Effects Of Biotin Deficiency Research Articles

Biotin effects on fatty acid synthesis in chicks.

Data are summarized from several papers on the effects of biotin deficiency on lipid metabolism, especially fatty acid synthesis, in chicks. Biotin deficiency inhibits in vivo lipogenesis and hepatic acetyl-CoA carboxylase (ACC) activity. Although acetate incorporation into fatty acids is inhibited in biotin-deficient chicks, malonate incorporation is not inhibited. In fact, dietary malonic acid stimulates lipogenesis during biotin deficiency as measured by total carcass fatty acid content. Biotin-deficient chicks exhibit altered hepatic and whole body fatty acid composition in comparison with control chicks. The deficiency results in an increased proportion of the 16-carbon to 18-carbon fatty acids, and the most striking increase is for palmitoleic (16:1) acid. Biotin deficiency increases the relative incorporation of palmitate and stearate into phospholipids and decreases the relative incorporation of these fatty acids into triglycerides. Finally, mercury stimulates lipogenesis in biotin-deficient, but not in control, chicks by an unknown mechanism.

Effects of Biotin Deficiency on Polyunsaturated Fatty Acid Metabolism in Rats

The effects of biotin and protein-calorie deficiency on metabolism of liver phospholipids in rats were determined. Weanling male Long-Evans rats were fed ad libitum a biotin-deficient (0.4 µg biotin/g diet) or a biotin-adequate (2.4 µg biotin/g diet) diet for 49 days. A pair-fed group was fed biotin-adequate diet but restricted to the amount consumed by biotin-deficient rats. The effects of these diets on food intake, weight gain, biotin content of serum and fatty acid composition of liver phospholipid were determined. Growth and food intake were significantly depressed in biotin-deficient and pair-fed rats. Biotin concentration in serum was significantly reduced in biotin-deficient and in pair-fed rats. Biotin deficiency caused significantly increased concentrations of 15:0, 17:0 and total odd-chain fatty acids in liver phospholipids. Combined biotin and protein-calorie deficiency and protein-calorie deficiency alone caused significantly increased concentrations of 18:2ω6 in liver phospholipids. Biotin deficiency caused significant reduction in liver phospholipid 20:3ω6. Reduced arachidonic acid (20:4ω6) level was due to combined biotin protein-calorie deficiency. Protein-calorie deficiency alone was primarily responsible for reduced levels of 22:5ω6. Biotin deficiency alone caused significant increases in liver phospholipids 18:3ω3 and 22:6ω3.

The effect of biotin deficiency and dietary protein content on lipogenesis, gluconeogenesis and related enzyme activities in chick liver.

Chicks were given biotin-deficient diets containing either suboptimal (low) or supraoptimal (high) concentrations of protein from 1-d-old until they were used during their fourth week of life. The low-protein diet predisposed chicks to develop fatty liver and kidney syndrome and the high-protein diet to develop classical biotin deficiency signs. Two other groups, as controls, received biotin-supplemented rations. Low dietary protein increased lipogenesis by isolated hepatocytes but had little effect on gluconeogenesis compared to high dietary protein. Low dietary protein decreased activities of hepatic isocitrate dehydrogenase (EC 1.1.1.42), fructose-1,6-bisphosphatase (EC 3.1.3.11) and glucose-6-phosphatase (EC 3.1.3.9; GP) and increased activities of fatty acid synthase (FAS), citrate cleavage enzyme (EC 4.1.3.8; CCE) and malate dehydrogenase (decarboxylating) (EC 1.1.1.39). When biotin deficiency was superimposed, the rate of lipogenesis by isolated hepatocytes (from fed birds) was decreased. Gluconeogenesis from lactate and glycerol was also depressed. Activity of GP was further decreased by biotin deficiency on the low-protein regimen and FAS and CCE were further increased. PK activity was increased by biotin deficiency.

Effects of biotin deficiency on serum proteins and plasma amino acids.

In biotin-deficient rats, a decrease of total proteins, attributable to a decrease of albumin and alpha1-globulin fractions, a decrease of the pre-beta-lipoproteins and an increase of the alpha-lipoproteins, was observed, together with a rise of total amino acids. Such a situation may be related to the influence of biotin on the synthesis of RNA and proteins.

Effects of Biotin Deficiency on Growth, Morphology and Sporulation in Bacillus megaterium NCIB7581

Summary: Bacillus megaterium strain ncib7581 grew at 30 °C in a simple chemically defined medium without biotin. At 37 °C the bacteria grew more slowly in the same medium and were deformed, especially during the earlier stages of growth, as filaments or with swollen ends. Addition of biotin restored the normal appearance and rate of growth at 37 °C. The organisms synthesized more biotin at 30 °C (11 ng 1−1 in a stationary phase culture) than at 37 °C (1·4 ng 1−1). Addition of either aspartate, malate, fumarate or acetate to minimal medium also restored normal morphology and accelerated the growth rate in biotin-deficient medium at 37 °C. Neither acetate nor aspartate increased synthesis of biotin at 37 °C. After growth in medium containing only 0·2% glucose almost every organism in the culture was able to sporulate at 30 °C whether or not biotin was added. About 50 times fewer spores were formed at 37 °C without biotin; the yield of spores increased about 20-fold at this temperature when biotin, aspartate or dipicolinate was added.

Effect of biotin deficiency on some properties of Staphylococcus aureus isolates from humans and other animals

Staphylococcus aureus isolates from humans and other animals were grown in biotin assay medium containing 12 mug of biotin per liter and compared to isolates from the same sources grown concurrently in medium containing adequate biotin. The two cultures were tested for production of coagulase, phosphatase, and fibrinolysin enzymes and for responses to various antimicrobial agents and bacteriophages. Organisms grown in biotin-deficient medium produced less phosphatase; coagulase and fibrinolytic activity was reduced, and they were more susceptible to antimicrobial agents than were normal organisms, but phage susceptibility was not greatly affected.

Effect of Biotin Deficiency on the Catabolism of Linoleate in the Rat

Effect of Biotin Deficiency on the Catabolism of Linoleate in the Rat

Glycogen synthesis in biotin-deficient rat liver.

SummaryThe effect of biotin deficiency on the in vivo synthesis and the level of glycogen in livers of rats during various stages of the deficiency was investigated. A glycogenic dose of labeled glucose was administered by stomach tube to 24-hr fasted control and deficient animals and glycogen synthesis in liver was measured after 3 hr. The deficient animals which were on the basal diet for 6 weeks were able to synthesize the same amount of hepatic glycogen as that by the controls. A marked reduction in the level of glycogen in the livers of deficient animals compared to controls was observed during the day but there was no change in the level between the two groups when examined during the night at all stages of biotin deficiency. The observed decrease during the day was the result of diurnal variation. The results show that in the rat the synthesis of hepatic glycogen is not impaired in biotin deficiency.

Depletion of biotin from brain and liver in biotin deficiency.

The effects of biotin deficiency on the metabolism of glucose (Bhagavan, Coursin and Dakshinamurti, 1965; Bhagavan, Maruyama and Coursin, 1967; Bhagavan, Coursin and Stewart, 1969) and central nervous system function (Bhagavan, Stewart, Dakshinamurti and Coursin, 1966; Stewart, Bhagavan, Coursin and Dakshinamurti, 1966; Stewart, Bhagavan and Coursin, 1967a, b; 1968) have already been reported. In a study of the biochemical changes in the brain and other tissues of the rat in biotin deficiency, the depletion of biotin from the brain and liver during the course of the deficiency has been followed. We found that while the liver lost over 90 per cent of its biotin, the depletion from the brain was only about 50 per cent after 8 weeks on the deficient diet. These data comprise the present report.

Lipogenesis in biotin deficiency.

The effect of biotin deficiency on the lipid composition of rat liver, epididymal fat pad, and carcass was investigated. The incorporation of acetate-1-14C into liver lipids, the concentration of liver acetyl-CoA, and the in vitro activities of mitochondrial and supernatant pathways were also studied in biotin-deficient and pair-weighed controls.Biotin-deficient rats had higher levels of carcass cholesterol, though there was no significant difference in liver cholesterol levels between deficient and control rats. These results indicate that the malonyl-CoA pathway proposed for cholesterol synthesis may not be the major route for cholesterogenesis.The reduction in esterified fatty acids of adipose tissue and carcass of biotin-deficient rats was greater than that of liver suggesting that biotin deficiency might have a more marked effect on the metabolism of the adipose tissue than of liver.

Effect of dietary biotin on fatty acid composition of the silkworm, Bombyx mori L.

The effect of biotin deficiency on lipid metabolism of larvae of the silkworm, Bombyx mori, was investigated. Biotin deficiency resulted in a significant decrease in fatty acid content of the larva. Oleic acid content decreased conspicuously in larvae receiving biotin-free diet. A little decrease was found in the amount of palmitic and stearic acids, whereas the amount of palmitoleic acid increased with biotin deficiency. No significant change was found for other fatty acids. The minimal optimal level of biotin for larval growth was 0·2 μg/g of dry diet, which also did not result in any alteration of fatty acid composition. The rôle of biotin in silkworm nutrition in relation to fatty acid synthesis is briefly discussed.

The Effects of Biotin Deficiency Upon Oviduct Growth and the Water-Soluble Oviduct Proteins of the Female Chick Treated with Gonadal Hormones

ANY information concerning the composition of the oviduct in the fowl is of value considering the importance of this organ in reproduction. As the most important function of the oviduct in the fowl is its implication in protein deposition in the egg any information on its protein composition is of interest.Mistri and Dakshinamurti (1964) have shown that protein synthesis is markedly reduced in biotin-deficient animals. They showed that this reduction in the synthesis of protein was probably the result of a decreased formation of ribonucleic acid, due to an alteration in the nature of soluble ribonucleic acid. Hertz et al. (1943, 1949) through investigations into avidin formation in the avian oviduct obtained evidence to suggest that the avidin-biotin complex might play a role in the physiology of avian reproduction. In the fowl there is a rapid increase in oviduct size just prior to lay as a result of stimulation .

Aspects of Liver Lipid Metabolism in the Biotin-deficient Rat

The effect of biotin deficiency on some aspects of lipid metabolism in the liver of female and male rats was investigated. No significant difference was found either in total lipid content or in lipid composition in the liver of biotin-deficient rats of both sexes when compared with biotin-treated controls. Significant changes were observed in the percentage fatty acid composition, namely more 16:1 and 18.2 and less 18:0 fatty acid were found in total liver lipids of the biotin-deficient rats. The incorporation of 32P into liver phospholipids in intact biotin-deficient rats was not altered. The rate of incorporation in vitro of acetate-1-14C into total liver lipids was significantly decreased in biotin deficiency. These data appear to indicate that biotin deficiency in the rat may result in some changes in liver lipid metabolism.

The effect of biotin deficiency on the biosynthesis of the fatty acids in a blowfly, Aldrichina grahami during metamorphosis under aseptic conditions.

(1967). The Effect of Biotin Deficiency on the Biosynthesis of the Fatty Acids in a Blowfly, Aldrichina Grahami During Metamorphosis Under Aseptic Conditions. Archives Internationales de Physiologie et de Biochimie: Vol. 75, No. 1, pp. 65-76.

Relationships of biotin to ethionine-induced fatty liver

The effect of ethionine on the biotin content of liver as well as the effect of biotin deficiency on the development of fatty liver and on lipogenesis in vitro in ethionine-treated rats are reported. The amount of biotin in the livers of ethionine-treated rats was lower than in the controls. In biotin-deficient rats, the development of ethionine-induced fatty liver was inhibited. The incorporation of acetate-1-C 14 into total lipids was decreased in slices from livers of biotin-deficient rats and also from livers of ethionine-treated rats fed on a biotin-free and on a biotin-supplemented diet. The data suggest that there may be a relationship between biotin and ethionine-induced fatty infiltration of the liver.

Effect of Biotin Deficiency on Escape and Avoidance Learning in Rats

The effect of biotin deficiency on the ability of Sprague-Dawley rats to acquire conditioned avoidance and escape reactions was investigated. Avoidance learning was impaired with both 5.0-second and 2.0-second intervals between conditional and unconditional stimuli. Escape learning was not affected, suggesting that the defect in avoidance learning was not due to motor impairment. Behavioral and biochemical evidence suggests that effects of the deficiency on the central nervous system may be expected.

Effects of biotin deficiency on pyruvate metabolism.

SummaryBiotin-deficient animals show a reduction in incorporation of pyruvate-214C into glucose with progressive onset of the deficiency. The oxidation and utilization of pyruvate is reduced by 50 per cent. The pyruvate carboxylase activity was greatly decreased whereas PEP carboxykinase activity was found to be slightly decreased in biotin deficiency. In vitro administration of biotin to biotin-deficient animals almost restored the pyruvate carboxylase activity and PEP carboxykinase activity was only slightly altered. In addition, it is observed that pyruvate carboxylase can be extracted from the mitochondria by homogenizing at room temperature and is quite stable under these conditions.

In vivo oxidation of glucose-C 14 to C 14O 2 in biotin deficiency

The effect of biotin deficiency on the in vivo oxidation of glucose-C 14 labeled in various positions has been studied in the rat. In all cases there is more C 14O 2 output by the biotin-deficient animal as compared with controls. Incorporation of glucose-C 14 into liver glycogen is also reduced markedly in biotin deficiency. These findings are in agreement with the role of biotin in CO 2 fixation reactions.

Biochemistry of Biotin

Publisher Summary This chapter focuses on a host of indirect effects observed in biotin deficiency and offers possible explanations for some of these findings. The discussions primarily deal with the results on certain aspects of biotin in intermediary metabolism. The chapter discusses some of the recent data on the biochemistry of biotin. It also discusses the characterization of five biotin enzymes. The effects of biotin deficiency are felt in very many reactions in the intact organism. Biotin has been implicated to play a role in the deamination of aspartate, serine, and threonine in bacteria in the deamination of serine in animals in the reductive carboxylation of pyruvate by the malic enzyme, in the carboxylation of phosphoenolpyruvate by the phosphoenolpyruvate carboxykinase in carbamylation reactions, in tryptophan metabolism, in purine synthesis, in protein synthesis, and in carbohydrate metabolism. As avidin specifically binds biotin, biotin enzymes do not directly mediate these reactions and the effects observed are indirect results of biotin deficiency.

Effects of biotin deficiency on carbohydrate metabolism

The interrelationship between insulin deficiency and biotin deficiency and its relation to carbohydrate metabolism has been studied. Severe biotin-deficient animals show no change in blood sugar levels. Administration of equal amount of anti-insulin serum increased the blood sugar levels to the same extent in normal and biotin-deficient animals, indicating insulin levels were unaltered in biotin deficiency. Oxidation of C 14-glucose to CO 2 is also unaltered. C 14O 2 incorporation into glucose is slightly decreased in biotin-deficient animals. Anti-insulin serum treated biotin-deficient animals show three- to fourfold increase in C 14O 2 incorporation into glucose. Incorporation of 2-C 14-acetate and 2-C 14-propionate into glucose, glycogen, and CO 2, and C 14O 2 into glucose and glycogen is unaltered in biotin-deficient animals. However, there is a significant decrease in the incorporation of these substrates into long-chain fatty acids.