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Biomedical subjects

C C Whitehead

Publications and source records attributed to C C Whitehead.

At least 109 records · Page 6Linked to original sources
PubMed1978

Blood pyruvate carboxylase (EC 6.4.1.1) activity as a criterion of biotin status in chickens and turkeys.

1. Blood pyruvate carboxylase (pyruvate-CO2 ligase (ADP-forming); EC 6.4.1.1; PC) activities in young chickens and turkeys given low-biotin diets supplemented with biotin at graded levels were studied in three experiments. 2. In both species PC activity was related positively to the supplemental biotin level. The relationship was sigmoid and maximum activity was attained with supplemental levels above those required to give maximal growth response. 3. Enzyme activity decreased between 2 and 4 weeks of age but remained almost constant thereafter. 4. Activity in chicks was not affected by alterations in the fat or protein content of the diet. 5. Changing poults from high to low and from low to high supplemental biotin levels resulted in reversals in the levels of enzyme activity. 6. It is concluded that blood PC activity is a promising new criterion for assessing the biotin status of young chickens and turkeys.

Aging↗
PubMed1978

Metabolic changes associated with the occurrence of fatty liver and kidney syndrome in chicks.

1. The changes in a number of metabolic measurements brought about by low-biotin diets associated with high and low incidences of fatty liver and kidney syndrome (FLKS) were studied in healthy 4-week-old broiler chicks. 2. Liver pyruvate carboxylase (pyruvate: CO2 ligase (ADP); EC 6.4.1.1) activity was low in birds fed on a diet causing a high incidence FLKS but the addition of fat or protein to this diet, to decrease the incidence of FLKS, increased enzyme activity. 3. Liver weights, blood lactate concentrations, plasma lactate dehydrogenase (L-lactate: NAD oxidoreductase; EC 1.1.1.27) activitvities and values for C16:1 : C18:0 fatty acid in liver, adipose tissue and plasma triglyceride were highest in birds fed on the high-FLKS diet and all measurements were negatively correlated with pyruvate carboxylase activity. 4. Birds with high plasma lactate dehydrogenase activity or triglyceride C16:1 : C18:0 values were the most likely to develop FLKS when fasted. 5. There was no evidence that increased liver weight was associated with increase activities of certain other liver enzymes. 6. It is concluded that FLKS occurs in birds with little or no hepatic gluconeogenic capacity via pyruvate carboxylase as a result of a dietary insufficiency of biotin but that the initiation of the syndrome in probably associated with the inhibition of other pathways of gluconeogenesis.

Animals↗
PubMed1977

Changes in plasma lipid and glucose levels during the onset of fatty liver and kidney syndrome in chics.

Plasma glucose, free fatty acid and triglyceride levels were measured during the onset of fatty liver and kidney syndrome in chicks. Intial studies indicated that behavioural and clinical changes characteristically associated with the syndrome were observed only during the 24 h preceding death. A more detailed examination of the blood changes was made on fasted birds. Typically, affected birds could be distinguished from healthy fasted birds by a hypoglycaemia which developed within 2.5 h of the removal of food, and a slightly higher and more sustained elevation of free fatty acid levels. Triglyceride values were not generally different from those found in normal birds. Although moderate to large amounts of lipid were occasionally observed in the kidneys of healthy fasted birds, only in affected birds was significant lipid infiltration of the kidneys associated with a similar level of lipid infiltration of the liver. In extreme cases death from fatty liver and kidney syndrome could occur within 4 h of the removal of food.

Animals↗
PubMed1976

Biotin deficiency and fatty liver and kidney syndrome in chicks given purified diets containing different fat and protein levels.

1. The occurence of biotin deficiency and fatty liver and kidney syndrome (FLKS) in chicks was studied using a 2x2x2x2 factorial-design experiment in which the variables were dietary biotin, fat and protein, and starvation. 2. The severity of biotin deficiency, using growth retardation and severity of dermal lesions as criteria, was least when the low-biotin diet also contained low levels of fat and protein. Addition of fat or protein increased the severity of the deficiency. Tissue fatty acid composition was affected by biotin deficiency only in those birds given the low-protein, low-fat diet. The main change was an increase in the ratio, 16:1 fatty acids :18:0 fatty acids. Plasma glucose and free fatty acid levels in non-fasted birds were unaffected by the dietary variables. 3. Mortality from FLKS with the diet containing low biotin, fat and protein levels was 52% at 28d, but was reduced or eliminated when the dietary level of any of these ingredients was increased. 4. Starvation considerably increased the incidnece of FLKS in the period immediately after fasting, and also affected plasma glucose and free fatty acid concentrations. Liver fatty acid composition, indicated an increase in the proportion of 18:0 at the expense of 16:1 and concentrations increased in proportion, at the expense of 18:0. 5. The relationship between biotin deficiency and FLKS, and a possible mechanism for the induction of FLKS by starvation are discussed.

Adipose Tissue↗
PubMed1976

Effect of dietary palmitic acid on broiler chicks fed on various concentrations of calcium.

1. The effect of dietary palmitic acid on body weight and bone-ash of chicks fed three concentrations of calcium was studied in a 2 X 3 factorial design (0 and 10% palmitic acid, 0.4, 0.7 and 1.0% calcium). 2. Body weight of chick not influenced by the calcium concentration when palmitic acid was not included in the diet. 3. When 10% palmitic acid was included the body weight of chicks fed 0.4 and 0.7% calcium was lower (P less than 0.01) than for the other groups. 4. Bone-ash was lower (P less than 0.01) for chicks fed 0.4% calcium than for the other two calcium concentrations when palmitic acid was not added and palmitic acid at 10% of the diet reduced bone-ash of the chicks fed 0.4 and 0.7% calcium (P less than 0.01).

Animal Feed↗
PubMed1976

An assessment of the optimal range of dietary sodium for inducing a pause in laying.

Laying hens were fed on a diet containing 0-9 g sodium/kg until 34 weeks of age, then groups were fed on diets containing 0-2, 0-3,0-4, 0-5, 0-6 or 0-9 g sodium/kg for 16 weeks before that containing 0-9 g sodium/kg was reintroduced for all birds. 2. Egg production and food consumption were depressed by the low-sodium diets in proportion to the dietary sodium content. 3. Birds receiving 0-3 to 0-6 g sodium/kg diet lost weight initially but subsequently gained weight; birds receiving 0-2 sodium/kg diet lost weight continouosly. 4. In birds receiving 0-2 g sodium/kg diet, the reproductive organs were completely regressed, whereas these organs resembled those of point-of-lay pullets in birds fed on 0-3 or 0-4 g sodium/kg. 5. When the control diet was reintroduced, birds which had received the low-sodium diets resumed normal egg production and food consumption and regained body weight. 6. The optimal range of dietary sodium for inducing a pause in egg laying is 0-3 to 0-4 g/kg.

Animal Feed↗
PubMed1976

The involvement of biotin in preventing the fatty liver and kidney syndrome in chicks.

Three experiments were carried out to investigate the involvement of vitamins in the fatty liver and kidney syndrome. The compounds studied, singly and in combination, were thiamin, riboflavin, nicotinic acid, pyridoxine, pantothenic acid, biotin, folic acid vitamin B12, ascorbic acid, choline and inositol and of these, only biotin prevented the syndrome. The minimum levels of supplemental dietary biotin required to prevent mortality varied from 0-05 to 0-15 mg/kg, depending on the diet. These levels were higher than the amounts required for maximum liveweight.

Animal Feed↗
PubMed1976

The involvement of further nutritional factors in the fatty liver and kidney syndrome in chicks.

Supplementing chick diets causing fatty liver and kidney syndrome (FLKS) with a wide range of minerals or with antibiotics did not affect mortality significantly but supplements of isolated soy protein or a mixture of crystalline amino acids were both equally effective in reducing mortality. Biotin supplementation of the parent flock diet subsequent mortality among the progeny by 30 per cent. Data on the age-distribution of the syndrome and the general conclusions from a whole series of experiments are presented.

Age Factors↗
PubMed1975

The utilisation of various fats by turkeys of different ages.

1. The utilisation of fat and fatty acids supplied as maize oil, tallow or lard in the diet of 2-, 4- and 8-week old turkeys has been investigated: a mixture of 10% fat and 15% cellulose replaced glucose monohydrate in a low-fat basal diet. 2. At 2 weeks of age the absorbabilities of the fats were 96, 57 and 91% for maize oil, tallow and lard respectively; at 4 and 8 weekds of age the corresponding figures were 97, 70 and 92% and 98, 74 and 90%. 3. The unsaturated fatty acids (18:1, 18:2) were highly absorbed from all fats; this was true also of the saturated acids (16:0, 18:0) in the maize oil, but in lard and, especially, tallow the absorbability of these fatty acids was lower. 4. The effect of age on the utilisation of tallow could be explained by the improvement in the absorption of these fatty acids. 5. The determined and calculated ME values of the fats are given.

Age Factors↗
PubMed1975

The involvement of dietary fat and vitamins, stress, litter and starvation on the incidence of the fatty liver and kidney syndrome in chicks.

Dietary and environmental factors involved in the fatty liver and kidney syndrome (FLKS) were studied. Addition of maize oil, tallow or olive oil isoenergetically at the expense of starch to the standard highmortality diet reduced mortality from 19 to 7 per cent. Supplementation of the standard diet with a mixture of vitamins reduced mortality to 1 per cent whereas supplementation with thiamin alone reduced it to 11 per cent. Mortality was 53 per cent higher among females than males. At 25 days of age mortality was 94 per cent higher among birds that had been subjected to repeated stressing. Withdrawal of food on day 36 resulted in a marked increase in mortality.

Animal Feed↗
PubMed1975

Tissue lipid composition in fatty liver and kidney syndrome in chicks.

The lipid composition of the liver, kidneys, heart and adipose tissue of chicks affected by the fatty liver and kidney syndrome were analysed. Livers and kidneys showed 400 to 500 per cent increases in heart lipid levels. Liver and kidney triglycerides contained increased proportions of mono-unsaturated fatty acids, mainly palmitoleic acid, at the expense of the saturated fatty acids, mainly stearic acid. Phospholipid and adipose tissue fatty acid composition were not markedly altered. The abnormalities were regressing in birds recovering from the syndrome.

Adipose Tissue↗
PubMed1975

The effect of dietary fat and protein levels, form and cereal type on fatty liver and kidney syndrome in chicks.

A total of 4200 day-old Ross I broiler chicks were subjected to an ambient temperature 2 to 3C degrees higher than normal and were fed various diets to determine the effects of dietary factors and sex on mortality from fatty liver and kidney syndrome (FLKS). In a first experiment mortality was not significantly influenced by cereal type (barley or wheat) but was influenced significantly by fat content of the diet. In a second experiment mortality was increased significantly with a low protein diet and with a pelleted one compared with a mash diet. In both experiments mortality was signigicantly higher in females than in males. High levels of protein and fat in the diet had a protective influence on mortality but the results, especially with pelleted diets, suggested that some other nutrient(s) might be involved in the syndrome.

Animal Feed↗
PubMed1975

Carbohydrate absorption by chicks affected with the fatty liver and kidney syndrome.

Chicks with fatty liver and kidney syndrome (FLKS) were given oral doses of one of the following test solutions: water, glucose, maltose, starch. Plasma glucose concentration was measured during the four subsequent hours. All FLKS-affected chicks were hypoglycaemic before treatment. Although in some cases plasma glucose concentration increased slightly in the FLSK-chicks given water alone, significantly greater increases were invariably observed following the administration of carbohydrate to sick birds. Results obtained from dietary experiments in which starch was replaced by glucose in a ration causing high mortality from the syndrome revealed no beneficial effect due to the substitution. It was concluded that FLKS does not involve any major impairmant of carbohydrate digestion or absorption.

Animals↗
PubMed1975

Some aspects of lipid metabolism in fatty liver and kidney syndrome in chicks.

Various aspects of lipid metabolism were examined in broiler chicks affected with fatty liver and kidney syndrome (FLKS). Plasma free fatty acid concentrations were invariably elevated. Plasma triglyceride concentrations were increased amounts of triglyceride-rich lipoproteins. Lipoprotein lipase activity in adipose tissue was considerably reduced, but in heart tissue the enzyme activity was increased. Hepatic lipogenesis was reduced. Rates of oxidation of palmitic and succinic acids by liver, heart and kidney were normal. The increased oxidation rate of palmitic acid following the addition of carnitine was also normal. These findings indicate that elevated blood lipid levels are likely to be an important factor contributing to the development of fatty deposition, particularly in extrahepatic tissues.

Adipose Tissue↗
PubMed1975

Evidence for a lesion in carbohydrate metabolism in fatty liver and kidney syndrome in chicks.

Liver and kidney slices from chicks affected with fatty liver and kidney syndrome (FLKS) were incubated in vitro with a variety of non-carbohydrate precursors and their ability to form glucose was studied. The results show that the affected liver was unable to form significant quantities of glucose from the precursors (gluconeogenesis). Glycogen breakdown was also drastically reduced because the tissue was almost devoid of this carbohydrate store. Blood chemistry revealed no evidence of overall liver malfunction but reflected the consequences of lack of gluconeogenesis. In contrast, kidney gluconeogenic activity was significantly higher than in the controls, suggesting an attempt by this organ to offset the reduced hepatic capability. Attempts to restore activity in vitro were made by adding known cofactors of gluconeogenesis. Asmall but significant improvement resulted from addition of biotin to liver slices.

Alanine↗