B. A. Watkins

Influences of biotin deficiency and dietary trans-fatty acids on tissue lipids in chickens.

1. The combined effects of feeding hydrogenated fats and varying the levels of biotin and linoleate (18:2 omega 6) on polyunsaturated fatty acids were studied in the chicken. 2. Biotin deficiency signs were not exacerbated by feeding hydrogenated fats or by diets low in linoleate for 21 d. 3. Biotin deficiency resulted in proportionately higher levels of 18:2 omega 6 and gamma-linolenate (18:3 omega 6) in liver triglycerides, and lower levels of dihomo-gamma-linolenate (20:3 omega 6) in liver and heart phospholipids irrespective of the 18:2 omega 6 level in the diet. 4. Biotin deficiency did not alter arachidonate (20:4 omega 6) levels in tissue lipids at 21 d. 5. Feeding high levels of trans-18:1 isomers with adequate biotin led to reduced 20:3 omega 6 and 20:4 omega 6 levels in liver and heart phospholipids with compensatory increases in omega 3 fatty acids. 6. The trans-isomers of 18:1 were incorporated into several tissues of the chick. Incorporation was dependent on the levels fed. Very small amounts were incorporated into brain compared with other tissues when dietary trans-isomer levels were high, but were similar when dietary trans-isomer levels were low. The trans-18:1 isomers appear to be preferentially incorporated into phospholipids as opposed to triglycerides in heart and liver.

Eicosanoic fatty acid reduction in the tibiotarsus of biotin-deficient chicks

SummaryDay-old male broiler chicks (Hubbard x Hubbard) were fed a purified diet containing biotin at 0 μg/kg of diet (biotin-deficient) or 500 μg/kg of diet (biotin-adequate). Biotin-deficient (BD) chicks had decreased growth and feed efficiency and greater twisted leg and dermatitis symptoms than biotin-adequate (BA) chicks. Lipids in cortical bone of the tibiotarsi in BD chicks contained higher levels of linoleate, γ-linolenate, and α-linolenate. Prostaglandin precursors, dihomo-γ-linolenate (20∶3ω6), arachidonate (20∶4ω6), and eicosapentaenoate (20∶5ω3) were all lower in BD chicks compared with BA chicks. Periosteal bone appositional and bone formation rates, and percent new bone formation were reduced in the tibiotarsi of BD chicks. Anatomically there were two different bone modeling patters at the mid-diaphysis. The cortex was thickest laterally in chicks fed the BA diet and thickest medially in chicks fed the BD diet. The quantitative differences in bone growth and the distinct bone modeling patterns, coupled with corresponding decreases in PG precursors, suggest that biotin deficiency may alter bone growth and modeling via a PG-dependent mechanism.

Dietary biotin effects on desaturation and elongation of 14C-linoleic acid in the chicken

Abstract Newly hatched male chicks were fed a purified diet containing added biotin at 0 μg (biotin-deficient, BD) or 500 μg (biotin-adequate, BA) per kg for 26 days. The metabolism of 14 C-linoleic acid (59 μCi/μmol) was studied in vitro using liver slices (ca. 100 mg) from BD and BA chickens at 15 and 19 days. Less radioactivity was found in the desaturation and elongation products of linoleic acid in BD chickens compared with their BA controls at 15 days. A higher substrate level did not increase the production of arachidonic acid in vitro . Injection of 14 C-linoleate into BD and BA chickens at 15 and 26 days revealed that biotin-deficient chicks had lowered formation of elongation products at 15 and 26 days in vivo . These data would support a hypothesis that biotin participates in chain elongation of polyunsaturates in the chicken, however, an exact mechanism is lacking.

Progression of biotin deficiency and influence of reduced food intake on fatty acids in the chick

Abstract Experiments were conducted with chickens to study the progression of biotin deficiency on fatty acids in liver subcellular organelles and pair feeding effects on fatty acids in liver. In Experiment 1, fatty acid profiles of liver subcellular organelles were determined at 7, 21 and 26 days of age in relation to biotin status in male chicks fed biotin-deficient (BD) or biotin-adequate (BA) purified diets. Liver biotin content of newly hatched chicks was 2820 ng/g of wet tissue. Liver biotin levels in BD chicks (0 μg added biotin/kg diet) dropped to 655 ng/g at Day 7 and to 321 ng/g at Day 21. In BA chicks (500 μg added biotin/kg diet) liver biotin decreased to 1480 ng/g at Day 7 but increased to 2450 ng/g at Day 21. Fatty acid profiles determined by capillary gas-liquid chromatography were influenced by age and dietary biotin. In liver microsomes and mitochondria of BD chicks, linoleate and γ-linolenate were elevated over time. Levels of arachidonate were not affected by dietary biotin level, but decreases in dihomo-γ-linolenate suggest that elongation of γ-linolenate is impaired during biotin deficiency. In Experiment 2, the fatty acid compositions of total lipids (TLs) and phospholipids (PLs) in liver were measured in pair-fed (PF), BD and BA chicks at 21 days of age. Liver TLs and PLs of BD chicks contained higher levels of linoleate and γ-linolenate and lower levels of dihomo-γ-linolenate compared to PF and BA chicks. These data indicate that changes in fatty acid profiles of liver lipids result from biotin deficiency and not from reduced feed intake.

ALTERATIONS IN CHICK BONE GROWTH AND BONE TISSUE EICOSANOIC FATTY ACIDS: RELATIONSHIP TO BIOTIN STATUS, PAIR-FEEDING, AND TREADMILL EXERCISE

Abstract Day-old male broiler chicks were fed a balanced, purified diet ad libitum and trained to exercise on a motorized treadmill. At 10 days of age, chicks were fed purified diets containing one of three biotin levels and received either no exercise or 5 minutes of treadmill exercise per day. Diet and exercise regimens were followed until the chicks were 32 days old. Liver biotin levels at 32 days were decreased in chicks fed biotindeficient (BD) diets compared with chicks fed biotin-adequate (BA) diets and pair-fed (PF) chicks (737 ng/g liver tissue vs. 1309 ng/g and 1098 ng/g, respectively). Chicks fed BD diets had poorer feed conversion ratios, reduced average weight gains, and shortened tibiotarsi compared with PF chicks and chicks fed BA diets. Periosteal bone appositional rate, bone formation, and percent cortical bone were increased in chicks fed BD diets compared with PF chicks. Levels of 16:0 and 18:0 fatty acids were higher but levels of 20:4ω6 and 22:4ω6 were lower in cortical bone phospholipids (PLs) of PF chicks compared with chicks fed BD and BA diets. There were no statistically significant effects due to treadmill exercise on any of the measurements made. The results indicate that chicks fed BD diets have decreased longitudinal bone growth and increased radial bone growth compared to chicks pair-fed a BA diet.

Dietary trans 181 isomers and biotin depletion altered mitochondrial and microsomal lipid compositions in chick heart and liver

Abstract To study the effects of dietary trans -181 (t-181) and biotin depletion on the fatty acid compositions in liver and heart phospholipids (PL), and in mitochondria and microsomes chicks were fed a purified basal diet containing one of three lipid mixtures. All diets fed were adequate in biotin (400 μ g) for the first 14 days, then biotin was withdrawn from the diet for half of the chicks for the last 14 days resulting in a 3×2 (lipid × biotin) factorial arrangement of treatments. The lipid mixtures were prepared to contain as a percent of the diet: A, 1.4% linoleate + 0% t-181; B, 1.4% linoleate + 1.2% t-181; C, 0.23% linoleate + 2.0% t-181. Argentation thin-layer chromatography and gas-liquid chromatography were used to determine fatty acid compositions. Feeding diet C with no biotin resulted in the lowest (p ω 6 in all cases, except in mitochondria, and decreased the level of 203 ω 6 in heart PL. Dietary t-181 and biotin depletion both suppressed the levels of 204 ω 6 in all cases. The product/ substrate ratio 204 ω 6/182 ω 6 was decreased due to the presence of t-181 in the diet and/or biotin depletion. The data revealed that both dietary t-181 and biotin can influence linoleate metabolism by altering fatty acid profiles in chicken tissues.