scholarly journals Pentose cycle and reducing equivalents in rat mammary-gland slices

1972 ◽  
Vol 128 (4) ◽  
pp. 879-899 ◽  
Author(s):  
Joseph Katz ◽  
P. A. Wals
Keyword(s):  
Amino Acids ◽  
Fatty Acids ◽  
Mammary Gland ◽  
Fatty Acid ◽  
Specific Radioactivity ◽  
Acid Synthesis ◽  
Glucose Carbon ◽  
Rat Mammary Gland ◽  
Reducing Equivalents

1. Slices of mammary gland of lactating rats were incubated with glucose labelled uniformly with 14C and in positions 1, 2, 3 and 6, and with 3H in all six positions. Glucose carbon atoms are incorporated into CO2, fatty acids, lipid glycerol, the glucose and galactose moieties of lactose, lactate, soluble amino acids and proteins. C-3 of glucose appears in fatty acids. The incorporation of 3H into fatty acids is greatest from [3-3H]glucose. 3H from [5-3H]glucose appears, apart from in lactose, nearly all in water. 2. The specific radioactivity of the galactose moiety of lactose from [1-14C]- and [6-14C]-glucose was less, and that from [2-14C]- and [3-14C]-glucose more, than that of the glucose moiety. There was no randomization of carbon atoms in the glucose moiety, but it was extensive in galactose. 3. The pentose cycle was calculated from 14C yields in CO2 and fatty acids, and from the degradation of galactose from [2-14C]glucose. A method for the quantitative determination of the contribution of the pentose cycle, from incorporation into fatty acids from [3-14C]glucose, is derived. The rate of the reaction catalysed by hexose 6-phosphate isomerase was calculated from the randomization pattern in galactose. 4. Of the utilized glucose, 10–20% is converted into lactose, 20–30% is metabolized via the pentose cycle and the rest is metabolized via the Embden–Meyerhof pathway. About 10–15% of the triose phosphates and pyruvate is derived via the pentose cycle. 5. The pentose cycle is sufficient to provide 80–100% of the NADPH requirement for fatty acid synthesis. 6. The formation of reducing equivalents in the cytoplasm exceeds that required for reductive biosynthesis. About half of the cytoplasmic reducing equivalents are probably transferred into mitochondria. 7. In the Appendix a concise derivation of the randomization of C-1, C-2 and C-3 as a function of the pentose cycle is described.

scholarly journals Synthesis of fatty acids in the perfused mouse liver

1974 ◽  
Vol 142 (3) ◽  
pp. 611-618 ◽  
Author(s):  
D. Michael W. Salmon ◽  
Neil L. Bowen ◽  
Douglas A. Hems
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
De Novo ◽  
Saturated Fatty Acids ◽  
Carbon Sources ◽  
Acid Synthesis ◽  
Hepatic Glycogen ◽  
Total Rate ◽  
Glucose Carbon

1. Fatty acid synthesis de novo was measured in the perfused liver of fed mice. 2. The total rate, measured by the incorporation into fatty acid of3H from3H2O (1–7μmol of fatty acid/h per g of fresh liver), resembled the rate found in the liver of intact mice. 3. Perfusions with l-[U-14C]lactic acid and [U-14C]glucose showed that circulating glucose at concentrations less than about 17mm was not a major carbon source for newly synthesized fatty acid, whereas lactate (10mm) markedly stimulated fatty acid synthesis, and contributed extensive carbon to lipogenesis. 4. The identification of 50% of the carbon converted into newly synthesized fatty acid lends further credibility to the use of3H2O to measure hepatic fatty acid synthesis. 5. The total rate of fatty acid synthesis, and the contribution of glucose carbon to lipogenesis, were directly proportional to the initial hepatic glycogen concentration. 6. The proportion of total newly synthesized lipid that was released into the perfusion medium was 12–16%. 7. The major products of lipogenesis were saturated fatty acids in triglyceride and phospholipid. 8. The rate of cholesterol synthesis, also measured with3H2O, expressed as acetyl residues consumed, was about one-fourth of the basal rate of fatty acid synthesis. 9. These results are discussed in terms of the carbon sources of hepatic newly synthesized fatty acids, and the effect of glucose, glycogen and lactate in stimulating lipogenesis, independently of their role as precursors.

scholarly journals Sterol regulatory element binding protein and dietary lipid regulation of fatty acid synthesis in the mammary epithelium

2010 ◽  
Vol 299 (6) ◽  
pp. E918-E927 ◽  
Author(s):  
Michael C. Rudolph ◽  
Jenifer Monks ◽  
Valerie Burns ◽  
Meridee Phistry ◽  
Russell Marians ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Mammary Gland ◽  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
De Novo ◽  
Regulatory Element ◽  
Acid Synthesis ◽  
De Novo Lipogenesis ◽  
Mrna Levels ◽  
Sterol Regulatory Element

The lactating mammary gland synthesizes large amounts of triglyceride from fatty acids derived from the blood and from de novo lipogenesis. The latter is significantly increased at parturition and decreased when additional dietary fatty acids become available. To begin to understand the molecular regulation of de novo lipogenesis, we tested the hypothesis that the transcription factor sterol regulatory element binding factor (SREBF)-1c is a primary regulator of this system. Expression of Srebf1c mRNA and six of its known target genes increased ≥2.5-fold at parturition. However, Srebf1c-null mice showed only minor deficiencies in lipid synthesis during lactation, possibly due to compensation by Srebf1a expression. To abrogate the function of both isoforms of Srebf1, we bred mice to obtain a mammary epithelial cell-specific deletion of SREBF cleavage-activating protein (SCAP), the SREBF escort protein. These dams showed a significant lactation deficiency, and expression of mRNA for fatty acid synthase ( Fasn), insulin-induced gene 1 ( Insig1), mitochondrial citrate transporter ( Slc25a1), and stearoyl-CoA desaturase 2 ( Scd2) was reduced threefold or more; however, the mRNA levels of acetyl-CoA carboxylase-1α ( Acaca) and ATP citrate lyase ( Acly) were unchanged. Furthermore, a 46% fat diet significantly decreased de novo fatty acid synthesis and reduced the protein levels of ACACA, ACLY, and FASN significantly, with no change in their mRNA levels. These data lead us to conclude that two modes of regulation exist to control fatty acid synthesis in the mammary gland of the lactating mouse: the well-known SREBF1 system and a novel mechanism that acts at the posttranscriptional level in the presence of SCAP deletion and high-fat feeding to alter enzyme protein.

scholarly journals Transacylation as a chain-termination mechanism in fatty acid synthesis by mammalian fatty acid synthetase. Synthesis of butyrate and hexanoate by lactating cow mammary gland fatty acid synthetase

1980 ◽  
Vol 186 (1) ◽  
pp. 287-294 ◽  
Author(s):  
J K Hansen ◽  
J Knudsen
Keyword(s):  
Fatty Acids ◽  
Mammary Gland ◽  
Fatty Acid ◽  
Fatty Acid Synthetase ◽  
Short Chain Fatty Acids ◽  
Acid Synthesis ◽  
Chain Termination ◽  
Short Chain ◽  
Esterified Fatty Acids ◽  
A Chain

1. Purified cow mammary gland fatty acid synthetase synthesized long-chain unesterified and short-chain esterified fatty acids. 2. A direct relationship was observed between the amount of short-chain products synthesized and the concentration of acetyl-CoA in the incubation medium. 3. The short-chain products were identified as butyryl-CoA and hexanoyl-CoA. 4. Inhibition of the terminating thioester hydrolase of the fatty acid synthetase complex with phenylmethanesulphonyl fluoride did not inhibit the synthesis of short-chain products. 5. It is suggested that the synthesis of short-chain fatty acids involves the reverse of the ‘loading’ reaction.

FATTY ACID AND GLYCERIDE GLYCEROL SYNTHESIS FROM GLUCOSE DURING HIGH RATES OF GLUCOSE UPTAKE IN THE INTACT RAT

1965 ◽  
Vol 43 (4) ◽  
pp. 437-450 ◽  
Author(s):  
A. S. W. de Freitas ◽  
Florent Depocas
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Glucose Uptake ◽  
Fatty Acid Synthesis ◽  
Acid Synthesis ◽  
Component Fatty Acid ◽  
Rat Tissues ◽  
Total Lipids ◽  
Glucose Carbon ◽  
Total Glucose

The extent of incorporation of glucose carbon into total lipids and component fatty acid, neutral glyceride glycerol, and phosphoglyceride glycerol moieties of carcass, liver, and epididymal tissue has been measured in 20 rats under conditions of constant plasma glucose concentration and specific activity. Rates of fatty acid synthesis from glucose and absolute rates of synthesis have also been estimated. Each rat received 750 mg glucose per hour by continuous infusion. The incorporation of glucose carbon into carcass, liver, and epididymal fat was, respectively, 6.2, 0.75, and 0.06% of the total glucose carbon taken up by the rat tissues. Fifty percent of the C14 found in total lipids of carcass and liver was in the fatty acid fraction. Corresponding glyceride glycerol moieties contained approximately 40% of the total activity. The low level of incorporation of glucose carbon into fatty acids and glyceride glycerol indicates that lipogenesis from glucose can only account for a small proportion of the total glucose taken up by the tissues, even at high rates of glucose uptake. Rates of synthesis from glucose of carcass and liver fatty acids were estimated as 1.5 and 0.11 mmoles fatty acid per tissue per day respectively, with corresponding half-lives of 57 and 7.6 days. Absolute rates of fatty acid synthesis were estimated as 2.6 and 0.55 mmoles fatty acid per day for carcass and liver tissue respectively, with corresponding half-lives of 34 and 4.6 days.

scholarly journals Transacylation as a chain-termination mechanism in fatty acid synthesis by mammalian fatty acid synthetase. Synthesis of medium-chain-length (C8-C12) acyl-CoA esters by goat mammary-gland fatty acid synthetase

1982 ◽  
Vol 202 (1) ◽  
pp. 139-143 ◽  
Author(s):  
J Knudsen ◽  
I Grunnet
Keyword(s):  
Fatty Acids ◽  
Mammary Gland ◽  
Fatty Acid ◽  
Fatty Acid Synthetase ◽  
Acid Synthesis ◽  
Medium Chain ◽  
Medium Chain Fatty Acids ◽  
Medium Chain Length ◽  
A Chain ◽  
Chain Fatty Acids

1. Ruminant mammary-gland fatty acid synthetases can, in contrast with non-ruminant mammary enzymes, synthesize medium-chain fatty acids. 2. Medium-chain fatty acids are only synthesized in the presence of a fatty acid-removing system such as albumin, beta-lactoglobulin or methylated cyclodextrin. 3. The short- and medium-chain fatty acids synthesized were released as acyl-CoA esters from the fatty acid synthetase.

THE EFFECT OF PROLACTIN AND GROWTH HORMONE ON FATTY ACID SYNTHESIS BY PREGNANT MOUSE MAMMARY GLAND IN ORGAN CULTURE

1972 ◽  
Vol 53 (2) ◽  
pp. 311-321 ◽  
Author(s):  
D. Y. WANG ◽  
R. C. HALLOWES ◽  
J. BEALING ◽  
C. R. STRONG ◽  
R. DILS
Keyword(s):  
Fatty Acids ◽  
Growth Hormone ◽  
Mammary Gland ◽  
Fatty Acid ◽  
Organ Culture ◽  
Fatty Acid Synthesis ◽  
Acid Synthesis ◽  
Pregnant Mouse ◽  
Mouse Mammary Gland ◽  
Gas Liquid Chromatography

SUMMARY The effect of various hormones on the incorporation of [14C]acetate into the fatty acids of pregnant mouse mammary gland explants in organ culture was studied. Of the hormones insulin (I), ovine prolactin (P), bovine growth hormone (GH) and cortisol (F) tested singly, only insulin stimulated fatty acid synthesis. There was synergism between cortisol or prolactin with insulin. The greatest stimulation in fatty acid synthesis occurred when explants were incubated in a medium containing either I + F + P or I + F + GH. Analysis by radio-gas-liquid chromatography of the fatty acids synthesized by explants after 14C labelling, showed that the pattern of fatty acids formed in the presence of I + F was distinctly different from that produced in the presence of I + F + P or I + F + GH. In the presence of I + F, the pattern of fatty acids resembled that found in mouse adipose tissue, whilst with I + F + P or I + F + GH the pattern resembled that of mouse milk fat. Synthesis of RNA was essential for the stimulation of fatty acid synthesis in explants incubated in medium containing I + F + P or I + F + GH. Results obtained when DNA synthesis was blocked with mitomycin C suggest that mitosis is important for the induction of milk-fatty acid synthesis. Puromycin had no effect for up to 8 h on explants which had been previously cultured in medium containing I + F, I + F + P or I + F + GH. This suggests a slow turnover rate of the enzymes involved in the synthesis of milk fatty acids.

Responses in rumen fermentation and milk-fat secretion in cows receiving low-roughage diets supplemented with protected tallow

1974 ◽  
Vol 41 (2) ◽  
pp. 165-173 ◽  
Author(s):  
J. E. Storry ◽  
P. E. Brumby ◽  
A. J. Hall ◽  
V. W. Johnson
Keyword(s):  
Fatty Acids ◽  
Mammary Gland ◽  
Fatty Acid ◽  
Dietary Supplement ◽  
Fatty Acid Synthesis ◽  
Milk Fat ◽  
Acid Synthesis ◽  
Rumen Fermentation ◽  
Total Fatty Acids ◽  
Friesian Cows

SummaryThe effects on rumen fermentation and milk-fat secretion of a dietary supplement of protected tallow given to 4 Friesian cows established on a low-roughage ration and with depressed milk fat is reported. The ratios of acetate to propionate in the rumen were unaffected by the supplement and remained typical of those associated with low-roughage diets in that the proportion of propionate was increased. The supplement produced almost complete recoveries in yield and content of milk fat without any increase in intramammary fatty-acid synthesis. The recoveries were due to transfer of about 20% of the total fatty acids of the tallow supplement. These results are discussed in relation to the effects of low-roughage diets on milk-fat secretion and it is concluded that in the ‘low-fat syndrome’ the capacity of the mammary gland to absorb preformed fatty acids is not impaired.

scholarly journals Rat mammary-gland acetyl-coenzyme A carboxylase. Interaction with milk fatty acids

1970 ◽  
Vol 118 (4) ◽  
pp. 645-657 ◽  
Author(s):  
A. L. Miller ◽  
Mary E. Geroch ◽  
H. Richard Levy
Keyword(s):  
Fatty Acids ◽  
Mammary Gland ◽  
Complex Mixture ◽  
Acid Synthesis ◽  
Acetyl Coa Carboxylase ◽  
High Concentration ◽  
Acetyl Coa ◽  
Milk Fatty Acids ◽  
Low Concentrations ◽  
Rat Mammary Gland

1. Highly purified rat mammary-gland acetyl-CoA carboxylase was inhibited by milk obtained from rats 12h after their young were weaned. 2. All the inhibitory activity was found in the particulate fraction (R105) obtained on centrifuging the milk. It could be extracted from milk fraction R105 with acetone and identified as a complex mixture of non-esterified fatty acids, present in high concentration (nearly 10mm) in the milk. 3. Inhibition of acetyl-CoA carboxylase was observed at low concentrations (0.2–20μm) of several of these fatty acids when fresh fully active enzyme was used. Enzyme that had been partly inactivated by aging, or by storing in the absence of citrate, was stimulated by low concentrations but inhibited by high concentrations of fatty acids. 4. Various experiments suggested that fatty acids produce irreversible inactivation of acetyl-CoA carboxylase. 5. The effects of palmitoyl-CoA on mammary-gland acetyl-CoA carboxylase were found to resemble those of fatty acids, except that palmitoyl-CoA was effective at lower concentration. 6. The effect of milk fraction R105 was tested on six other enzymes previously shown to decline to various extents after weaning. Although several of these enzymes were affected by unfractionated milk fraction R105, none was significantly inhibited by the acetone extract or by low concentrations of lauric acid. 7. The findings are consistent, both qualitatively and quantitatively, with a regulatory mechanism whereby milk fatty acids shut off fatty acid synthesis in the mammary gland after weaning by inhibiting acetyl-CoA carboxylase.

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