc\. wt. Sci. 19. 173-184.
.I
hi,W. BANNISTER
patible with present knowledge. Firstly, depletion of hepatic glycogen, leaving the bird with inadequate means of maintaining blood glucose concentration. Secondly, raised blood lactate (derived from muscular contraction) that cannot be disposed of normally, and that gives rise to a metabolic acidosis (Balnave rr al.. 1977a). The reduced glucose concentration stimulates adipose tissue lipolysis (hormonally mediated?) leading to elevated plasma free fatty acid concentration. These changes occur very rapidly, they are well established by 6 hr after precipitating the syndrome by removing food (Evans er al. 1977). indeed the hypoglycemia was becoming evident within 2.5 hr. The fatty acids are then taken up by a variety of tissues at a greater rate than they can be oxidised. The excess is esterified and formed into lipid droplets within the cells: this imposes a further burden on the diminishing amount of glucose present because of the requirement for glycerol 3-phosphate. The metabolic acidosis provides an additional threat to survival by altering blood pH and electrolyte balance. Furthermore the increased reductive capacity of hepatic cytoplasm, caused by elevated lactate, may inhibit gluconeogenesis from precursors such as glycerol leading to the observed complete collapse of this fundamental metabolic pathway. It is not known how some birds survive the clinical stage of FLKS. Perhaps, as mentioned earlier, the kidnewcompensate sufficiently to maintain glucose concentrations compatible with life and concomitantly remove lactate from the blood: how the liver subsequently regains its function is unknown. Other aspects of the syndrome are also less well understood for example, the origin and significance of elevated very-low-density lipoproteins in a proportion of affected chicks (Evans et al., 1975) and their possible contribution to fatty infiltration. There is also the appearance of elevated plasma urate levels in some birds (Balnave et al.. 1977a; Bannister et nl.. 1974) that might indicate renal failure despite the gluconeogenic function of the organs being maintained. Clearly then there is still much to be learned about this nutritionally-induced metabolic disorder, which is a fascinating example of interaction between major and micronutrients affecting the development of fundamental pathways. REFERENCES ACHUTAMURTHYP. N. & MISTRYS. P. (1972) Synthesis of biotindependent carboxvlases from their aoooroteins and biotin. 3. scienf. ind. R-es. 31, 554-563. ’ . BALNAVED. & JACKSONN. (1974) The influence of biotin and gonadal hormones on glutamate-metabolizing enzymes in the liver and oviduct of the immature female chick. Inr. J. Biochem. 5, 780-786. BALNAVED. & PEARCEJ. (1976) Aspects of lipid and carbohydrate metabolism, dietary biotin and fatty liver and kidney syndrome in broilers. Br. Pod?. Sci. 17, 627-636. BALNAVED., BERRYM. N. & GUMMINGR. B. (1977a) Clinical signi of fatty liver and kidney syndrome in broilers and their alleviation by the short-term use of biotin or animal tallow. Br. Pot&. Sci. 18, 749-753. BALNAVED.. GUMMINGR. B. & SUTHERLAND T. M. (1977b) A biochemical explanation for the fatty liver and kidney syndrome of broilers: its alleviation by the short-term use of dietary fat. Br. J. Nutr. 38, 319-328. BALNAVED., WOLFENDEN J., BALLF. M.. GUMMINGR. B. & LENG R. A. (1977~) Studies of fatty liver and kidney
syndrome in chickens: dynamics of glucose metabolism. Br. J. Nutr.
38, 329-334.
BANNISTERD. W. (1976a) Hepatic gluconeogenesis in chicks: effect of biotin on gluconeogenesis in biotin-deficiency and fatty liver and kidney syndrome. Camp. Biochrm. Phpsiol. 53B, 57>579. BANNISTERD. W. (1976b) The biochemistry of fatty liver and kidney syndrome: biotin-mediated restoration of hepatic gluconeogenesis in vitro and its relationship to pyruvate carboxylase activity. B&hem. J. 156, 167173. BANNISTERD. W. & EVANS A. J. (1974) The fatty liver and kidney syndrome in poultry: biochemical aspects. In Cosf/Eficrireness of Micro-Nutrient Supplementation, pp 63-70. Roche Symposium. BANNISTER D. W. & CLELANDM. E. (1977) The biochemistry of fatty liver and kidney syndrome of the fowl (Callus domesticus): reduced gluconeogenesis from precursors that are independent of pyruvate carboxylase. Inr. J. Biothem.
8, 869-875.
BANNISTER D. W. & CLELANDM. E. (1978) The biochemistry of fatty liver and kidney syndrome of the fowl (GUI/US domesticus): effects of fasting and fastinglre-reeding on renal gluconeogenesis in chicks fed on the syndromeinducing diet. Int. J. Biochem. 9, 531-537. BANNISTER D. W.. EVANSA. J. & WHITEHEAD C. C. (1975a) Evidence for a lesion in carbohydrate metabolism in fatty liver and kidney syndrome in chicks. Res. ret. Sci. 18, 149-156. BANNISTER D. W.. EVANSA. J. & WHITEHEAD C. C. (1975b) Carbohydrate absorption by chicks affected with the fatty liver and kidney syndrome. Res. ref. Sci. 19. 9C-92. BANNISTERD. W., BURNSA. B.. EVANSA. J. & MARTINDALEL. (1974) Interference by urate in the determination of plasma glucose. Br. Poulr: SC;. 15, 421-425. BAXTERR. M. & OUASTELJ. H. (1953) The enzymatic breakdown of d-biotin in vitro. J. hiol. Chek 201, 751-764. BELL D. J. (1971) Plasma glucose. In Physiology and Biochemisrrj, of rhe Domesric Fowl (Edited by BELL D. J. & FREEMANB. M.) Vol. 2, pp. 913-920. Academic Press, London. BHAGAVANH. N. & COURSIND. B. (1974) Nucleic acid incorporation of and protein contents, and L-[U-“Clleucine into proteins of brain and liver in biotin-deficient rats. Int. J. cit. Nutr. Res. 44, 363-369. BLAIR R.. BOLTONW. & DUFF R. H. (1969) Fatty liver and kidney disease in broiler chickens receiving diets with varying contents of protein. Vet. Rec. 84, 41-43. BLAIRR., WHITEHEADC. C. & TEAGUEP. W. (1975) The effect of dietary fat and protein levels. form and cereal type on fatty liver and kidney syndrome in chicks. Res. ref. SC;. 18, 76-81. BLAIR R.. WHITEHEADC. C.. BANNISTER D. W. & EVANS A. J. (1973) Involvement of diet in fatty liver and kidney syndrome in broiler chickens. Vet. Rec. 92, 118-l 19. BOECKX R. L. & DAKSHINAMURTIK. (1974) Biotinmediated protein biosynthesis. Biochem. J. 140, 549-556. BOECKXR. L. & DAKSHINAMURTt K. (1975) Effect of biotin on ribonucleic acid synthesis. Biochim. hiophys. Acrcr 383. 2X2-289.
DAKSH~NAMURTI K. & CHEAH-TAN C. (1968) Biotinmediated synthesis of hepatic glucokinase in the rat. Archs Biochem. Biophys. 127, 17-21. EVANSA. J. (1972) III ritro lipogenesis in the liver and adipose tissue of the female Aylesbury duck at different ages. Br. Pod?. Sri. 13, 59>602. EVANSA. J., BANNISTER D. W. & WHITEHEAD C. C. (1975) Some aspects of lipid metabolism in fatty liver and kidney synd’rome in chicks. Res. ref. Sci. 18. 2&31. EVANSA. J.. BANNISTER D. W.. WHITEHEADC: C.. SILLER W. G. & WIGH~ P. A. L. (1977) Changes in plasma lipid and glucose levels during the onset of fatty liver and kidney syndrome in chicks. Res. ret. Sri. 23, 275-279.
Recent GOODRIIXX A. G. (1968a)
advances
in avian
Citrate-cleavage enzyme. ‘malic’ enzyme and certain dehydrogenases in embryonic and growing chicks. Biorhem. J. 108, 663-666. GOODRIDGE A. G. (1968b) The effect of starvation and starvation followed by feeding on enzyme activity and the metabolism of [U-‘4C]glucose in liver from growing chicks. Biorhem. J. 108, 667-673. GOODRID~E A. G. & BALL E. G. (1966) Lipogenesis in the oieeon: in vitro studies. Am. J. Phvsiol. 211, 803-808. G&RIDC;E A. G. & BALL E. G. (196?) Lipogenesis in the pigeon: in ciao studies, Am. J. Physiol. 213, 245-249. HEMSLEY L. A. (1965) The fatty liver and kidney syndrome of young chickens. Vet. Rec. 77, 124-126. HEMSLEY L. A. (1973) The effect of sugar, molasses and litter age on the fatty liver and kidney syndrome of voune chickens. Vet. Rec. 93. 25&257. HOOD i. L., JOHNSON A. R.. FOC~ERTYA. C. & PEARSON J. A. (1976) Fatty liver and kidney syndrome in chicks. II. Biochemical role of biotin. Au.@. J. hid. Sci. 29, 429-44 I. JANSEN G. R.. HUT~HISON C. F. & ZANETTI M. E. (1966) Studies on lipogenesis in rice: effect of dietary fat or starvation on conversion of [‘4C]glucose into fat and turnover of newly synthesised fat. Biochem. J. 99, 323--33X KREBS H. A. (1972) The Pasteur effect and the relations between respiration and fermentation. In E.ssc~~s i!l Biochemistry (Edited by CAMPBELL P. N. & DICKENS F.) Vol. 8. pp. l-34. Academic Press. London. LAURSEN-JONES A. P. (1971) Fatty liver and kidney syndrome in chickens: a review. Proc. XIXrh W/d. Vet. Conp-. 3, 1165-l 168. LEvEtLLE G. A., ROMS~S D. R., YEH Y-Y. & O’HEA E. K. (1975) Lipid biosynthesis in the chick. A consideration of site of synthesis. influence of diet and possible regulatory mechanisms. Poulr. Sci. 54, 1075-1093. MAJERUS P. W. & KILBURN E. (1969) Acetyl-CoA carboxylase. The roles of synthesis and degradation in regulation of enzyme levels in rat liver. J. hid. Chem. 244. 6254-6262. O’H~A E. K. & LEVEILLE G. A. (1969) Lipid biosynthesis and transport in the domestic chick (Gullus domesticus). Camp. Biochem. Physiol. 30, 149-159. PAYNE C. G.. GILCHRIST P., PEARSON J. A. & HEMSLEY L. A. (1974) Involvement of biotin in the fatty liver and kidney syndrome of broilers. Br. Poulf. Sci. 15, 489-498. PEARCE J. (1975) The effects of choline and inositol on hepatic lipid metabolism and the incidence of the fatty liver and kidney syndrome in broilers. Br. Poult. Sci. 16, 565-570. PEARCE J. (1977) Minireview: some differences between avian and mammalian biochemistry. Int. J. Biochem. 8, 269-275. PEARCE J. & BROWN W. 0. (1971) Carbohydrate metabolism. In Physioloyy und Biochemistry sf the Domestic
biochemistry
I99
Fotil/ (Edited by BELL D. J. & FREIIMAN B. M.) Vol. I, pp. 295-319. Academic Press, London. PEARSON J., JOHNSON A. R.. HOOD R. L. & FO~;I.RTY A. C. (1976) Fatty liver and kidney syndrome in chicks. 1. EtTect of biotin in diet. Ausf. J. hid. Sci. 29. 4 19-428. RIDDELL C., OLSEN G. V. & GRIMSON R. E. (1971) Fatty liver and kidney syndrome in a broiler flock. Arictn t/is. 15, 398-405. ROLAND D. A. & EDWARDS H. M. (1971) Effect of essential fatty acid deficiency and type of dietary fat supplementation biotin-deficient chicks. J. Nutr. 101, 81 I -XIX. SHRAGO E.. GLENNON J. A. & GORDON E. S. (1971) Comparative aspects of lipogenesis in mammalian tissues. Mrruholism
20, 54-62.
SILLER W. G. & WIC;HT P. A. L. (1976) An ultrastructural study of the liver. kidney and myocardium in the fatty liver and kidney syndrome in the fowl. Res. WI. Ser. 21, 79-89. WHITEHEADC. C. (1975) Tissue
lipid composition in fatty liver and kidney syndrome. Res. wt. Sri. 18. 32-35. WHITEHEAD C. C. & BLAIR R. (1974a) Fatty liver and kidney syndrome in chicks: the involvement of dietary energy-protein ratio and house temperature. Rrs. ret. Sri. 17, 8690. WHtTEHEAD C. C. & BLAIR R. (1974b) The involvement of biotin in the fatty liver and kidney syndrome in broiler chickens. Wld. Poult. Sci. J. 30, 231. WHITEHEAD C. C.. BANNISTER D. W. & CLI..LANI) M. E. (1978) Metabolic changes associated with the occurrence of patty liver and kidney syndrome in chicks. Br. J. Nlrtv. 40. 22 I-234. WHITEHEAD C. C., BLAIR R., BANNISTER D. W. & EVANS A. J. (1975) The involvement of dietary fat and vitamins. stress, litter and starvation on the incidence of the Fatty liver and kidney syndrome in chicks. Res. ret. Sc,i. 18, lO&lO4. WHITEHEAD C. C., BANNISTER D. W.. EVANS A. J.. SII.LI:R W. G. 8~ WIGHT P. A. L. (1976a) Biotin deficiency and fatty liver and kidney syndrome in chicks given purified diets containing different fat and protein levels. Br. J. Nurr. 35, 115-125. WHITEHEAD C. C., BLAIR R.. BANNISTER D. W., EVANS A. J. & MORLEY JONES R. (1976b) The involvement of biotin in preventing the fatty liver and kidney syndrome in chicks. Res. ret. Sci. 20, 18&184. WIGHT P. A. L. (1975a) The neuropathology of the fatty liver and kidney syndrome of chicks. Neuroptrthol. upplied Neurohiol. I. 231-245. WIGHT P. A. L. (1975b) Histopathology of the adrenal glands in the fatty liver and kidney syndrome of chickens. J. romp. Poth. 85. 539-548. WIC;HT P. A. L. & ‘SILLERW. 6. (1975) The histopathology of fatty liver and kidney syndrome in chicks. Rc\. wt. Sci. 19. 173-184.
